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      Adipose tissue expression of adipose (WDTC1) gene is associated with lower fat mass and enhanced insulin sensitivity in humans

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          Abstract

          The overexpression of the adipose gene ( adp/WDTC1) in mice inhibits lipid accumulation and improves the metabolic profile.

          Objective

          We evaluated subcutaneous fat adp expression in humans and its relation to metabolic parameters.

          Design, Setting and Methods

          Abdominal subcutaneous fat adp expression, insulin sensitivity (clamp) and respiratory quotient (RQ; indirect calorimetry) were assessed in: 36 obese and 56 BMI-, race- and sex-matched type 2 diabetic volunteers (Look AHEAD Adipose Ancillary Study); 37 non-diabetic Pima Indians including obese (n=18) and non-obese (n=19) subjects and; 62 non-obese non-diabetic subjects at the Pennington Center in the ADAPT study.

          Results

          In the Look AHEAD Study, adp expression normalized for cyclophilin B was higher in males vs. females (1.27±0.06 vs. 1.11±0.04; p<0.01) but not after controlling for body fat. Adp expression was not influenced by the presence of diabetes but was related to body fat (r=−0.23; p=0.03), insulin sensitivity (r=0.23; p=0.03) and fasting/insulin-stimulated RQ (r=0.31 & 0.33; p<0.01). In Pima Indians, adp expression was also higher in males vs. females (1.00±0.05 vs. 0.77±0.05; p=0.02) and higher in non-obese vs. obese (1.02±0.05 vs. 0.80±0.06; p=0.03). In the ADAPT study, there was no difference in adp expression between males and females.

          Conclusion

          Consistent with animal studies, our results suggest that, high adp expression in human adipose tissue is associated with lower adiposity and enhanced glucose utilization.

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          Most cited references10

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          Obesity-associated improvements in metabolic profile through expansion of adipose tissue.

          Excess caloric intake can lead to insulin resistance. The underlying reasons are complex but likely related to ectopic lipid deposition in nonadipose tissue. We hypothesized that the inability to appropriately expand subcutaneous adipose tissue may be an underlying reason for insulin resistance and beta cell failure. Mice lacking leptin while overexpressing adiponectin showed normalized glucose and insulin levels and dramatically improved glucose as well as positively affected serum triglyceride levels. Therefore, modestly increasing the levels of circulating full-length adiponectin completely rescued the diabetic phenotype in ob/ob mice. They displayed increased expression of PPARgamma target genes and a reduction in macrophage infiltration in adipose tissue and systemic inflammation. As a result, the transgenic mice were morbidly obese, with significantly higher levels of adipose tissue than their ob/ob littermates, leading to an interesting dichotomy of increased fat mass associated with improvement in insulin sensitivity. Based on these data, we propose that adiponectin acts as a peripheral "starvation" signal promoting the storage of triglycerides preferentially in adipose tissue. As a consequence, reduced triglyceride levels in the liver and muscle convey improved systemic insulin sensitivity. These mice therefore represent what we believe is a novel model of morbid obesity associated with an improved metabolic profile.
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            Molecular regulation of adipogenesis.

            Adipogenesis, or the development of fat cells from preadipocytes, has been one of the most intensely studied models of cellular differentiation. In part this has been because of the availability of in vitro models that faithfully recapitulate most of the critical aspects of fat cell formation in vivo. More recently, studies of adipogenesis have proceeded with the hope that manipulation of this process in humans might one day lead to a reduction in the burden of obesity and diabetes. This review explores some of the highlights of a large and burgeoning literature devoted to understanding adipogenesis at the molecular level. The hormonal and transcriptional control of adipogenesis is reviewed, as well as studies on a less well known type of fat cell, the brown adipocyte. Emphasis is placed, where possible, on in vivo studies with the hope that the results discussed may one day shed light on basic questions of cellular growth and differentiation in addition to possible benefits in human health.
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              Look AHEAD (Action for Health in Diabetes): design and methods for a clinical trial of weight loss for the prevention of cardiovascular disease in type 2 diabetes.

              Overweight and obesity are major contributors to both type 2 diabetes and cardiovascular disease (CVD). Moreover, individuals with type 2 diabetes who are overweight or obese are at particularly high risk for CVD morbidity and mortality. Although short-term weight loss has been shown to ameliorate obesity-related metabolic abnormalities and CVD risk factors, the long-term consequences of intentional weight loss in overweight or obese individuals with type 2 diabetes have not been adequately examined. The primary objective of the Look AHEAD clinical trial is to assess the long-term effects (up to 11.5 years) of an intensive weight loss program delivered over 4 years in overweight and obese individuals with type 2 diabetes. Approximately 5000 male and female participants who have type 2 diabetes, are 45-74 years of age, and have a body mass index >or=25 kg/m(2) will be randomized to one of the two groups. The intensive lifestyle intervention is designed to achieve and maintain weight loss through decreased caloric intake and increased physical activity. This program is compared to a control condition given diabetes support and education. The primary study outcome is time to incidence of a major CVD event. The study is designed to provide a 0.90 probability of detecting an 18% difference in major CVD event rates between the two groups. Other outcomes include components of CVD risk, cost and cost-effectiveness, diabetes control and complications, hospitalizations, intervention processes, and quality of life.
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                Author and article information

                Journal
                101264860
                32902
                Obesity (Silver Spring)
                Obesity (Silver Spring)
                Obesity (Silver Spring, Md.)
                1930-7381
                1930-739X
                1 February 2013
                11 June 2013
                November 2013
                01 May 2014
                : 21
                : 11
                : 2244-2248
                Affiliations
                [1 ]Pennington Biomedical Research Center, Baton Rouge, USA
                [2 ]Department of Nutrition, Diabetes and Metabolism. School of Medicine. Pontifical Catholic University of Chile, Chile
                [3 ]Department of Medicine, University of Pittsburgh, Pittsburgh, USA
                [4 ]New York Obesity Nutrition Research Center, St. Luke’s Roosevelt Hospital, New York, NY, USA
                [5 ]Obesity and Diabetes Clinical Research Section. NIDDK, NIH. Phoenix, USA
                [6 ]Diabetes and Obesity Research Center. Sanford-Burnham Medical Research Institute, FL, USA
                Author notes
                Corresponding author: Eric Ravussin, PhD. Pennington Biomedical Research Center. 6400 Perkins Road, Baton Rouge, LA, 70808, USA. Phone: 225 763 3186. Fax: 225 763 2525.: Eric.Ravussin@ 123456pbrc.edu
                Article
                NIHMS435899
                10.1002/oby.20371
                3695019
                23512946
                a161f9b0-c1dd-4b63-8b88-e9891dbf122c
                History
                Categories
                Article

                Medicine
                obesity,insulin sensitivity,body fat
                Medicine
                obesity, insulin sensitivity, body fat

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