Distribution of in vivo insulin action in Pima Indians as mixture of three normal distributions

Bogardus, Clifton; Lillioja, Stephen; Nyomba, B. L.; Zurlo, F.; Swinburn, B.; Puente, A. Esposito-Del; Knowler, William C.; Ravussin, E.; Mott, D. M.; Bennett, P. H.

doi:10.2337/diabetes.38.11.1423

Cited by 65 publications

(49 citation statements)

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“…However, hyperglycemia, once manifest, also contributes to the worsening of insulin resistance (8,9). The magnitude and nature of insulin resistance that is primary, and presumably genetic in origin (55), versus that which is acquired secondarily to metabolic disturbances, such as hyperglycemia, is unclear. In vitro, high media glucose concentra- Data are means Ϯ SE.…”

Section: Discussionmentioning

confidence: 99%

Normalization of Plasma Glucose Concentration by Insulin Therapy Improves Insulin-Stimulated Glycogen Synthesis in Type 2 Diabetes

et al. 2002

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Considerable evidence suggests that skeletal muscle insulin resistance is an inherent feature of type 2 diabetes and contributes to the pathogenesis of the disease. In patients with poorly controlled diabetes, hyperglycemia is thought to produce additional insulin resistance in muscle. The magnitude and nature of hyperglycemia-induced insulin resistance is not known. The purpose of the present study was to determine the biochemical mechanisms responsible for increased insulin-stimulated glucose disposal after the achievement of tight glycemic control with a mixed-split regimen. We performed hyperinsulinemic-euglycemic clamps with indirect calorimetry and vastus lateralis muscle biopsies in eight type 2 diabetic patients who had poor glycemic control (HbA 1c 10.1%) and again after 3 months of intensive insulin therapy designed to produce nearnormoglycemia (HbA 1c 6.6%). Improved glycemic control increased insulin-stimulated glucose disposal

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Section: Discussionmentioning

confidence: 99%

Normalization of Plasma Glucose Concentration by Insulin Therapy Improves Insulin-Stimulated Glycogen Synthesis in Type 2 Diabetes

et al. 2002

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“…The gene or genes have not been identified but studies in non-diabetic Pima Indians demonstrate that insulin sensitivity has a familial aggregation and may be determined by a single gene with a codominant mode of inheritance (Bogardus et al, 1989) linked to chromosomal markers on 4q (Prochazka et al, 1993).…”

Section: Determinants Of Insulin Resistancementioning

confidence: 99%

The ‘carnivore connection’—evolutionary aspects of insulin resistance

Colagiuri

Brand-Miller

2002

Eur J Clin Nutr

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Insulin resistance is common and is determined by physiological (aging, physical fitness), pathological (obesity) and genetic factors. The metabolic compensatory response to insulin resistance is hyperinsulinaemia, the primary purpose of which is to maintain normal glucose tolerance. The 'carnivore connection' postulates a critical role for the quantity of dietary protein and carbohydrate and the change in the glycaemic index of dietary carbohydrate in the evolution of insulin resistance and hyperinsulinaemia. Insulin resistance offered survival and reproductive advantages during the Ice Ages which dominated human evolution, during which a high-protein low-carbohydrate diet was consumed. Following the end of the last Ice Age and the advent of agriculture, dietary carbohydrate increased. Although this resulted in a sharp increase in the quantity of carbohydrate consumed, these traditional carbohydrate foods had a low glycaemic index and produced only modest increases in plasma insulin. The industrial revolution changed the quality of dietary carbohydrate. The milling of cereals made starch more digestible and postprandial glycaemic and insulin responses increased 2 -3 fold compared with coarsely ground flour or whole grains. This combination of insulin resistance and hyperinsulinaemia is a common feature of many modern day diseases. Over the last 50 y the explosion of convenience and takeaway 'fast foods' has exposed most populations to caloric intakes far in excess of daily energy requirements and the resulting obesity has been a major factor in increasing the prevalence of insulin resistance.

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“…Genetic as well as shared environmental influences on insulin, insulin resistance, and obesity have been reported in family and twin studies [5][6][7][8][9][10][11]. Familial aggregation of NIDDM [12,13], elevated blood pressure levels [14,15], and lipid disorders [16,17] is well established.…”

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confidence: 99%

Familial components of the multiple metabolic syndrome: the ARIC Study

et al. 1997

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The clustering of multiple metabolic abnormalities including obesity, insulin resistance, non-insulin-dependent diabetes mellitus (NIDDM), hypertension, and dyslipidaemias has become known as the insulin resistance syndrome [1,2] or multiple metabolic syndrome (MMS) [3,4]. Genetic as well as shared environmental influences on insulin, insulin resistance, and obesity have been reported in family and twin studies [5][6][7][8][9][10][11]. Familial aggregation of NIDDM [12,13], elevated blood pressure levels [14,15], and lipid disorders [16,17] is well established. Metabolic disorders such as familial hypercholesterolaemia [18,19], familial combined hyperlipidaemia [20][21][22], and familial dyslipidemic hypertension [23] require a positive family history as part of their definition.Particularly within genetic epidemiology, studies on the MMS have frequently had a primary focus on a single, continuously distributed metabolic characteristic such as insulin [8,9]. Others have compared multiple metabolic variables among offspring of affected and unaffected parents [24][25][26][27][28][29][30][31]. Focusing on a single metabolic characteristic, however, limits the Diabetologia (1997) Summary The association of a parental history of diabetes mellitus and hypertension with the multiple metabolic syndrome (MMS) was studied in a population survey of middle-aged adults. The eligible population was drawn from the baseline examination of the Atherosclerosis Risk in Communities Study, a population-based, bi-ethnic, multi-centre cohort study. The MMS was defined as a multivariate, categorical phenotype of co-occurring diabetes, hypertension, and dyslipidaemia. MMS cases (n = 356) were compared to disorder-free control subjects (n = 6797) with respect to their parental history of diabetes and hypertension. MMS cases were more likely to report a history of diabetes in both parents (odds ratio [OR] 4.7, 95 % confidence interval (CI) 1.5-14.7) or a history of hypertension in both parents (OR 1.9, 95 % CI 1.1-3.0) than control subjects, adjusting for BMI, waist-to-hip ratio, age, gender, and ethnicity/centre. A parental history of diabetes and hypertension in both parents was associated with the greatest increase in odds of MMS (OR 8.3,. A dose-response relationship between the number of parental disorders (one; two; three to four) and the odds of MMS was observed (OR 1.2, 95 % CI 0.9-1.7; OR 2.0, 95 % CI 1.4-2.8; OR 4.0, 95 % CI 2.5-6.2). Based on the marked associations observed between a parental history of MMS components and the clustering of these metabolic disorders in the offspring generation, we conclude that genetic and/or non-genetic familial influences play a role in the development of the multiple metabolic syndrome. [Diabetologia (1997) 40: 963-970]

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Distribution of in vivo insulin action in Pima Indians as mixture of three normal distributions

Cited by 65 publications

References 0 publications

Normalization of Plasma Glucose Concentration by Insulin Therapy Improves Insulin-Stimulated Glycogen Synthesis in Type 2 Diabetes

Normalization of Plasma Glucose Concentration by Insulin Therapy Improves Insulin-Stimulated Glycogen Synthesis in Type 2 Diabetes

The ‘carnivore connection’—evolutionary aspects of insulin resistance

Familial components of the multiple metabolic syndrome: the ARIC Study

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