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Journal ArticleDOI

Gender differences in the association of visceral and subcutaneous adiposity with adiponectin in African Americans: the Jackson Heart Study

22 Feb 2013-BMC Cardiovascular Disorders (BioMed Central)-Vol. 13, Iss: 1, pp 9-9

TL;DR: The statistically significant inverse association of VAT and adiponectin persisted after additionally adjusting for SAT, body mass index (BMI) and waist circumference (WC), suggesting that VAT provides significant information above and beyond BMI and WC.

AbstractAdiponectin, paradoxically reduced in obesity and with lower levels in African Americans (AA), modulates several cardiometabolic risk factors. Because abdominal visceral adipose tissue (VAT), known to be reduced in AA, and subcutaneous adipose tissue (SAT) compartments may confer differential metabolic risk profiles, we investigated the associations of VAT and SAT with serum adiponectin, separately by gender, with the hypothesis that VAT is more strongly inversely associated with adiponectin than SAT. Participants from the Jackson Heart Study, an ongoing cohort of AA (n = 2,799; 64% women; mean age, 55 ± 11 years) underwent computer tomography assessment of SAT and VAT volumes, and had stored serum specimens analyzed for adiponectin levels. These levels were examined by gender in relation to increments of VAT and SAT. Compared to women, men had significantly lower mean levels of adiponectin (3.9 ± 3.0 μg/mL vs. 6.0 ± 4.4 μg/mL; p < 0.01) and mean volume of SAT (1,721 ± 803 cm3 vs. 2,668 ± 968 cm3; p < 0.01) but significantly higher mean volume of VAT (884 ± 416 cm3 vs. 801 ± 363 cm3; p < 0.01). Among women, a one standard deviation increment in VAT was inversely associated with adiponectin (β = − 0.13; p < 0.0001) after controlling for age, systolic blood pressure, fasting plasma glucose, high-density lipoprotein cholesterol, triglycerides, education, pack-years of smoking and daily intake of alcohol. The statistically significant inverse association of VAT and adiponectin persisted after additionally adjusting for SAT, body mass index (BMI) and waist circumference (WC), suggesting that VAT provides significant information above and beyond BMI and WC. Among men, after the same multivariable adjustment, there was a direct association of SAT and adiponectin (β = 0.18; p = 0.002) that persisted when controlling for BMI and WC, supporting a beneficial effect of SAT. Insulin resistance mediated the association of SAT with adiponectin in women. In African Americans, abdominal visceral adipose tissue had an inverse association with serum adiponectin concentrations only among women. Abdominal subcutaneous adipose tissue appeared as a protective fat depot in men.

Topics: Adiponectin (58%)

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Journal ArticleDOI
TL;DR: The role of adipocytokines and proinflammatory cytokines in the pathogenesis of NAFLD is explored, particularly on adiponectin, leptin and ghrelin, with a brief mention of resistin, visfatin and retinol-binding protein 4 among adipokines, and tumor necrosis factor-α, interleukin (IL)-6, IL-1, and briefly IL-18 among pro inflammatory cytokines.
Abstract: Nonalcoholic fatty liver disease (NAFLD) is a condition in which excess fat accumulates in the liver of a patient with no history of alcohol abuse or other causes for secondary hepatic steatosis. The pathogenesis of NAFLD and nonalcoholic steatohepatitis (NASH) has not been fully elucidated. The “two-hit“ hypothesis is probably a too simplified model to elaborate complex pathogenetic events occurring in patients with NASH. It should be better regarded as a multiple step process, with accumulation of liver fat being the first step, followed by the development of necroinflammation and fibrosis. Adipose tissue, which has emerged as an endocrine organ with a key role in energy homeostasis, is responsive to both central and peripheral metabolic signals and is itself capable of secreting a number of proteins. These adipocyte-specific or enriched proteins, termed adipokines, have been shown to have a variety of local, peripheral, and central effects. In the current review, we explore the role of adipocytokines and proinflammatory cytokines in the pathogenesis of NAFLD. We particularly focus on adiponectin, leptin and ghrelin, with a brief mention of resistin, visfatin and retinol-binding protein 4 among adipokines, and tumor necrosis factor-α, interleukin (IL)-6, IL-1, and briefly IL-18 among proinflammatory cytokines. We update their role in NAFLD, as elucidated in experimental models and clinical practice.

207 citations


Journal ArticleDOI
10 Dec 2014
TL;DR: It seems that in the pig and humans, INTMF and VAT share a similar pattern of distribution and a similar association of components dictating insulin sensitivity, while in pigs, the relationship between leanness and higher proportions of IN TMF fat in pigs was not observed in human studies and was not corroborated by other pig studies.
Abstract: Human studies of the influence of aging and other factors on intermuscular fat (INTMF) were reviewed. Intermuscular fat increased with weight loss, weight gain, or with no weight change with age in humans. An increase in INTMF represents a similar threat to type 2 diabetes and insulin resistance as does visceral adipose tissue (VAT). Studies of INTMF in animals covered topics such as quantitative deposition and genetic relationships with other fat depots. The relationship between leanness and higher proportions of INTMF fat in pigs was not observed in human studies and was not corroborated by other pig studies. In humans, changes in muscle mass, strength and quality are associated with INTMF accretion with aging. Gene expression profiling and intrinsic methylation differences in pigs demonstrated that INTMF and VAT are primarily associated with inflammatory and immune processes. It seems that in the pig and humans, INTMF and VAT share a similar pattern of distribution and a similar association of components dictating insulin sensitivity. Studies on intramuscular (IM) adipocyte development in meat animals were reviewed. Gene expression analysis and genetic analysis have identified candidate genes involved in IM adipocyte development. Intramuscular (IM) adipocyte development in human muscle is only seen during aging and some pathological circumstance. Several genetic links between human and meat animal adipogenesis have been identified. In pigs, the Lipin1 and Lipin 2 gene have strong genetic effects on IM accumulation. Lipin1 deficiency results in immature adipocyte development in human lipodystrophy. In humans, overexpression of Perilipin 2 (PLIN2) facilitates intramyocellular lipid accretion whereas in pigs PLIN2 gene expression is associated with IM deposition. Lipins and perilipins may influence intramuscular lipid regardless of species.

81 citations


Cites background from "Gender differences in the associati..."

  • ...The protective action of gluteal femoral SQF seems to be further limited to the femoral subcutaneous region and not necessarily with the gluteal region in black South African women further confounding the issue with ethnicity differences.(11,16,25,27,29-32) Indeed, even gender appears to have a profound influence on the responses by different adipose depots....

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  • ...Indeed, even gender appears to have a profound influence on the responses by different adipose depots.(16,32-34) One mechanism that seems universal in human adipose depot regulation of adipose tissue is insulin, although, with as much variation within one species (human) one can only imagine the differences which exist between species....

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  • ...Issues associated with adipose depot include disruption of normal function of organs due to infiltration with lipid-filled adipocytes—for example, nonalcoholic fatty livers are not capable of functioning as properly as normal livers, and is likely a precursor of fatty infiltration into other organs/tissues.(9,16) An interest of this paper is on the specific differences in INTMF vs....

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Journal ArticleDOI
TL;DR: Dietary intake of natural products endowed with anti-oxidant and anti-inflammatory activities may represent a valid interventional approach for preventing and/or attenuating the pathological consequences of obesity.
Abstract: Childhood obesity is characterized by a low grade inflammation status depending on the multicellular release of cytokines, adipokines and reactive oxygen species. In particular, the imbalance between anti-inflammatory T regulatory cells and inflammatory T helper 17 cells seems to sustain such a phlogistic condition. Alterations of gut microbiota since childhood also contribute to the maintenance of inflammation. Therefore, besides preventive measures and caloric restrictions, dietary intake of natural products endowed with anti-oxidant and anti-inflammatory activities may represent a valid interventional approach for preventing and/or attenuating the pathological consequences of obesity. In this regard, the use of prebiotics, probiotics, polyphenols, polyunsaturated fatty acids, vitamins and melatonin in human clinical trials will be described.

53 citations


Cites background from "Gender differences in the associati..."

  • ...They secrete in large amounts TNF-α, IL-6, IL-12, IL-1β, and monocyte chemotactic protein-1 (MCP-1), as well as nitric oxide (NO) (24)....

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  • ...Adiponectin exerts anti-inflammatory activities, inhibiting IL-6 and TNF-α production (112)....

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  • ...On the other hand, IL-1β, IL-6, and IL-8 serum levels were increased in asthmatic obese and obese children in comparison to asthmatic children and controls....

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  • ...Treated subjects exhibited a significant reduction in weight as well as in TNF-α and IL-6 with an increase in adiponectin in comparison to the placebo group....

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  • ...In view of its beneficial activities, melatonin has successfully been used in rats with MetS diminishing insulin resistance, release of TNF-α and IL-6 from adipocytes, low-density lipoprotein, and very low-density lipoprotein plasma levels and body weight (182)....

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Journal ArticleDOI
01 Mar 2014-Headache
TL;DR: The potential mechanisms for the migraine–obesity association are discussed, with a focus on the central and peripheral pathophysiological pathways which overlap between migraine and those modulating the drive to feed.
Abstract: Obesity and headache are both associated with a substantial personal and societal impact, and epidemiologic studies have consistently identified a positive association between obesity and headache in general, as well as obesity and migraine specifically (see part I). In the current manuscript, we will discuss the potential mechanisms for the migraine–obesity association, with a focus on the central and peripheral pathophysiological pathways which overlap between migraine and those modulating the drive to feed. We then discuss surgical, behavioral, and pharmacological treatment considerations for overweight and obese migraineurs as well as for those with idiopathic intracranial hypertension. We close by briefly discussing where future research may be headed in light of this data.

49 citations


Cites background from "Gender differences in the associati..."

  • ...The majority of studies also support that ADP levels are inversely associated with obesity, with obese individuals having lower fasting ADP levels.(36,37) In the first trial evaluating interictal ADP levels in episodic and chronic migraineurs,(38) ADP and its multimers were measured in 37 participants (EM: 13; CM: 12; Control 12)....

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Journal ArticleDOI
TL;DR: More work is needed to understand barriers to behavior change for black women, and knowledge gaps remain in identifying mechanisms by which pharmacologic and surgical treatments for obesity modify cardiovascular risk in black women.
Abstract: Black women in the United States are disproportionately affected by obesity, with almost two-thirds considered obese based on body mass index Obesity has been directly linked to cardiovascular morbidity and mortality in black women Therefore, understanding contributors to the genesis of obesity in black women is imperative While biologic differences likely result in varying obesity prevalence across racial/ethnic groups, behaviors such as post-partum weight retention and limited leisure-time physical activity, may especially contribute to obesity in black women Black women also appear to be particularly susceptible to cultural, psychosocial, and environmental factors that can promote weight gain Therapeutic interventions are being tailored to specifically address these social determinants of health and to foster lifestyle modification; however, more work is needed to understand barriers to behavior change for black women Knowledge gaps also remain in identifying mechanisms by which pharmacologic and surgical treatments for obesity modify cardiovascular risk in black women

43 citations


References
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Journal ArticleDOI
TL;DR: The correlation of the model's estimates with patient data accords with the hypothesis that basal glucose and insulin interactions are largely determined by a simple feed back loop.
Abstract: The steady-state basal plasma glucose and insulin concentrations are determined by their interaction in a feedback loop. A computer-solved model has been used to predict the homeostatic concentrations which arise from varying degrees beta-cell deficiency and insulin resistance. Comparison of a patient's fasting values with the model's predictions allows a quantitative assessment of the contributions of insulin resistance and deficient beta-cell function to the fasting hyperglycaemia (homeostasis model assessment, HOMA). The accuracy and precision of the estimate have been determined by comparison with independent measures of insulin resistance and beta-cell function using hyperglycaemic and euglycaemic clamps and an intravenous glucose tolerance test. The estimate of insulin resistance obtained by homeostasis model assessment correlated with estimates obtained by use of the euglycaemic clamp (Rs = 0.88, p less than 0.0001), the fasting insulin concentration (Rs = 0.81, p less than 0.0001), and the hyperglycaemic clamp, (Rs = 0.69, p less than 0.01). There was no correlation with any aspect of insulin-receptor binding. The estimate of deficient beta-cell function obtained by homeostasis model assessment correlated with that derived using the hyperglycaemic clamp (Rs = 0.61, p less than 0.01) and with the estimate from the intravenous glucose tolerance test (Rs = 0.64, p less than 0.05). The low precision of the estimates from the model (coefficients of variation: 31% for insulin resistance and 32% for beta-cell deficit) limits its use, but the correlation of the model's estimates with patient data accords with the hypothesis that basal glucose and insulin interactions are largely determined by a simple feed back loop.

26,901 citations


Journal ArticleDOI
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TL;DR: The ob gene product may function as part of a signalling pathway from adipose tissue that acts to regulate the size of the body fat depot.
Abstract: The mechanisms that balance food intake and energy expenditure determine who will be obese and who will be lean. One of the molecules that regulates energy balance in the mouse is the obese (ob) gene. Mutation of ob results in profound obesity and type II diabetes as part of a syndrome that resembles morbid obesity in humans. The ob gene product may function as part of a signalling pathway from adipose tissue that acts to regulate the size of the body fat depot.

11,990 citations


"Gender differences in the associati..." refers background in this paper

  • ..., leptin [42], adiponectin [43], tumor necrosis factor-α (TNF-α) [44], plasminogenactivator inhibitor type-1 (PAI-1) [45] and resistin [46]....

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Journal ArticleDOI
01 Jan 1993-Science
TL;DR: A role for TNF-alpha in obesity and particularly in the insulin resistance and diabetes that often accompany obesity is indicated.
Abstract: Tumor necrosis factor-alpha (TNF-alpha) has been shown to have certain catabolic effects on fat cells and whole animals. An induction of TNF-alpha messenger RNA expression was observed in adipose tissue from four different rodent models of obesity and diabetes. TNF-alpha protein was also elevated locally and systemically. Neutralization of TNF-alpha in obese fa/fa rats caused a significant increase in the peripheral uptake of glucose in response to insulin. These results indicate a role for TNF-alpha in obesity and particularly in the insulin resistance and diabetes that often accompany obesity.

6,903 citations


Additional excerpts

  • ...Several studies have demonstrated that adipose tissue actively produces a variety of locally and systemically functioning bioactive molecules that interact in various obesity-related diseases, e.g., leptin [42], adiponectin [43], tumor necrosis factor-α (TNF-α) [44], plasminogenactivator inhibitor type-1 (PAI-1) [45] and resistin [46]....

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  • ..., leptin [42], adiponectin [43], tumor necrosis factor-α (TNF-α) [44], plasminogen-activator inhibitor type-1 (PAI-1) [45] and resistin [46]....

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Journal ArticleDOI
TL;DR: Plasma concentrations of adiponectin in obese subjects were significantly lower than those in non-obese subjects, although adip onectin is secreted only from adipose tissue.
Abstract: We isolated the human adipose-specific and most abundant gene transcript, apM1 (Maeda, K., et al.,Biochem. Biophys. Res. Commun.221, 286–289, 1996). The apM1 gene product was a kind of soluble matrix protein, which we named adiponectin. To quantitate the plasma adiponectin concentration, we have produced monoclonal and polyclonal antibodies for human adiponectin and developed an enzyme-linked immunosorbent assay (ELISA) system. Adiponectin was abundantly present in the plasma of healthy volunteers in the range from 1.9 to 17.0 mg/ml. Plasma concentrations of adiponectin in obese subjects were significantly lower than those in non-obese subjects, although adiponectin is secreted only from adipose tissue. The ELISA system developed in this study will be useful for elucidating the physiological and pathophysiological role of adiponectin in humans.

4,718 citations


Journal ArticleDOI
18 Jan 2001-Nature
TL;DR: It is shown that adipocytes secrete a unique signalling molecule, which is named resistin (for resistance to insulin), which circulating resistin levels are decreased by the anti-diabetic drug rosiglitazone, and increased in diet-induced and genetic forms of obesity.
Abstract: Diabetes mellitus is a chronic disease that leads to complications including heart disease, stroke, kidney failure, blindness and nerve damage. Type 2 diabetes, characterized by target-tissue resistance to insulin, is epidemic in industrialized societies and is strongly associated with obesity; however, the mechanism by which increased adiposity causes insulin resistance is unclear. Here we show that adipocytes secrete a unique signalling molecule, which we have named resistin (for resistance to insulin). Circulating resistin levels are decreased by the anti-diabetic drug rosiglitazone, and increased in diet-induced and genetic forms of obesity. Administration of anti-resistin antibody improves blood sugar and insulin action in mice with diet-induced obesity. Moreover, treatment of normal mice with recombinant resistin impairs glucose tolerance and insulin action. Insulin-stimulated glucose uptake by adipocytes is enhanced by neutralization of resistin and is reduced by resistin treatment. Resistin is thus a hormone that potentially links obesity to diabetes.

4,355 citations


Additional excerpts

  • ..., leptin [42], adiponectin [43], tumor necrosis factor-α (TNF-α) [44], plasminogen-activator inhibitor type-1 (PAI-1) [45] and resistin [46]....

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