Showing papers in "Food & Nutrition Research in 2022"
TL;DR: In healthy, well-nourished children of Western populations, there is probably a causal relationship between a high-protein intake in early childhood – particularly protein of animal origin – and higher BMI later in childhood, with consistent findings across cohort studies.
Abstract: Objectives The aim of this study was to examine the evidence for an association between the dietary protein intake in children and the growth and risk of overweight or obesity up to 18 years of age in settings relevant for the Nordic countries. Methods We searched MEDLINE, Embase, Cochrane Central Register of Controlled Trials, and Scopus up to February 26, 2021 for randomized controlled trials (RCTs) or prospective cohort studies assessing for protein intake from foods (total and from different sources) in children. The outcomes include weight, height/length, adiposity indices, and/or risk of overweight and/or obesity. The risk of bias was evaluated with instruments for each respective design (Cochrane’s Risk of Bias 2.0 and RoB-NObS). A meta-analysis of five cohort studies was performed. The evidence was classified according to the criteria of the World Cancer Research Fund. Results The literature search resulted in 9,132 abstracts, of which 55 papers were identified as potentially relevant. In total, 21 studies from 27 publications were included, of which five were RCTs and 16 were cohort studies. The RCTs found generally null effects of high-protein intake in infants on weight gain, nor that lower protein diets negatively affected growth. All included RCTs had some concern regarding the risk of bias and were limited by small sample sizes. Total protein intake and BMI were assessed in 12 cohorts, of which 11 found positive associations. The meta-analysis revealed a pooled effect estimate of 0.06 (95% CI 0.03, 0.1) kg/m2 BMI per one E% increment in total protein (I2 = 15.5). Therefore, the evidence for a positive relationship between total protein intake and BMI was considered probable. Furthermore, there was probable evidence for an association between higher intake of animal protein and increased BMI. There was limited, suggestive evidence for an effect of total protein intake and higher risk of overweight and/or obesity, while no conclusions could be made on the associations between animal vs. plant protein intake and risk of overweight and/or obesity. Discussion In healthy, well-nourished children of Western populations, there is probably a causal relationship between a high-protein intake in early childhood (≤ 18 months) – particularly protein of animal origin – and higher BMI later in childhood, with consistent findings across cohort studies. A lack of RCTs precluded a stronger grading of the evidence.
14 citations
TL;DR: CLA potentially contributed to ameliorating hepatic steatosis in OB mice via modulating liver inflammation, intestinal permeability, and gut microbiota, which suggests CLA is more suitable for people with obesity or overweight.
Abstract: Background Conjugated linoleic acid (CLA) is an effective supplement for reducing fat mass, but its effect on hepatic steatosis remains controversial. Objective This study aims to evaluate the effect of CLA on liver fat accumulation, inflammation, gut microbiome, and intestinal barrier integrity. Design Wild-type (WT) mice and ob/ob (OB) mice were randomly divided into four groups according to the treatment with/without 1% CLA: WT, WT mice treated with CLA (WT-CLA), OB, and OB mice treated with CLA (OB-CLA). Lipid metabolism and hepatic fat accumulation were evaluated by changes in histological and biochemical parameters. Gene expressions related to liver inflammation and intestinal barrier integrity were examined. The effect of CLA on the gut microbiota population was investigated. Results The body weight, fatty tissue mass, and serum lipid levels of the WT-CLA group and OB-CLA group were separately lower than those of the WT group and OB group, but the livers of the WT-CLA group had more fatty lipids, higher triglyceride properties, and saturated fatty acid (FA) composition than those of the WT group, which was contrary to the effect of CLA on OB mice. Real time quantitative PCR results showed that CLA increased hepatic inflammation and intestinal permeability in the WT mice, while it significantly decreased the mRNA expression of liver TNF-α, IFN-γ, and IL-1β and markedly ameliorated intestinal tight junction proteins in the OB mice. The gut microbiota testing indicated a higher abundance of beneficial bacteria (e.g., Lachnoclostridium, Roseburia, Dubosiella, Oscillibacter, and Anaerostipes) and a lower abundance of pro-inflammatory bacteria (e.g., Tyzzerella and Alistipes) in the OB-CLA group than those of the OB group. Correlation analysis suggested that gut microbiota correlated with liver inflammation, intestinal permeability, and hepatic FA composition. Conclusion CLA potentially contributed to ameliorating hepatic steatosis in OB mice via modulating liver inflammation, intestinal permeability, and gut microbiota, which suggests CLA is more suitable for people with obesity or overweight.
13 citations
TL;DR: It is found that the lighter the fermentation, the greater the potential for inhibiting the production of uric acid, and the inhibitory effects of polyphenols rich in lightly fermented tea were significantly stronger than caffeine rich in highly fermented tea.
Abstract: Background The health benefits of tea are as diverse including the reduction of uric acid levels. Xanthine oxidase is the most directly mediated enzyme in the production of uric acid. Objective To explore the inhibitory effects of different teas and its main bioactive components on the production of uric acid. Design Experimental study. The experiments were conducted in vitro using human immortalized normal liver cell line HL-7702 (L-02). Results The inhibition of the xanthine oxidase activities and the expression level of xanthine dehydrogenase mRNA stimulated in the hyperuric hepatocyte cell model showed that the unfermented green tea and th1e lightly fermented yellow tea, white tea, and oolong tea significantly stronger than the highly fermented black tea and dark tea. The main bioactive compound, gallic acid, showed the strongest inhibitory effect on uric acid production, followed by tea polyphenols and theaflavins. Discussion All teas exhibited significant inhibition of xanthine oxidase activities, and the degree of fermentation of tea may be inversely proportional to its ability to inhibit the production of uric acid. Compared with tea polyphenols rich in tea, gallic acid may be a more potential uric acid-lowering component. Conclusion In this article, we first compared the effects of six traditional Chinese tea made from a single variety in stabilizing the synthesis of uric acid and found that the lighter the fermentation, the greater the potential for inhibiting the production of uric acid. Furthermore, we analyzed the inhibitory effects of its main biochemical active ingredients and found that the inhibitory effects of polyphenols rich in lightly fermented tea were significantly stronger than caffeine rich in highly fermented tea. Our findings will be helpful for people to choose a proper tea for alleviating hyperuricemia and provide a scientific basis for uric acid-lowering tea processing.
12 citations
TL;DR: Antcin K dose-dependently inhibited VCAM-1 expression and monocyte adhesion in RASFs and appeared to be mediated by MEK1/2-ERK, p38, and AP-1 signaling, which seems promising for the treatment of RA.
Abstract: Background Antcin K, an extract of Antrodia cinnamomea (a medicinal mushroom endemic to Taiwan commonly used in Chinese medicine preparations), inhibits proinflammatory cytokine production and angiogenesis in human rheumatoid arthritis synovial fibroblasts (RASFs), major players in RA disease. Antcin K also inhibits disease activity in mice with collagen-induced arthritis (CIA). Up until now, the effects of Antcin K upon cell adhesion molecules (CAMs) were unknown. Methods RA and healthy synovial tissue samples (n = 10 in each group) were retrieved from the Gene Expression Omnibus (GEO) database (accession code: GDS5401) to compare CAM and monocyte marker expressions. In addition, synovial tissue samples from six RA patients and six patients undergoing arthroscopy for trauma/joint derangement (healthy controls) were subjected to immunohistochemical (IHC) analysis. mRNA and protein expression levels were analyzed in RASFs using RT-qPCR (Reverse transcription-quantitative polymerase chain reaction) and Western blot. RASFs were incubated with Antcin K and examined for monocyte adherence by fluorescence microscopy. Ankle joint tissue specimens from a CIA mouse model and healthy controls were stained with hematoxylin and eosin (H&E) and Safranin-O/Fast Green to examine histological changes and evidence of bone loss. IHC analysis determined levels of vascular cell adhesion molecule 1 (VCAM-1) and CD11b in CIA ankle tissue and clinical synovial tissue. Results Levels of VCAM-1 expression were higher in the GEO database specimens and the study’s clinical samples of RA synovial tissue compared with the healthy specimens. Antcin K dose-dependently inhibited VCAM-1 expression and monocyte adhesion in RASFs. Antcin K also significantly inhibited levels of VCAM-1 and monocyte CD11b expression in CIA tissue. These effects appeared to be mediated by MEK1/2-ERK, p38, and AP-1 signaling. Conclusions Antcin K seems promising for the treatment of RA and deserves further investigations.
10 citations
TL;DR: It is demonstrated that mcIRBP-19-BGE possesses a hypoglycemic effect, and can have a significant reduction in FBG and HbA1c when the antidiabetic drugs are ineffective.
Abstract: Background The fruits of Momordica charantia L., also named as bitter gourd or bitter melon in popular, is a common tropical vegetable that is traditionally used to reduce blood glucose. A peptide derived from bitter gourd, Momordica charantia insulin receptor binding peptid-19 (mcIRBP-19), had been demonstrated to possess an insulin-like effect in vitro and in the animal studies. However, the benefit of the mcIRBP-19-containing bitter gourd extracts (mcIRBP-19-BGE) for lowering blood glucose levels in humans is unknown. Objective This aim of this study was to evaluate the hypoglycemic efficacy of mcIRBP-19-BGE in subjects with type 2 diabetes who had taken antidiabetic medications but failed to achieve the treatment goal. Whether glucose lowering efficacy of mcIRBP-19-BGE could be demonstrated when the antidiabetic medications were ineffective was also studied. Design Subjects were randomly assigned to two groups: mcIRBP-19-BGE treatment group (N = 20) and placebo group (N = 20), and were orally administered 600 mg/day investigational product or placebo for 3 months. Subjects whose hemoglobin A1c (HbA1c) continued declining before the trial initiation with the antidiabetic drugs were excluded from the subset analysis to further investigate the efficacy for those who failed to respond to the antidiabetic medications. Results The oral administration of mcIRBP-19-BGE decreased with a borderline significance at fasting blood glucose (FBG; P = 0.057) and HbA1c (P = 0.060). The subgroup analysis (N = 29) showed that mcIRBP-19-BGE had a significant effect on reducing FBG (from 172.5 ± 32.6 mg/dL to 159.4 ± 18.3 mg/dL, P = 0.041) and HbA1c (from 8.0 ± 0.7% to 7.5 ± 0.8%, P = 0.010). Conclusion All of these results demonstrate that mcIRBP-19-BGE possesses a hypoglycemic effect, and can have a significant reduction in FBG and HbA1c when the antidiabetic drugs are ineffective.
10 citations
TL;DR:
Abstract: Background Inflammatory liver diseases present a significant public health problem. Probiotics are a kind of living microorganisms, which can improve the balance of host intestinal flora, promote the proliferation of intestinal beneficial bacteria, inhibit the growth of harmful bacteria, improve immunity, reduce blood lipids and so on. Probiotics in fermented foods have attracted considerable attention lately as treatment options for liver injury. Objective The aim of this study was selected probiotic strain with well probiotic properties from naturally fermented foods and investigated the underlying mechanisms of screened probiotic strain on lipopolysaccharide (LPS)-induced liver injury, which provided the theoretical foundation for the development of probiotics functional food. Design The probiotic characteristics of Lactobacillus plantarum Lp2 isolated from Chinese traditional fermented food were evaluated. Male KM mice were randomly assigned into three groups: normal chow (Control), LPS and LPS with L. plantarum Lp2. L. plantarum Lp2 were orally administered for 4 weeks before exposure to LPS. The liver injury of LPS-induced mice was observed through the evaluation of biochemical indexes, protein expression level and liver histopathology. Results and discussions After treatment for 4 weeks, L. plantarum Lp2 administration significantly reduced the LPS-induced liver coefficient and the levels of serum or liver aspartate transaminase (AST), alanine aminotransferase (ALT), tumor necrosis factor α (TNF-α), interleukin-6 (IL-6) and LPS, as well as decreasing the histological alterations and protein compared with the LPS group. Western-blotting results showed that L. plantarum Lp2 activated the signal pathway of TLR4/MAPK/NFκB/NRF2-HO-1/CYP2E1/Caspase-3 and regulated the expression of related proteins. Conclusions In summary, L. plantarum Lp2 suppressed the LPS-induced activation of inflammatory pathways, oxidative injury and apoptosis has the potential to be used to improve liver injury.
9 citations
TL;DR: Kimchi intake helps alleviate IBS by increasing dietary fiber intake and reducing serum inflammatory cytokine levels and harmful fecal enzyme activities, and these reductions were greatest in the functional kimchi, nLpSK and FK groups as mentioned in this paper .
Abstract: Background Irritable bowel syndrome (IBS) can be caused by abnormal bowel movements, altered brain-gut axis, gut microbiota change, and low levels of inflammation or immune activation. The intake of food containing much fiber and lactic acid bacteria (LABs) can alleviate IBS. Objective This study was undertaken to confirm the alleviative effect of kimchi on symptoms of IBS. Design Three types of kimchi (standard kimchi, SK; dead nano-sized Lactobacillus plantarum nF1 (nLp) added to standard kimchi, nLpSK; or functional kimchi, FK) were given to 30 individuals in each of three groups, that is, the SK group (n = 30), the nLpSK group (n = 30), or the FK group (n = 30) at 210 g a day for 12 weeks. Food intake records, serum levels of inflammatory factors, fecal levels of harmful enzymes, and microbiome changes were investigated over the 12-week study period. Results After intervention, dietary fiber intake was increased in all groups. Typical IBS symptoms (abdominal pain or inconvenience, desperation, incomplete evacuation, and bloating), defecation time, and stool type were also improved. In serum, all groups showed reductions in tumor necrosis factor (TNF)-α (P < 0.001) levels. In addition, serum IL-4 (P < 0.001), IL-10 (P < 0.001), and IL-12 (P < 0.01) were significantly reduced in the nLpSK and FK groups, and serum monocyte chemotactic protein (MCP)-1 (P < 0.05) was significantly reduced in the nLpSK group. Furthermore, activities of fecal β-glucosidase and β-glucuronidase were significantly decreased in all three groups, and these reductions were greatest in the nLpSK group. Gut microbiome analysis showed that kimchi consumption increased Firmicutes populations at the expense of Bacteroidetes and Tenericutes populations. In addition, the Bifidobacterium adolescentis population increased significantly in the FK group (P = 0.026). Conclusion Kimchi intake helps alleviate IBS by increasing dietary fiber intake and reducing serum inflammatory cytokine levels and harmful fecal enzyme activities. Notably, nLp improved the immune system, and several functional ingredients in FK promoted the growth of Bifidobacterium adolescentis in gut.
9 citations
TL;DR: Short-term moderate CR decreases obesity, increases the thermogenesis, and inhibits inflammation in a mouse model of obesity, probably via the activation of the AMPK/SIRT1 pathway in WAT and liver.
Abstract: Background Obesity is a growing problem for public health worldwide. Calorie restriction (CR) is a safety and effective life intervention to defend against obesity. Short-term moderate CR may be a more favorable strategy against this pathology. However, the mechanisms behind the effects of CR remain to be clarified. Increased energy expenditure in the liver and brown adipose tissue could potentially be manipulated to modulate and improve metabolism in obesity. Moreover, nicotinamide adenine dinucleotide (NAD)-dependent deacetylase sirtuin-1 (SIRT1) and AMP-activated protein kinase (AMPK) are well-characterized metabolic modulators. We aim to explore the anti-obesity effects of short-term moderate CR by improving energy metabolism via the SIRT1/AMPK pathway in white adipocytes and liver in a mouse model of obesity. Methods Male C57BL/6 mice were randomized into two groups receiving either a standard or a high-fat diet (HFD) for 8 weeks to induce obesity. The HFD-induced obese mice were further randomized into two groups: HFD group or CR group (received 75% of the food eaten by HFD group). Their energy metabolism, white adipose tissue (WAT) contents, hepatic fat deposition, the expression of AMPK, SIRT1, peroxisome proliferators γ-activated receptor coactivator-1α (PGC-1α), nuclear factor kappa B (NF-κB), endothelial nitric oxide synthase (eNOS) in WAT, and hepatic tissues were determined. Results After 4 weeks, body weight, total serum cholesterol, fasting blood glucose, and insulin levels were significantly lower in the CR group. Moreover, CR ameliorated hepatocyte steatosis, attenuated white adipogenesis, and increased energy expenditure and expressions of SIRT1, PGC-1α, and phosphorylated AMPK in subcutaneous WAT and the hepatic tissues. In addition, CR reduced the protein levels of NF-κB and increased the eNOS expression. Conclusion Short-term moderate CR decreases obesity, increases the thermogenesis, and inhibits inflammation in a mouse model of obesity, probably via the activation of the AMPK/SIRT1 pathway in WAT and liver.
8 citations
TL;DR: CAP can reduce fat accumulation by regulating BAs, microorganisms, and short-chain fatty acids by regulating lipid metabolism, fasting plasma glucose and insulin resistance.
Abstract: Capsaicin (CAP) is one of the active ingredients found in chili peppers and has been shown to reduce fat. This study aimed to explore the mechanisms of CAP activity by investigating intestinal microorganisms and bile acids (BAs). This study utilized 16S RNA sequencing to detect gut microbiota in cecal contents, and BAs in Sprague Dawley (SD) rats were also investigated. The results showed that 1) CAP increased the levels of chenodeoxycholic acid (CDCA), deoxycholic acid (DCA), β-muricholic acid (β-MCA), and tauro-β-muricholic acid sodium salt (T-β-MCA), which can regulate farnesoid X receptor (FXR) to inhibit Fgf15, increased CYP7A1 expression to lower triglycerides (TG) and total cholesterol (TC); 2) CAP decreased the abundance of Firmicutes and promoted the presence of specific fermentative bacterial populations, like Akkermansia; meanwhile, less optimal dose can reduce Desulfovibrio; 3) CAP decreased inflammatory factors IL-6 and IL-1β, and increased transient receptor potential channel of vanilloid subtype 1 (TRPV1) to regulate lipid metabolism, fasting plasma glucose and insulin resistance. In conclusion, CAP can reduce fat accumulation by regulating BAs, microorganisms, and short-chain fatty acids.
5 citations
TL;DR: The intake of long chain n-3 fatty acid supplements during pregnancy may reduce the risk of asthma and/or wheeze in the offspring, but the strength of evidence is low.
Abstract: Objective To assess whether supplementation with long chain n-3 fatty acids during pregnancy, lactation, or infancy reduces the risk of developing asthma or atopic disease during childhood. Methods Searches were performed in MEDLINE, Embase, Cochrane Central Register of Controlled Trials, and Scopus up to 2021-09-20, for randomized controlled trials (RCTs) that investigated the effect of supplemental long chain n-3 fatty acids during pregnancy, lactation, or infancy for the prevention of childhood asthma or allergy. Article selection, data extraction, and risk of bias assessment (Cochrane’s Risk of Bias 2.0) were independently conducted by two assessors. The evidence was synthesized qualitatively according to the criteria of the World Cancer Research Fund and meta-analyzed. Results A total of nine RCTs met inclusion criteria; six were conducted during pregnancy, two during infancy, and one during both pregnancy and infancy. Meta-analysis showed that long chain n-3 fatty acid supplementation during pregnancy significantly reduced the risk of asthma/wheeze in the child (RR 0.62 [95% confidence interval 0.34–0.91], P = 0.005, I2 = 67.4%), but not other outcomes. Supplementation during lactation of infancy showed no effects on any outcome. The strength of evidence that long chain n-3 fatty acid supplementation during pregnancy reduces risk of asthma/wheeze in the offspring was considered limited – suggestive. No conclusion could be made for the effects of long chain n-3 fatty acid supplementation during pregnancy for other atopic diseases, or for supplementation during lactation or infancy for any outcome. Conclusion The intake of long chain n-3 fatty acid supplements during pregnancy may reduce the risk of asthma and/or wheeze in the offspring, but the strength of evidence is low. There is inconclusive evidence for the effects of long chain n-3 fatty acid supplements during pregnancy for other outcomes, as well as for supplementation during lactation or infancy.
5 citations
TL;DR: Troxerutin could significantly alleviate cisplatin-induced renal dysfunction, such as increased levels of blood urea nitrogen and creatinine, as well as improved abnormal renal tissue microstructure and ultrastructure, and the underlying mechanism might be attributed to the regulation of Phosphoinositide 3 kinase/Protein kinase B (PI3K/AKT) pathway via enhancing MAP4 expression to attenuate cellular apoptosis, alleviating oxidative stress and inflammatory response.
Abstract: Background Troxerutin is a flavonoid compound and possesses potential anti-cancer, antioxidant, and anti-inflammatory activities. Besides, cisplatin is one of the most widely used therapeutic agents, but the clinical uses of cisplatin are often associated with multiple side effects, among which nephrotoxicity is more common. Objective and design This study explored the protective effects of troxerutin (150 mg kg−1 day−1 for 14 days) against cisplatin-induced kidney injury and the potential mechanism using Wistar rats as an experimental mammalian model. Results We discovered that troxerutin could significantly alleviate cisplatin-induced renal dysfunction, such as increased levels of blood urea nitrogen and creatinine (P < 0.01), as well as improved abnormal renal tissue microstructure and ultrastructure. Additionally, troxerutin significantly decreased malondialdehyde (MDA), hydrogen peroxide (H2O2), NO, inducible nitric oxide synthase (iNOS) levels (P < 0.01), p-NF-κB p65/NF-κB p65, TNF-α, Pro-IL-1β, IL-6, B cell lymphoma-2 (Bcl-2)/Bcl-xl associated death promoter (Bad), Cytochrome C (Cyt C), Cleaved-caspase 9, Cleaved-caspase 3, and Cleaved-caspase 8 protein levels (P < 0.01) in the kidney tissues of cisplatin-treated rats; and increased superoxide dismutase (SOD), catalase (CAT), glutathione (GSH), total antioxidant capacity (T-AOC) activities (P < 0.01), IL-10, Bcl-2 protein levels (P < 0.01). Conclusion These results suggested that the underlying mechanism might be attributed to the regulation of Phosphoinositide 3 kinase/Protein kinase B (PI3K/AKT) pathway via enhancing MAP4 expression to attenuate cellular apoptosis, alleviating oxidative stress and inflammatory response.
TL;DR: Findings highlight the relationship between the gut microbiota, diet, and metabolic markers in healthy individuals and highlight the need to address whether these findings are causally linked and whether targeting these gut bacteria can prevent metabolic diseases.
Abstract: Background Metabolic diseases have been related to gut microbiota, and new knowledge indicates that diet impacts host metabolism through the gut microbiota. Identifying specific gut bacteria associated with both diet and metabolic risk markers may be a potential strategy for future dietary disease prevention. However, studies investigating the association between the gut microbiota, diet, and metabolic markers in healthy individuals are scarce. Objective We explored the relationship between a panel of gut bacteria, dietary intake, and metabolic and anthropometric markers in healthy adults. Design Forty-nine volunteers were included in this cross-sectional study. Measures of glucose, serum triglyceride, total cholesterol, hemoglobin A1c (HbA1c), blood pressure (BP), and body mass index (BMI) were collected after an overnight fast, in addition to fecal samples for gut microbiota analyzes using a targeted approach with a panel of 48 bacterial DNA probes and assessment of dietary intake by a Food Frequency Questionnaire (FFQ). Correlations between gut bacteria, dietary intake, and metabolic and anthropometric markers were assessed by Pearson’s correlation. Gut bacteria varying according to dietary intake and metabolic markers were assessed by a linear regression model and adjusted for age, sex, and BMI. Results Of the 48 gut bacteria measured, 24 and 16 bacteria correlated significantly with dietary intake and metabolic and/or anthropometric markers, respectively. Gut bacteria including Alistipes, Lactobacillus spp., and Bacteroides stercoris differed according to the intake of the food components, fiber, sodium, saturated fatty acids, and dietary indices, and metabolic markers (BP and total cholesterol) after adjustments. Notably, Bacteroides stercoris correlated positively with the intake of fiber, grain products, and vegetables, and higher Bacteroides stercoris abundance was associated with higher adherence to Healthy Nordic Food Index (HNFI) and lower diastolic BP after adjustment. Conclusion Our findings highlight the relationship between the gut microbiota, diet, and metabolic markers in healthy individuals. Further investigations are needed to address whether these findings are causally linked and whether targeting these gut bacteria can prevent metabolic diseases.
TL;DR: Children’s intake of the favorite food item groups, fruit and berries, vegetables and fish, was associated with the use of positive feeding practices, such as involvement, environment, modeling and encouragement.
Abstract: Background Parental feeding practices may be important determinants for children’s diets. In Norway, few studies have assessed this association and to our knowledge, no studies have included fish as an outcome. Objective The purpose of this study was to explore the association between multiple parental feeding practices and children’s food intake. Design Parents (n = 111) of preschool children aged 1–5 years in the Gardermoen Region in Norway were recruited. The parents completed a web–based questionnaire regarding the use of 12 feeding practices measured by the Comprehensive Feeding Practices Questionnaire (CFPQ). Children’s weekly food intake was measured using a food frequency questionnaire (FFQ). The association between parental feeding practices and food intake was assessed by logistic regression. Results The feeding practices involvement and environment increased the likelihood of children having a higher intake of fruit and berries (OR = 1.99, 95% CI = 1.15, 3.44 and OR = 2.10, 95% CI = 1.17, 3.78, respectively) when controlling for potential confounders. A positive association was found between the feeding practice environment and the children’s intake of vegetables (OR = 2.94, CI = 1.55, 5.55), and between modeling and intake of vegetables (OR = 2.14, CI = 1.26, 3.63). Also, the feeding practice encourage balance and variety increased the likelihood of a higher consumption of vegetables (OR = 5.18, CI = 1.63, 16.5). Parents who more frequently encouraged the child to eat balanced and varied were more likely to have children with a higher consumption of fish (OR = 5.03, CI = 1.62, 15.7). If parents used more restriction for weight, the child was less likely to have a high SSB consumption (OR = 0.43, CI = 0.22, 0.83). Conclusion Findings suggest that children’s intake of the favorite food item groups, fruit and berries, vegetables and fish, was associated with the use of positive feeding practices, such as involvement, environment, modeling and encouragement. For unfavorable food groups, only restriction for weight was negatively associated with SSB consumption. Findings should be interpreted carefully due to the relatively small sample size.
TL;DR: It is demonstrated that JXGT treatment has a potential protection on HFD-induced obesity mice via activating the AMPK/CPT-1A and down-regulating FAS/GSK-3β/PGC-1α and IL-6/TNFα.
Abstract: Background Obesity is a global public health concern and increases the risk of metabolic syndrome and other diseases. The anti-obesity effects of various plant-derived bioactive compounds, such as tea extracts, are well-established. The mechanisms underlying the anti-obesity activity of Jinxuan green tea (JXGT) from different storage years are still unclear. Objective The aim of this study was to evaluate the effects of JXGTs from three different years on the high fat diet (HFD)-fed mouse model. Design The mice were divided into six groups, the control group received normal diet and the obese model group received HFD. We analyzed the effects of JXGTs from 2005, 2008, and 2016 on HFD-fed obese mice over a period of 7 weeks. Results The JXGTs reduced the body weight of the obese mice, and also alleviated fat accumulation and hepatic steatosis. Mechanistically, JXGTs increased the phosphorylation of AMP-activated protein kinase (p-AMPK)/AMP-activated protein kinase (AMPK) ratio, up-regulated carnitine acyl transferase 1A (CPT-1A), and down-regulated fatty acid synthase (FAS), Glycogen synthase kinase-3beta (GSK-3β), Peroxisome proliferator-activated receptor-gamma co-activator-1alpha (PGC-1α), Interleukin 6 (IL-6), and Tumour necrosis factor alpha (TNFα). Thus, JXGTs can alleviate HFD-induced obesity by inhibiting lipid biosynthesis and inflammation, thereby promoting fatty acid oxidation via the AMPK pathway. Discussion The anti-obesity effect of three aged JXGTs were similar. However, JXGT2016 exhibited a more potent activation of AMPK, and JXGT2005 and JXGT2008 exhibited a more potent inhibiting glycogen synthase and inflammation effect. Furthermore, the polyphenol (–)-epicatechin (EC) showed the strongest positive correlation with the anti-obesity effect of JXGT. Conclusions These findings demonstrate that JXGT treatment has a potential protection on HFD-induced obesity mice via activating the AMPK/CPT-1A and down-regulating FAS/GSK-3β/PGC-1α and IL-6/TNFα. Our study results also revealed that different storage time would not affect the anti-obesity and anti-inflammation effect of JXGT. Graphical abstract
TL;DR: No clear association was found between the intake of various classes of fatty acids and the risk of AD and dementia in adults and the certainty of the overall evidence was inconclusive.
Abstract: Objective To identify, critically appraise, and synthesize evidence on the effect of quality of dietary fat intake and different classes of fatty acids on the risk of Alzheimer’s disease (AD) and dementia in adults aged ≥50 years. Methods We searched MEDLINE, EMBASE, Cochrane Central of Controlled Trials, and Scopus for clinical trials and prospective cohort studies published until May 2021. Two reviewers independently screened retrieved literature, extracted relevant data, and performed risk of bias assessment. Classes of fatty acids included were saturated fatty acids (SFAs), trans fatty acids (TFAs), monounsaturated fatty acids (MUFAs), poly-unsaturated fatty acids (PUFAs), and their subtypes and sources. Given between-study heterogeneity, we did not perform meta-analyses but narratively described findings from the studies. Results From 4,491 identified records, five articles (based on four prospective cohort studies) met the inclusion criteria. Three studies had an overall serious risk of bias, while one study had a moderate risk. Overall, we found no robust association between intake of any fatty acids type and the development of AD and dementia. For example, for SFA and TFA, there was contradictory associations reported on AD: one study found that each unit increase in energy-adjusted intake of SFA (risk ratio [RR] 0.83, 95%CI 0.70–0.98) and TFA (RR 0.80, 95%CI 0.65–0.97) was associated with a decreased risk of AD, but not dementia. For PUFA, one study found that higher quintile intake of marine-based n-3 PUFA was associated with a decreased risk of AD. The intake of other fatty acids was not associated with the outcomes. The certainty of the overall evidence was inconclusive. Conclusion We found no clear association between the intake of various classes of fatty acids and the risk of AD and dementia in adults. More well-designed prospective studies are required to clarify these findings.
TL;DR: In this article , the effect of quercetin on bacterial enteritis and pyroptosis was evaluated using rat intestinal microvascular endothelial cells divided into seven groups: control group (no treatment), model group (10 μg/mL lipopolysaccharide (LPS)+1 mM adenosine triphosphate [ATP]), LPS group ( 10 μg/dL LPS), ATP group (1 mM ATP), and treatment groups (10 mM/mL LPS+1 mM ADP and 5, 10, and 20 μM quercETin).
Abstract: Background Inflammatory bowel diseases are characterized by the alterations of the mucosa and gastrointestinal physiology, and the core of these alterations is endothelial cells. Quercetin is a flavonoid presents in some traditional Chinese medicine, plants, and fruits. Its protective effects in several gastrointestinal tumors have been demonstrated, but its effects on bacterial enteritis and pyroptosis-related diseases have rarely been studied. Objective This study aimed to evaluate the effect of quercetin on bacterial enteritis and pyroptosis. Design In vitro experiments were performed using rat intestinal microvascular endothelial cells divided into seven groups: control group (no treatment), model group (10 μg/mL lipopolysaccharide (LPS)+1 mM adenosine triphosphate [ATP]), LPS group (10 μg/mL LPS), ATP group (1 mM ATP), and treatment groups (10 μg/mL LPS+1 mM ATP and 5, 10, and 20 μM quercetin). The expression of pyroptosis-associated proteins, inflammatory factors, tight junction proteins, and the percentage of late apoptotic and necrotic cells were measured. In vivo analysis was performed using specific pathogen-free Kunming mice pretreated with quercetin and the water extract of Cacumen Platycladi for 2 weeks followed by 6 mg/kg LPS on day 15. Inflammation in the blood and intestinal pathological changes were evaluated. Results Quercetin used in vitro significantly reduced the expression of Toll-like receptor 4 (TLR4), NOD-like receptor 3 (NLRP3), caspase-1, gasdermin D, interleukin (IL)-1β, IL-18, IL-6, and tumor necrosis factor-α. It also inhibited phosphorylation of nuclear factor-kappa B (NF-κB) p65 and increased cell migration and the expression of zonula occludens 1 and claudins, while reduced the number of late apoptotic cells. The in vivo results showed that Cacumen Platycladi and quercetin significantly reduced inflammation, protected the structure of the colon and cecum, and prevent fecal occult blood induced by LPS. Conclusions These findings suggested the ability of quercetin to reduce inflammation induced by LPS and pyroptosis through TLR4/NF-κB/NLRP3 pathway.
TL;DR: WP administration effectively alleviated intestinal mucosal impairment in aged mice, suggesting that WP have a potential effect on inhibiting aging-induced inflammatory responses by blocking TLR4/Myd88/MAPK signal transduction.
Abstract: Background Aging can induce oxidative stress, inflammation and mucosal impairment, and few works have been conducted to investigate the protective effects of WP on the natural intestinal aging process. Objective The present work aimed to examine the protective effect of wheat oligopeptides (WP) on intestine mucosal impairment in aged mice, and investigate the potential antioxidation, anti-inflammatory effects of WP. Design Seventy-two aged mice (24 months old) were randomly divided into six groups, 12 for each group. Twelve young mice (6 months old) were regarded as the young control group. WP (25, 50, 100, 200, or 400 mg/kg) or distilled water were administered daily by gavage for 30 days. Results Histological observations showed that intestinal mucosal degeneration was attenuated by WP pretreatment. WP exhibited remarkable antioxidant activity via increasing superoxide dismutase, glutathione peroxidase, total antioxidant capacity and catalase activities, and decreasing the malondialdehyde levels in small intestine mucosa. WP pretreatment significantly suppressed intestinal mucosa inflammation through the reduction of TNF-α, TGF-β, IFN-γ IL-1β and IL-6. WP markedly protect the intestinal mucosal barrier by decreasing the ICAM-1 level, and increasing ZO-1 and JAMA-A levels. WP significantly down-regulated protein expression levels of TLR4, Myd88, and MAPK, suggesting that WP have a potential effect on inhibiting aging-induced inflammatory responses by blocking TLR4/Myd88/MAPK signal transduction. Conclusion WP administration effectively alleviated intestinal mucosal impairment in aged mice. The potential mechanism was associated with enhancement of antioxidation and anti-inflammatory action and protection of the intestinal mucosal barrier.
TL;DR: SUNCA might prevent obesity by suppressing the adipogenesis/lipogenesis pathway and stimulating the lipolysis/thermogenesis pathway in HFD-induced obese mice.
Abstract: Background: Obesity, abnormal fat accumulation in the adipose tissue, has become a serious global public health problem as it increases an individual’s risk of developing various diseases.
Objective: This study sought to determine whether the extract from sunflower seed (SUNCA) prevents the development of obesity in high-fat diet (HFD)-induced obese mice.
Design: C57BL/6J mice were fed with AIN93G normal diet (Normal diet), 60% HFD, HFD containing Catechin 100 mg/kg body weight (b.w.) (Catechin), HFD containing SUNCA 25 mg/kg b.w. (SUNCA 25), HFD containing SUNCA 50 mg/kg b.w. (SUNCA 50), or HFD containing SUNCA 100 mg/kg b.w. (SUNCA 100) for 15 weeks.
Results: Body weight gain, food efficiency rate, adipose tissue weight, adipose tissue mass, size of adipocytes, and serum levels of triglyceride, total cholesterol, very low-density lipoprotein/low-density lipoprotein (VLDL/LDL)-cholesterol, aspartate aminotransferase, and alanine aminotransferase were significantly decreased by SUNCA supplementation in HFD-fed mice. Furthermore, SUNCA supplementation decreased the expression of proteins related to the adipogenesis and lipogenesis pathways and increased the expression of proteins related to the lipolysis and thermogenesis pathways in the adipose tissues of HFD-induced obese mice.
Conclusions: Altogether, SUNCA might prevent obesity by suppressing the adipogenesis/lipogenesis pathway and stimulating the lipolysis/thermogenesis pathway in HFD-induced obese mice.
TL;DR: It is shown for the first time that Arborinine showed inhibitory effect on ccRCC via KDM1A/UBE2O signaling.
Abstract: Background Arborinine is a natural product isolated from Globigerina parva (G. parva) leaf extract that shows strong anticancer activity with its role in clear-cell renal cell carcinoma (ccRCC) unreported. Objective We aim to evaluate the role of Arborinine in ccRCC. Design Arborinine was tested for its effects in ccRCC cell lines in vitro and in silico. Results Arborinine conferred inhibitory effect to ccRCC cells at reasonable doses. Arborinine showed inhibitory effects on Lysine Demethylase 1A (KDM1A) in ccRCC cells and decreased levels of KDM1A outputs and on epithelial mesenchymal transition (EMT) markers. Arborinine significantly inhibited proliferation, apoptosis, and cell cycle progression and migration of ccRCC cells. Using in silico ChIP analysis and luciferase activity validation, we identified Ubiquitin-conjugating enzyme E2O (UBE2O) as an active transcription target downstream of KDM1A. UBE2O expression was not only correlated with KDM1A expression but also associated with worsened prognosis in ccRCC. Overexpression of UBE2O abrogated cancer-inhibitory effect of Arborinine. Discussion Arborinine holds promise as an additive in the treatment of ccRCC. Conclusions We have shown for the first time that Arborinine showed inhibitory effect on ccRCC via KDM1A/UBE2O signaling.
TL;DR: The nutrient intake and, especially, food consumption differ between the Nordic and Baltic countries because of differences in food patterns and factors related to the dietary surveying, food grouping, and calculation procedures in each country.
Abstract: Background Knowledge about the nutrient intakes and food consumption in the Nordic and Baltic countries is important for the formulation of dietary reference values (DRVs) and food-based dietary guidelines (FBDGs), as part of the Nordic Nutrition Recommendations 2022 project (NNR2022). Objective To describe nutrient intake and food consumption at a broad level in the adult population of each Nordic and Baltic country. This paper also provides guidance on where to find more information on the nutrient intake and food consumption reported from each country. Design Information about the dietary surveys as well as the daily mean intakes was retrieved from the national dietary surveys in each of the Nordic and Baltic countries. Tabulation of the population intakes divided by sex for macronutrients, 20 micronutrients, and for the following broader food groups, Beverages, Cereals, Potatoes, Vegetables, Fruits and berries, Fish and seafood, Meat and meat products, Milk and dairy products, Cheese, Eggs, Fats and oils, and Sweets and sweet bakery products, was done. Results and Discussion The Nordic and Baltic countries share not only similarities but also differences in food consumption patterns, which is reflected in differences in average food consumption and nutrient intakes between the countries. This may be related to the dietary assessment method, prevalence of misreporting, and participation rates in the different dietary surveys. Other factors that may play a role are differences in the calculation procedures in the food composition databases and the definition of food groups. Conclusion The nutrient intake and, especially, food consumption differ between the Nordic and Baltic countries because of differences in food patterns and factors related to the dietary surveying, food grouping, and calculation procedures in each country. To facilitate future comparisons between countries, it would be of interest to harmonize food groupings and the age groups reported on.
TL;DR: Household food insecurity was a main predictor of dietary diversity among school-age children in Ghana in this study, and caregiver knowledge in nutrition may not be enough, particularly in the presence of food insecurity to guarantee adequate nutrition for school-aged children.
Abstract: Background Dietary diversity is generally considered as a good indicator of nutrient adequacy and is influenced by various factors at the national, household, and individual levels. Objective The present study sought to determine the relationships between household food insecurity, primary caregivers’ nutrition knowledge, and dietary diversity of school-aged children in Ghana. Methods This forms part of a longitudinal study conducted in the Ayawaso West Municipal district in Accra (urban setting) and the Upper Manya Krobo district (rural setting) in Ghana. Data were collected from a total of 116 caregiver-child dyads using 24-h dietary recall and a short version of the US 12-month Household Food Security Survey Module. Nutrition knowledge and sociodemographic data were obtained using a structured questionnaire. Multivariable logistic regression was used to check for factors associated with children’s dietary diversity. Results Majority of households reported food insecurity, with a higher percentage of insecure households located in the rural area (88.9% vs. 46.5%, P ≤ 0.0001), compared to the urban setting. Diet diversity among the study children was low, with a mean (standard deviation [SD]) of 5.8 (2.1) out of 14 food groups. Children living in food insecure households were three times more likely to have received low diverse diet compared to those from food secure households (adjusted odds ratio [OR] =3.3, 95% confidence interval [CI]: 1.4–8.0). Caregivers’ nutrition knowledge was, however, not related to children’s dietary diversity. Discussion and conclusion Household food insecurity was a main predictor of dietary diversity among school-age children in this study. Thus, caregiver knowledge in nutrition may not be enough, particularly in the presence of food insecurity to guarantee adequate nutrition for school-aged children.
TL;DR: This study demonstrates that a single administration of Jerusalem artichoke tubers reduces postprandial glucose and active GIP concentrations in prediabetic and healthy individuals.
Abstract: Background The consumption of Jerusalem artichoke has multiple beneficial effects against diabetes and obesity. Objective The aim of this study was to determine the effect of a single administration of Jerusalem artichoke tubers on postprandial glycemia and the concentrations of incretin hormones in humans. Method Grated Jerusalem artichoke was administered prior to a meal (Trial 1; white rice for prediabetic participants, n = 10). Dose-dependent effect of Jerusalem artichoke (Trial 2; white rice for prediabetic participants, n = 4) and effect prior to the fat-rich meal were also investigated (Trial 3; healthy participants, n = 5) in this pilot study. Circulating glucose, insulin, triglyceride, glucagon, active glucagon-like peptide-1 (GLP-1), and active glucose-dependent insulinotropic polypeptide (GIP) concentrations were subsequently measured in all the trials. Results Jerusalem artichoke significantly reduced the glucose and GIP concentrations after the consumption of either meal in Trial 1 and Trial 3, whereas there were no differences in the insulin, glucagon, and active GLP-1 concentrations. Also, there was no significant difference in the triglyceride concentration after the ingestion of the fat-rich meal in Trial 3. The glucose and GIP-lowering effects were dose-dependent, and the consumption of at least 100 g of Jerusalem artichoke was required to have these effects in Trial 2. Conclusion This study demonstrates that a single administration of Jerusalem artichoke tubers reduces postprandial glucose and active GIP concentrations in prediabetic and healthy individuals.
TL;DR: Dynamic changes in the nascent proteome and transcriptome in response to resveratrol in HEK 293T cells are revealed and it is demonstrated that resver atrol downregulates Hsp60 by activating SIRT1, which may be a possible mechanism by which res veratrol prevents p53-dependent apoptosis by regulating Hsp 60.
Abstract: Background Resveratrol, a well-known natural compound and nutrient, activates the deacetylation ability of SIRT1, demonstrating p53-dependent apoptosis functions in many diseases. However, the nascent proteomic fluctuation caused by resveratrol is still unclear. Objective In this study, we investigated the effect of resveratrol on the nascent proteome and transcriptome initiated by SIRT1 activation, and we explored the mechanism of resveratrol in HEK 293T cells. Methods Bioorthogonal noncanonical amino acid tagging (BONCAT) is a method used to metabolically label nascent proteins. In this strategy, L-azidohomoalanine (AHA) was used to replace methionine (Met) under different conditions. Taking advantage of the click reaction between AHA and terminal alkyne- and disulfide-functionalized agarose resin (TAD resin), we were able to efficiently separate stimulation responsive proteins from the pre-existing proteome. Resveratrol responsive proteins were identified by Liquid Chromatograph-Mass Spectrometer/Mass Spectrometer (LC-MS/MS). Furthermore, changes in mRNA levels were analyzed by transcriptome sequencing. Results Integrational analysis revealed a resveratrol response in HEK 293T cells and showed that Hsp60 was downregulated at both the nascent protein and mRNA levels. Knockdown of SIRT1 and Hsp60 provides evidence that resveratrol downregulated Hsp60 through SIRT1 and that Hsp60 decreased p53 through the Akt pathway. Conclusions This study revealed dynamic changes in the nascent proteome and transcriptome in response to resveratrol in HEK 293T cells and demonstrated that resveratrol downregulates Hsp60 by activating SIRT1, which may be a possible mechanism by which resveratrol prevents p53-dependent apoptosis by regulating Hsp60.
TL;DR: Serological and liver biochemical indicators suggest that CMT reduced dyslipidemia and liver damage caused by fatty liver, and suggested that the active ingredients of CMT might be beneficial in NAFLD therapy.
Abstract: Background Nonalcoholic fatty liver disease (NAFLD) is a chronic metabolic disease that easily induces hepatitis, cirrhosis, and even liver cancer. The long-term use of NAFLD therapeutic drugs produces toxicity and drug resistance. Therefore, it is necessary to develop high efficiency and low-toxicity active ingredients to alleviate NAFLD. Objective This study aimed to reveal the role and mechanism of a new functional food CMT in alleviating NAFLD. Results In the ob/ob fatty liver mice models, the CMT extracts significantly inhibited the weight gain of the mice and reduced the accumulation of white fat. The anatomical and pathological results showed that CMT relieved fatty liver in mice and reduced excessive lipid deposition and inflammatory infiltration. Serological and liver biochemical indicators suggest that CMT reduced dyslipidemia and liver damage caused by fatty liver. CMT obviously activated the adenosine 5′-monophosphate-activated protein kinase (AMPK)/acetyl-coA carboxylase (ACC) and AMPK/fatty acid synthase (FAS) signaling pathways, promoted fat oxidation, and inhibited synthesis. Moreover, CMT regulated the expression of inflammatory factors to relieve hepatitis caused by NAFLD. Conclusion The study explained the role and mechanism of CMT in alleviating NAFLD and suggested that the active ingredients of CMT might be beneficial in NAFLD therapy.
TL;DR: Findings suggested that L. plantarum FRT4 had beneficial effects against obesity in HFD-induced obese mice and can be used as a potential functional food for the prevention of obesity.
Abstract: Background Obesity has become a global epidemic recognized by the World Health Organization. Probiotics supplementation has been shown to contribute to improve lipid metabolism. However, mechanisms of action of probiotics against obesity are still not clear. Lactobacillus plantarum FRT4, a probiotic previously isolated from a kind of local yogurt, had good acid and bile salt tolerance and lowered cholesterol in vitro. Objective This study aimed to evaluate the effect of L. plantarum FRT4 on serum and liver lipid profile, liver metabolomics, and gut microbiota in mice fed with a high-fat diet (HFD). Design Mice were fed with either normal diet or HFD for 16 weeks and administered 0.2 mL of 1 × 109 or 1 × 1010 CFU/mL dosage of L. plantarum FRT4 during the last 8 weeks of the diet. Cecal contents were analyzed by 16S rRNA sequencing. Hepatic gene expression and metabolites were detected by real-time quantitative polymerase chain reaction (PCR) and metabolomics, respectively. Results L. plantarum FRT4 intervention significantly reduced the HFD-induced body weight gain, liver weight, fat weight, serum cholesterol, triglyceride, and alanine aminotransferase (ALT) levels in the liver (P < 0.05). Liver metabolomics demonstrated that the HFD increased choline, glycerophosphocholine, and phosphorylcholine involved in the glycerophospholipid metabolism pathway. All these changes were reversed by FRT4 treatment, bringing the levels close to those in the control group. Further mechanisms showed that FRT4 favorably regulated gut barrier function and pro-inflammatory biomediators. Furthermore, FRT4 intervention altered the gut microbiota profiles and increased microbial diversity. The relative abundances of Bacteroides, Parabateroides, Anaerotruncus, Alistipes, Intestinimonas, Butyicicoccus, and Butyricimonas were significantly upregulated. Finally, Spearman’s correlation analysis revealed that several specific genera were strongly correlated with glycerophospholipid metabolites (P < 0.05). Conclusions These findings suggested that L. plantarum FRT4 had beneficial effects against obesity in HFD-induced obese mice and can be used as a potential functional food for the prevention of obesity.
TL;DR: The results showed that A12 effectively alleviated relieved weight gain and dyslipidemia, inhibited liver adipose accumulation, and improved leptin resistance in HFD-fed mice, and the anti-obesity effects of B. lactis A12 were closely related to the assembly of short-chain fatty acids, SCFAs, SCFA-downstream receptors, and glucagon-like peptide-1 (GLP-1) secretion.
Abstract: Background: Bifidobacterium lactis A12 (B. lactis A12) has been shown to have the potential to prevent obesity. However, the mechanisms by which it affects the control of energy metabolism have not been fully elucidated.
Objective: The present work aimed to clarify the mechanisms by that B. lactis A12 has an effect on the management of energy metabolism.
Design: Three- to five-week-old male C57BL/6J mice were randomly divided into five groups, 15 mice for each group. Low-fat diet (LFD) group and high-fat diet (HFD) group were fed with phosphate-buffered saline (PBS) on a daily basis. Cell-free supernatant (CFS), A12, and B. lactis BB12 (BB12) groups were fed with daily probiotics for 10 weeks (1 × 109 CFU of every strain).
Results: The results showed that A12 effectively alleviated relieved weight gain and dyslipidemia, inhibited liver adipose accumulation, and improved leptin resistance in HFD-fed mice (p < 0.05). The anti-obesity effects of B. lactis A12 were closely related to the assembly of short-chain fatty acids (SCFAs), SCFA-downstream receptors, and glucagon-like peptide-1 (GLP-1) secretion. Additionally, high-throughput sequencing of the 16S rRNA showed that B. lactis A12 supplementation reversed HFD-induced gut microbiota dysbiosis, which was possible related to the augmented abundance of SCFA-producing bacterium and a minimized ratio of Bacteroidetes to Firmicutes in mice.
Conclusions: B. lactis A12 prevents obesity in some pathways, including the downregulation of sterol regulatory element binding protein-1 mRNA levels in the liver, modulation of the structure of gut microbiota in a gut microbiota-dependent manner, and the upregulation of the SCFA-producing bacteria-related G protein-coupled receptor 43 pathway.
TL;DR: In this article , the authors evaluated the relationship of habitual nutrient intake and protein adequacy to the prevalence of child malnutrition and found that higher consumption of grains and cereal products, meat, and high-quality protein foods was associated with a lower risk of stunting.
Abstract: Background: Adequate nutrition during childhood is essential to promote child growth and development. Objective: The study evaluated the relationship of habitual nutrient intake and protein adequacy to the prevalence of child malnutrition. Methods: Data were derived from a nationally representative sample of children aged 6–12 years. Two nonconsecutive day 24-h dietary recalls (24hR) were collected to estimate the individual food intake. PC-SIDE version 1.0 software (Software for Intake Distribution Estimation) was used to estimate the habitual intake of key nutrients accounting for between- and within-person differences in dietary intake. The 2007 WHO Protein Digestibility Corrected Amino Acid Score (PDCAAS) method was used to measure the protein quality or the utilizable protein intake. The nutritional status of the participants is reflected in the weight-for-age, height-for-age, and body mass index (BMI)-for-age z-scores using the WHO Growth Reference Standard (WHO, 2007). Results: Undernourished school-aged children were found to have high protein inadequacy. Higher consumption of grains and cereal products, meat, and high-quality protein foods was associated with a lower risk of stunting. Higher intake of milk and milk products, grains and cereal products, high-quality protein foods, calcium, riboflavin, and vitamin C was associated with a lower risk of underweight. Higher consumption of grains and cereal products, riboflavin, thiamine, and fiber was associated with a lower risk of wasting. On the contrary, higher consumption of meat, milk and milk products, grains and cereal products, high-quality protein foods, and vitamin C was associated with a higher risk of obesity. Furthermore, linear growth of children was found to be associated with high-quality protein foods, calcium, vitamin B12, vitamin C, and vitamin D. Conclusions: Malnutrition among Filipino children is influenced by nutrient intakes. However, the existence of malnutrition among children may be specifically attributed to the quality of protein consumed. Therefore, the study suggests that nutrition interventions and policies focusing on child malnutrition should improve not just the quantity but also the quality of protein sources consumed by children to aid in proper growth and development.
TL;DR: In this paper , the authors evaluated the hepatoprotective effect of rosmarinic acid (RA) on carbon tetrachloride (CCl4)-induced liver injury.
Abstract: Background Rosmarinic acid (RA) has biological and pharmaceutical properties and shows hepatoprotective potential. However, the hepatoprotective mechanism of RA needs to be further elucidated in vivo and in vitro. Objective This study was aimed to evaluate the protective effect of RA on carbon tetrachloride (CCl4)-induced liver injury and elucidate the hepatoprotective mechanism of RA in vivo and in vitro. Design In vivo, the mice were orally administrated with RA (10, 20, and 40 mg/kg bw) daily for 28 consecutive days, and 1% CCl4 (5 mL/kg bw, dissolved in peanut oil) was used to induce liver injury. In vitro, the big rat liver (BRL) hepatocytes were pretreated with RA (0.2, 0.4, and 0.8 mg/mL) for 3 h, and then the hepatocytes were treated with CC14 (final concentration, 14 mM) for 3 h to induce cell injury. The related indexes, including hepatic function, oxidative stress, protein expression of nuclear-factor erythroid 2-related factor 2 (Nrf2) pathway, inflammation, histopathological change, hepatocyte apoptosis, and mitochondrial membrane potential, were evaluated. Results Oral administration of RA to mice considerably decreased the CCl4-induced elevation of serum alanine aminotransferase (ALT), alkaline phosphatase (ALP), triacylglycerols (TG), total cholesterol (TC), total bilirubin (TBIL), hepatic reactive oxygen species (ROS), malondialdehyde (MDA), nitric oxide (NO), 8-hydroxydeoxyguanosine (8-OHdG), tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6), and interleukin-8 (IL-8). RA also increased the levels of hepatic glutathione (GSH), superoxide dismutase (SOD), and catalase (CAT) and the protein expressions of Nrf2, quinine oxidoreductase (NQO1), and heme oxygenease-1 (HO-1). Histopathological examinations indicated that RA (20 and 40 mg/kg bw) alleviated the liver tissue injury induced by CCl4. Moreover, RA inhibited the hepatocyte apoptosis caused by CCl4 based on TUNEL assay. In vitro, RA pretreatment remarkably recovered the cell viability and reduced the CCl4-induced elevation of AST, ALT, lactate dehydrogenase (LDH), ROS, and 8-OHdG. Immunohistochemistry staining demonstrated that pretreatment with RA markedly inhibited the expression of IL-6, inducible nitric oxide synthase (iNOS), cyclooxygenase-2 (COX-2), and Caspase-3 in CCl4-treated hepatocytes. Additionally, RA pretreatment significantly decreased the elevation of mitochondrial membrane potential in CCl4-treated hepatocytes. Conclusions RA exerted a protective effect against CCl4-induced liver injury in mice through activating Nrf2 signaling pathway, reducing antioxidant damage, suppressing inflammatory response, and inhibiting hepatocyte apoptosis. RA could attenuate BRL hepatocyte ROS production, DNA oxidative damage, inflammatory response, and apoptosis induced by CCl4 exposure.
TL;DR: In this article , the effects of an Euterpe oleracea-enriched diet on motor performance, anxiety-like behavior, and memory retention were deeply investigated in Wistar rats.
Abstract: Background Açaí (Euterpe oleracea) has a rich nutritional composition, showing nutraceutical and protective effects in several organs. In this study, the effects of an açaí-enriched diet on motor performance, anxiety-like behavior, and memory retention were deeply investigated. Methods Eight-week male Wistar rats were fed with an Euterpe oleracea (EO) pulp-enriched diet, an olive oil-enriched (OO) diet (polyunsaturated fatty acid [PUFA] fat control diet), or a chow diet for 31 days (28 days pre-treatment and 3 days during behavioral tests). Afterward, animals were submitted to a battery of behavioral tests to evaluate spontaneous motor behavior (open-field test), anxiety-like behavior (elevated plus maze and open-field test), and memory retention (step-down). Oxidative stress in the hippocampus was evaluated by a lipid peroxidation assay. Results EO-enriched diet did not influence the body weight and food intake but increased the glucose plasmatic level after 31 days under this diet. However, a similar fat-enriched diet stimulated a marked weight gain and reduced the food intake, followed by changes in the plasmatic lipid markers. EO-enriched diet preserved the motor spontaneous performance, increased the exploration in the aversive environment (anxiolytic-like effects), and elevated the latency to step-down (improved memory retention). The EO-enriched diet also reduced the level of lipid peroxidation in the hippocampus. These positive effects of EO-enriched diet can greatly support the usage of this diet as a preventive therapy. Conclusion Taken together, the current study suggests that Euterpe oleracea-enriched diet promotes anxiolytic-like effects and improves memory consolidation, possibly due to the reduced levels of lipid peroxidation in the hippocampus.
TL;DR: The results implied that GJ-4 might be a promising drug to improve VD through the regulation of microglial M1/M2 polarization and the subsequent inhibition of neuro-inflammation.
Abstract: Background GJ-4 is extracted from Gardenia jasminoides J. Ellis (Fructus Gardenia) with crocin composition and has been demonstrated to improve memory deficits in several dementia models in our previous studies. Objective This study aimed to evaluate the effects of GJ-4 on hyperlipidemic vascular dementia (VD) and explore the underlying mechanisms. Design In the current study, we employed a chronic hyperlipidemic VD rat model by permanent bilateral common carotid arteries occlusion (2-VO) based on high-fat diet (HFD), which is an ideal model to mimic the clinical pathogenesis of human VD. Results Our results showed that GJ-4 could significantly reduce serum lipids level and improve cerebral blood flow in hyperlipidemic VD rats. Additionally, treatment with GJ-4 remarkedly ameliorated memory impairment and alleviated neuronal injury. Mechanistic investigation revealed that the neuroprotective effects of GJ-4 might be attributed to the inhibition of microglia-mediated neuro-inflammation via regulating the M1/M2 polarization. Our data further illustrated that GJ-4 could regulate the phenotype of microglia through activating the peroxisome proliferator-activated receptor-γ (PPAR-γ) and subsequently inhibited nuclear factor-κB (NF-κB) nuclear translocation and increased CCAAT/enhancer-binding protein β (C/EBPβ) expression. Conclusion Our results implied that GJ-4 might be a promising drug to improve VD through the regulation of microglial M1/M2 polarization and the subsequent inhibition of neuro-inflammation.