Contribution of visceral fat mass to the insulin resistance of aging
ABSTRACT Recent studies have shown that central obesity (increased waist to hip ratio [WHR]) is related to insulin resistance and aging. Furthermore, in central-obesity states, the intraabdominal fat (IAF) depot has been postulated to contribute most to the development of insulin resistance. Therefore, the observed insulin resistance of aging may be related more to changes in body composition than to aging per se. The purpose of this study was to explore the association of IAF with age and insulin sensitivity (SI) after controlling for obesity. We examined 60 healthy nondiabetic subjects (normal 75-g oral glucose tolerance test, aged 23 to 83, 15 men and 45 women). We chose subjects so that those < or = 125% and greater than 125% of ideal body weight were equally represented in each age decade. We quantified total and subcutaneous abdominal fat and IAF at the umbilicus using a validated magnetic resonance imaging (MRI) scanning technique and determined SI using a modified minimal model. IAF correlated significantly with age (r = .49, P = .0001) in the group as a whole, as well as in men (r = .58, P = .022) and women (r = .48, P = .0008) separately. In all subjects, SI was significantly related to IAF (r = -.50, P < .0001) but was not related to age (r = .00, P = .98). In multivariate analysis for various combinations of age, sex, and measures of fat distribution, WHR accounted for 28% and IAF for 51% of the variance in SI, whereas age, sex, and interactions of age and sex accounted for only 1%.(ABSTRACT TRUNCATED AT 250 WORDS)
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- "The AT from different anatomic locations differs in fatty acid metabolism . Visceral (vc) AT mass is more strongly correlated with IS , increased risk of developing diabetes type 2, and atherosclerosis  than subcutaneous (sc) AT. "
ABSTRACT: Adipose tissue (AT) depots are heterogeneous in terms of morphology and adipocyte metabolism. Adiponectin, one of the most abundant adipokines, is known for its insulin sensitising effects and its role in glucose and lipid metabolism. Very little is known about the presence of adiponectin protein in visceral (vc) and subcutaneous (sc) AT depots. We assessed serum adiponectin and adiponectin protein concentrations and the molecular weight forms in vc (mesenterial, omental and retroperitoneal) and sc (sternum, tail-head and withers) AT of primiparous dairy cows during early lactation. Primiparous German Holstein cows (n = 25) were divided into a control (CON) and a conjugated linoleic acid (CLA) group. From day 1 of lactation until slaughter, CLA cows were fed 100 g of a CLA supplement/d (about 6% of cis-9, trans-11 and trans-10, cis-12 isomers each), whereas the CON cows received 100 g of a fatty acid mixture/d instead of CLA. Blood samples from all animals were collected from 3 wk before calving until slaughter on day 1 (n = 5, CON cows), 42 (n = 5 each of CON and CLA cows) and 105 (n = 5 each of CON and CLA cows) of lactation when samples from different AT depots were obtained. Adiponectin was measured in serum and tissue by ELISA. In all AT depots adiponectin concentrations were lowest on day 1 compared to day 42 and day 105, and circulating adiponectin reached a nadir around parturition. Retroperitoneal AT had the lowest adiponectin concentrations, however, when taking total depot mass into consideration, the portion of circulating adiponectin was higher in vc than sc AT. Serum adiponectin was positively correlated with adiponectin protein concentrations but not with the mRNA abundance in all fat depots. The CLA supplementation did not affect adiponectin concentrations in AT depots. Furthermore, inverse associations between circulating adiponectin and measures of body condition (empty body weight, back fat thickness and vc AT mass) were observed. In all AT depots at each time, adiponectin was present as high (about 300 kDa) and medium (about 150 kDa) molecular weight complexes similar to that of the blood serum. These data suggest differential contribution of AT depots to circulating adiponectin.Domestic animal endocrinology 12/2013; DOI:10.1016/j.domaniend.2013.12.001 · 2.17 Impact Factor
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- "Obesity-related adverse health consequences, however, are less related to total body fat deposition, and more strongly associated with a precise fat distribution. More specifically, lower body1 and abdominal subcutaneous2-4 fat accumulation are associated with reduced metabolic perturbations whereas upper body fat distribution and increased visceral fat,5-8 is associated with metabolic dysregulation. Metabolic disorders associated with upper body/visceral obesity include dyslipidemia,9 hypertension,10,11 insulin resistance and type 2 diabetes.12,13 "
ABSTRACT: Increased visceral adiposity is a risk factor for metabolic disorders such as dyslipidemia, hypertension, insulin resistance and type 2 diabetes, whereas peripheral (subcutaneous) obesity is not. Though the specific mechanisms which contribute to these adipose depot differences are unknown, visceral fat accumulation is proposed to result in metabolic dysregulation because of increased effluent, e.g., fatty acids and/or adipokines/cytokines, to the liver via the hepatic portal vein. Pathological significance of visceral fat accumulation is also attributed to adipose depot/adipocyte-specific characteristics, specifically differences in structural, physiologic and metabolic characteristics compared with subcutaneous fat. Fat manipulations, such as removal or transplantation, have been utilized to identify location dependent or independent factors that play a role in metabolic dysregulation. Obesity-induced alterations in adipose tissue function/intrinsic characteristics, but not mass, appear to be responsible for obesity-induced metabolic dysregulation, thus "quality" is more important than "quantity." This review summarizes the implications of obesity-induced metabolic dysfunction as it relates to anatomic site and inherent adipocyte characteristics.10/2012; 1(4):192-199. DOI:10.4161/adip.21756
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- "there could be 75% of adults that are overweight or obese by 2015 . Obesity is a major risk factor for developing T2DM  . Moreover, obesity in middle-age subjects is a negative modifier of T2DM . "
ABSTRACT: Metabolic dysregulation, including abnormal glucose utilization and insulin resistance or deficiency, occurs at an early stage of AD independent of type II diabetes mellitus (T2DM). Thus, AD has been considered as type 3 diabetes. T2DM is a risk factor for AD; the coexistence of these two diseases in a society with an increasing mean age is a significant issue. Recently, research has focused on shared molecular mechanisms in these two diseases with the goal of determining whether treating T2DM can lessen the severity of AD. The progress in this field lends strong support to several mechanisms that could affect these two diseases, including insulin resistance and signaling, vascular injuries, inflammation, and the receptor for advanced glycation endproducts and their ligands. In this paper, we focus on inflammation-based mechanisms in both diseases and discuss potential synergism in these mechanisms when these two diseases coexist in the same patient.International Journal of Alzheimer's Disease 06/2012; 2012:918680. DOI:10.1155/2012/918680