Anti-diabetic and anti-obesity: Efficacy evaluation and exploitation of polyphenols in fruits and vegetables.

The gastrointestinal tract of humans is a complex microbial ecosystem known as gut microbiota. The microbiota is involved in several critical physiological processes such as digestion, absorption, and related physiological functions and plays a crucial role in determining the host’s health. The habitual consumption of specific dietary components can impact beyond their nutritional benefits, altering gut microbiota diversity and function and could manipulate health. Phytochemicals are non-nutrient biologically active plant components that can modify the composition of gut microflora through selective stimulation of proliferation or inhibition of certain microbial communities in the intestine. Plants secrete these components, and they accumulate in the cell wall and cell sap compartments (body) for their development and survival. These compounds have low bioavailability and long time-retention in the intestine due to their poor absorption, resulting in beneficial impacts on gut microbiota population. Feeding diets containing phytochemicals to humans and animals may offer a path to improve the gut microbiome resulting in improved performance and/or health and wellbeing. This review discusses the effects of phytochemicals on the modulation of the gut microbiota environment and the resultant benefits to humans; however, the effect of phytochemicals on the gut microbiota of animals is also covered, in brief.

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The Impact of Plant Phytochemicals on the Gut Microbiota of Humans for a Balanced Life

With the increase in cannabis use due to policy changes and areas of decriminalization, it is important to recognize the potential impact of these substances on endocrine processes. Cannabinoids have many effects by activating the endocannabinoid system. This system plays a role in the normal functioning of nearly every organ and consists of the body’s natural endocannabinoids, the cannabinoid receptors, and the enzymes and processes that regulate endocannabinoids. Exogenous cannabinoids such as Δ9-tetrahydrocannabinol (THC) are known to act through cannabinoid type 1 and 2 receptors, and have been shown to mimic endocannabinoid signaling and affect receptor expression. This review summarizes the known impacts of cannabis on thyroid, adrenal, and gonadal function in addition to glucose control, lipids, and bone metabolism, including: reduced female fertility, increased risk of adverse pregnancy outcomes, reduced sperm counts and function, lower thyroid hormone levels with acute use, blunting of stress response with chronic use, increased risk of prediabetes but lower risk of diabetes, suggested improvement of high density lipoproteins and triglycerides, and modest increase in fracture risk. The known properties of endocannabinoids, animal data, population data, and the possible benefits and concerns of cannabinoid use on hormonal function are discussed. The interconnectivity of the endocrine and endocannabinoid systems suggests opportunities for future therapeutic modalities which are an area of active investigation.

The effects of cannabis and cannabinoids on the endocrine system

Secoiridoid dimers and their biogenetic precursors from the fruits of Cornus officinalis with potential therapeutic effects on type 2 diabetes.

The type 2 diabetes mellitus (T2DM) is an urgent global health problem. T2DM patients are in a state of high oxidative stress and inflammation. Vitamin D and glutathione (GSH) play crucial roles in antioxidation and anti‐inflammation. However, T2DM patients have lower vitamin D and GSH levels than healthy persons. A randomized controlled trial was conducted to see the effect of the vitamin D supplementation on oxidative stress and inflammatory factors in T2DM patients. In this study, a total of 178 T2DM patients were randomly enrolled, 92 patients received regular treatment (T2DM group) and 86 patients in Vitamin D group received extra vitamin D 400 IU per day in addition to regular treatment. Serum vitamin D, GSH, GSH metabolic enzyme GCLC and GR, inflammatory factor MCP‐1, and IL‐8 levels were investigated. We found that the T2DM group has significantly higher concentrations of MCP‐1 and IL‐8 than those in the healthy donor group. After vitamin D supplementation for 90 days, T2DM patients had a 2‐fold increase of GSH levels, from 2.72 ± 0.84 to 5.76 ± 3.19 μmol/ml, the concentration of MCP‐1 decreased from 51.11 ± 20.86 to 25.42 ± 13.06 pg/ml, and IL‐8 also decreased from 38.21 ± 21.76 to 16.05 ± 8.99 pg/ml. In conclusion, our study demonstrated that vitamin D could regulate the production of GSH, thereby reducing the serum levels of MCP‐1 and IL‐8, alleviating oxidative stress and inflammation, providing evidence of the necessity and feasibility of adjuvant vitamin D treatment among patients with T2DM. On the other hand, vitamin D and GSH levels have important diagnostic and prognostic values in T2DM patients.

https://onlinelibrary.wiley.com/doi/pdfdirect/10.1002/jcla.24430

Effect of vitamin D on oxidative stress and serum inflammatory factors in the patients with type 2 diabetes

Anti-inflammatory phytochemicals for the treatment of diabetes and its complications: Lessons learned and future promise.

https://doi.org/10.1016/j.fochx.2022.100307

Eugenol treatment delays the flesh browning of fresh-cut water chestnut (Eleocharis tuberosa) through regulating the metabolisms of phenolics and reactive oxygen species

Dysfunctional triglyceride‐very low‐density lipoprotein (TG‐VLDL) metabolism is linked to metabolic‐associated fatty liver disease (MAFLD); however, the underlying cause remains unclear. The study shows that hepatic E3 ubiquitin ligase murine double minute 2 (MDM2) controls MAFLD by blocking TG‐VLDL secretion. A remarkable upregulation of MDM2 is observed in the livers of human and mouse models with different levels of severity of MAFLD. Hepatocyte‐specific deletion of MDM2 protects against high‐fat high‐cholesterol diet‐induced hepatic steatosis and inflammation, accompanied by a significant elevation in TG‐VLDL secretion. As an E3 ubiquitin ligase, MDM2 targets apolipoprotein B (ApoB) for proteasomal degradation through direct protein–protein interaction, which leads to reduced TG‐VLDL secretion in hepatocytes. Pharmacological blockage of the MDM2‐ApoB interaction alleviates dietary‐induced hepatic steatohepatitis and fibrosis by inducing hepatic ApoB expression and subsequent TG‐VLDL secretion. The effect of MDM2 on VLDL metabolism is p53‐independent. Collectively, these findings suggest that MDM2 acts as a negative regulator of hepatic ApoB levels and TG‐VLDL secretion in MAFLD. Inhibition of the MDM2‐ApoB interaction may represent a potential therapeutic approach for MAFLD treatment.

https://onlinelibrary.wiley.com/doi/pdfdirect/10.1002/advs.202200742

Hepatic MDM2 Causes Metabolic Associated Fatty Liver Disease by Blocking Triglyceride‐VLDL Secretion via ApoB Degradation

Oligochitosan-based nanovesicles for nonalcoholic fatty liver disease treatment via the FXR/miR-34a/SIRT1 regulatory loop.

Browning inhibition in fresh-cut Chinese water chestnut under high pressure CO2 treatment: Regulation of reactive oxygen species and membrane lipid metabolism.

Mengjie Kong

Papers

Anti-inflammatory phytochemicals for the treatment of diabetes and its complications: Lessons learned and future promise.

Eugenol treatment delays the flesh browning of fresh-cut water chestnut (Eleocharis tuberosa) through regulating the metabolisms of phenolics and reactive oxygen species

Hepatic MDM2 Causes Metabolic Associated Fatty Liver Disease by Blocking Triglyceride‐VLDL Secretion via ApoB Degradation

Oligochitosan-based nanovesicles for nonalcoholic fatty liver disease treatment via the FXR/miR-34a/SIRT1 regulatory loop.

Browning inhibition in fresh-cut Chinese water chestnut under high pressure CO2 treatment: Regulation of reactive oxygen species and membrane lipid metabolism.