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      Obesity and Type 2 Diabetes: What Can Be Unified and What Needs to Be Individualized?

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          There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.

          Abstract

          Objective:

          This report examines what is known about the relationship between obesity and type 2 diabetes and how future research in these areas might be directed to benefit prevention, interventions, and overall patient care.

          Research Design and Methods:

          An international working group of 32 experts in the pathophysiology, genetics, clinical trials, and clinical care of obesity and/or type 2 diabetes participated in a conference held on 6–7 January 2011 and cosponsored by The Endocrine Society, the American Diabetes Association, and the European Association for the Study of Diabetes. A writing group comprising eight participants subsequently prepared this summary and recommendations. Participants reviewed and discussed published literature and their own unpublished data.

          Results:

          The writing group unanimously supported the summary and recommendations as representing the working group's majority or unanimous opinions.

          Conclusions:

          The major questions linking obesity to type 2 diabetes that need to be addressed by combined basic, clinical, and population-based scientific approaches include the following: 1) Why do not all patients with obesity develop type 2 diabetes? 2) Through what mechanisms do obesity and insulin resistance contribute to β-cell decompensation, and if/when obesity prevention ensues, how much reduction in type 2 diabetes incidence will follow? 3) How does the duration of type 2 diabetes relate to the benefits of weight reduction by lifestyle, weight-loss drugs, and/or bariatric surgery on β-cell function and glycemia? 4) What is necessary for regulatory approval of medications and possibly surgical approaches for preventing type 2 diabetes in patients with obesity? Improved understanding of how obesity relates to type 2 diabetes may help advance effective and cost-effective interventions for both conditions, including more tailored therapy. To expedite this process, we recommend further investigation into the pathogenesis of these coexistent conditions and innovative approaches to their pharmacological and surgical management.

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          Most cited references46

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          Reduction in the incidence of type 2 diabetes with lifestyle intervention or metformin.

          Type 2 diabetes affects approximately 8 percent of adults in the United States. Some risk factors--elevated plasma glucose concentrations in the fasting state and after an oral glucose load, overweight, and a sedentary lifestyle--are potentially reversible. We hypothesized that modifying these factors with a lifestyle-intervention program or the administration of metformin would prevent or delay the development of diabetes. We randomly assigned 3234 nondiabetic persons with elevated fasting and post-load plasma glucose concentrations to placebo, metformin (850 mg twice daily), or a lifestyle-modification program with the goals of at least a 7 percent weight loss and at least 150 minutes of physical activity per week. The mean age of the participants was 51 years, and the mean body-mass index (the weight in kilograms divided by the square of the height in meters) was 34.0; 68 percent were women, and 45 percent were members of minority groups. The average follow-up was 2.8 years. The incidence of diabetes was 11.0, 7.8, and 4.8 cases per 100 person-years in the placebo, metformin, and lifestyle groups, respectively. The lifestyle intervention reduced the incidence by 58 percent (95 percent confidence interval, 48 to 66 percent) and metformin by 31 percent (95 percent confidence interval, 17 to 43 percent), as compared with placebo; the lifestyle intervention was significantly more effective than metformin. To prevent one case of diabetes during a period of three years, 6.9 persons would have to participate in the lifestyle-intervention program, and 13.9 would have to receive metformin. Lifestyle changes and treatment with metformin both reduced the incidence of diabetes in persons at high risk. The lifestyle intervention was more effective than metformin.
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            Mechanisms linking obesity to insulin resistance and type 2 diabetes.

            Obesity is associated with an increased risk of developing insulin resistance and type 2 diabetes. In obese individuals, adipose tissue releases increased amounts of non-esterified fatty acids, glycerol, hormones, pro-inflammatory cytokines and other factors that are involved in the development of insulin resistance. When insulin resistance is accompanied by dysfunction of pancreatic islet beta-cells - the cells that release insulin - failure to control blood glucose levels results. Abnormalities in beta-cell function are therefore critical in defining the risk and development of type 2 diabetes. This knowledge is fostering exploration of the molecular and genetic basis of the disease and new approaches to its treatment and prevention.
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              Obesity is associated with macrophage accumulation in adipose tissue

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                Author and article information

                Journal
                The Journal of Clinical Endocrinology & Metabolism
                The Endocrine Society
                0021-972X
                1945-7197
                June 01 2011
                June 01 2011
                : 96
                : 6
                : 1654-1663
                Affiliations
                [1 ]Division of Endocrinology, Metabolism and Diabetes, and Cardiology (R.H.E.), Department of Medicine, University of Colorado Anschutz Medical Campus, Aurora, Colorado 80045;
                [2 ]Division of Metabolism, Endocrinology and Nutrition (S.E.K.), Department of Medicine, VA Puget Sound Health Care System and University of Washington, Seattle, Washington 98108;
                [3 ]Department of Internal Medicine (E.F.), University of Pisa, 56100 Pisa, Italy;
                [4 ]Joslin Diabetes Center and Harvard Medical School (A.B.G.), Boston, Massachusetts 02115;
                [5 ]Clinical Research Center and Diabetes Center (D.M.N.), Massachusetts General Hospital and Harvard Medical School, Boston, Massachusetts 02114;
                [6 ]Division of Metabolism, Endocrinology and Nutrition (M.W.S.), Department of Medicine, University of Washington, Seattle, Washington 98109;
                [7 ]Division of Endocrinology and the Hallett Center for Diabetes and Endocrinology (R.J.S.), Alpert Medical School of Brown University, Providence, Rhode Island 02914;
                [8 ]Translational Research Institute for Metabolism and Diabetes (S.R.S.), Florida Hospital–Sanford/Burnham Research Institute, Orlando, Florida 32827
                Article
                10.1210/jc.2011-0585
                3206399
                21602457
                5a33c0c7-2d62-4ecb-8924-2b5e0db88f6f
                © 2011
                History

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