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C Bogardus

Researcher at National Institutes of Health

Publications -  91
Citations -  11766

C Bogardus is an academic researcher from National Institutes of Health. The author has contributed to research in topics: Insulin & Insulin resistance. The author has an hindex of 53, co-authored 91 publications receiving 11394 citations. Previous affiliations of C Bogardus include University of Vermont.

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Skeletal Muscle Triglyceride Levels Are Inversely Related to Insulin Action

TL;DR: The results suggest that in this human population, as in animal models, skeletal muscle insulin sensitivity is strongly influenced by local supplies of triglycerides, as well as by remote depots and circulating lipids.
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Skeletal muscle capillary density and fiber type are possible determinants of in vivo insulin resistance in man.

TL;DR: The data suggest that diffusion distance from capillary to muscle cells or some associated biochemical change, and fiber type, could play a role in determining in vivo insulin action and may provide at least a partial explanation for the insulin resistance associated with obesity.
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Enlarged subcutaneous abdominal adipocyte size, but not obesity itself, predicts type II diabetes independent of insulin resistance.

TL;DR: Although enlarged mean subcutaneous abdominal adipocyte size is associated with insulin resistance cross-sectionally, prospectively, both abnormalities are independent and additive predictors of Type II diabetes.
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Low ratio of fat to carbohydrate oxidation as predictor of weight gain: study of 24-h RQ

TL;DR: It is concluded that in Pima Indians fed a standard diet 1) family membership is the principal determinant of the ratio of fat to carbohydrate oxidation, and 2) a low ratio of fats to carbohydrates is associated with subsequent weight gain independent of low energy expenditure and may contribute to the familial aggregation of obesity.
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Relationships between insulin secretion, insulin action, and fasting plasma glucose concentration in nondiabetic and noninsulin-dependent diabetic subjects.

TL;DR: Decreased peripheral insulin availability leads to increased FFA concentrations and lipid oxidation rates (and probably also increased concentrations of gluconeogenic precursors) that together stimulate gluconeogenesis, hepatic glucose production, and progressive hyperglycemia.