Variations in Insulin-Stimulated Glucose Uptake in Healthy Individuals with Normal Glucose Tolerance*

Hollenbeck, C. B.; Reaven, Gerald M.

doi:10.1210/jcem-64-6-1169

Cited by 294 publications

(158 citation statements)

References 35 publications

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“…This dynamic interaction between insulin secretion and insulin resistance is essential to the maintenance of NGT [1,3,6,7,9,14,15,16,17,18] and interruption of this cross-talk between the beta cell and peripheral tissues results in the progressive deterioration of glucose homeostasis [1,3,14,17,18,19]. Among individuals with NGT it has been proposed that about 20% are insulin resistant [15,20,21,22]. Using the hyperglycaemic clamp technique, we have shown that these NGT, insulinresistant individuals are able to appropriately augment both first-and second-phase insulin secretion to offset the insulin resistance [13,15]; similar results have been reported by others [16,17,18,19].…”

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confidence: 99%

Beta-cell dysfunction and glucose intolerance: results from the San Antonio metabolism (SAM) study

et al. 2004

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Aims/hypothesis. Both insulin resistance and beta-cell dysfunction play a role in the transition from normal glucose tolerance (NGT) to Type 2 diabetes (T2DM) through impaired glucose tolerance (IGT). The aim of the study was to define the level of glycaemia at which beta-cell dysfunction becomes evident in the context of existing insulin resistance. Methods. Insulin response (OGTT) and insulin sensitivity (euglycaemic insulin clamp) were evaluated in 388 subjects in the San Antonio Metabolism (SAM) study (138 NGT, 49 IGT and 201 T2DM). In all subjects the insulin secretion/insulin resistance index (DeltaI/DeltaGdivided byIR) was calculated as the ratio of the increment in plasma insulin to the increment in plasma glucose during the OGTT divided by insulin resistance, as measured during the clamp. Results. In lean NGTs with a 2-h plasma glucose concentration (2-h PG) between 5.6 and 6.6 and between 6.7 and 7.7 mmol/l, there was a progressive decline in DeltaI/AGdivided byIR compared with NGTs with a 2-h PG less than 5.6 mmol/l. There was a further decline in DeltaI/DeltaGdivided byIR in IGTs with a 2-h PG between 7.8 and 9.3 and between 9.4 and 11.0 mmol/l, and in Type 2 diabetic patients with a 2-h PG greater than It. I mmol/l. Lean and obese subjects showed coincident patterns of relation of 2-h PG to DeltaI/DeltaGdivided byIR. Conclusion/interpreation. When the plasma insulin response to oral glucose is related to the glycaemic stimulus and severity of insulin resistance, there is a progressive decline in beta-cell function that begins in "normal" glucose tolerant individuals

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confidence: 99%

Beta-cell dysfunction and glucose intolerance: results from the San Antonio metabolism (SAM) study

et al. 2004

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“…Resistance of glucose elimination to insulin action (insulin resistance) is a major determinant of the plasma insulin concentration 8 and may have a stronger relation with cardiovascular disease risk factors than does plasma insulin concentration. 9 - 11 Determinants of insulin concentrations, such as insulin resistance, may therefore be more directly involved in the relations between insulin and cardiovascular disease risk than are the insulin concentrations themselves.…”

mentioning

confidence: 99%

Influence of insulin resistance, secretion, and clearance on serum cholesterol, triglycerides, lipoprotein cholesterol, and blood pressure in healthy men.

Godsland¹,

Crook²,

Walton³

et al. 1992

Arterioscler Thromb

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Relations between serum lipids, lipoproteins, blood pressure, and insulin metabolism were investigated in 158 healthy men aged 19-77 years and with body mass indexes (BMIs) of 19-41 kg • m" 2 . Mathematical modeling analysis of glucose, insulin, and C-peptide concentrations during an intravenous glucose tolerance test was used to measure parameters of insulin metabolism. In univariate analysis, both fasting and postglucose insulin concentrations showed significant positive associations with fasting serum triglyceride levels (r=0-33 and 0.38, respectively) and systolic (r=022 and 0.26) and diastollc (r=0.21 and 0.24) blood pressure and negative associations with high density lipoprotein subtraction 2 cholesterol (HDL 2 ; r=-0.21 and -0.25). In multivariate analysis, the associations between insulin and HDL 2 cholesterol concentrations were found to depend on triglyceride levels. Insulin resistance and basal pancreatic insulin secretion showed significant positive associations with serum triglycerides, which were independent of the effects of age, BMI, and fat distribution. Hepatic insulin throughput was independently associated with HDL 2 cholesterol. Associations of insulin-related variables with blood pressure were generally dependent on age and BMI. These results underline the importance of insulin sensitivity and insulin concentrations as determinants of triglyceride metabolism. They also indicate a close relation between hepatic insulin handling and HDL] concentration that is independent of triglyceride metabolism. has lent support to the possibility that elevated insulin concentrations may have a direct role in atherogenesis. 4 Furthermore, elevated insulin concentrations are associated with raised blood pressure 5 and serum triglyceride concentrations 6 and with reduced serum high density lipoprotein (HDL) cholesterol concentrations, 7 factors that in themselves may increase coronary heart disease risk.Resistance of glucose elimination to insulin action (insulin resistance) is a major determinant of the plasma insulin concentration 8 and may have a stronger relation with cardiovascular disease risk factors than does plasma insulin concentration.9 -11 Determinants of insulin concentrations, such as insulin resistance, may therefore be more directly involved in the relations between insulin and cardiovascular disease risk than are the insulin concentrations themselves. Computer modeling of plasma glucose, insulin, and C-peptide concentrations during an intravenous glucose tolerance test (FVGTT) allows quantification of the determinants of plasma insulin concentrations, which may be otherwise difficult to measure. We have used this technique in a large group of healthy men to investigate the associations of serum lipid and lipoprotein concentrations and blood pressure with insulinrelated variables. A wide range of variation in age and adiposity in this group provided the necessary variation in insulin metabolism against which these associations could be examined. Methods SubjectsWe studied 158 apparently heal...

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“…All of these dietary factors are characterised by their enhancing effect on insulin secretion or by their interference with insulin metabolism (Hollenbeck & Reaven, 1987;Greenberger et al, 1968;Montague & Taylor, 1968;Sanbar & Martin, 1967;Linscheer et al, 1967;Lardinois et al, 1987). Hyperinsulinaemia is sometimes accompanied by glucose intolerance (Hartog et al, 1987) because of down-regulation of insulin receptors.…”

Section: Resultsmentioning

confidence: 99%

Insulin-tumour interrelationships in thymoma bearing mice. Effects of dietary glucose and fructose

Yam

Fink²,

Nir³

et al. 1991

Br J Cancer

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Summary Control (C) or Thymoma (T) implanted male C57BL/6J mice received a basal diet containing 16.5% glucose (G) or fructose (F). Compared to the C-G group, the C-F mice consumed more food and less water, and gained more weight. The blood glucose, insulin and triglyceride levels were higher in the C-F than in the C-G mice. Thymoma implantation into the right flank caused a transient decrease in body weight followed by a steady increase due to tumour growth. Tumours were detected earlier and tumour size was greater in the T-F group than in the T-G mice. Tumour chemical composition was similar in both groups. Blood analysis showed that the T mice had lower glucose and higher insulin and triglyceride levels than the C group. Carcasses from the T groups contained more water and ash and less fat than their C counterparts, but the type of sugar did not affect the body composition of the C or T groups. The results suggest that dietary fructose may enhance the growth of tumour via its hyperinsulinaemic action.

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Variations in Insulin-Stimulated Glucose Uptake in Healthy Individuals with Normal Glucose Tolerance*

Cited by 294 publications

References 35 publications

Beta-cell dysfunction and glucose intolerance: results from the San Antonio metabolism (SAM) study

Beta-cell dysfunction and glucose intolerance: results from the San Antonio metabolism (SAM) study

Influence of insulin resistance, secretion, and clearance on serum cholesterol, triglycerides, lipoprotein cholesterol, and blood pressure in healthy men.

Insulin-tumour interrelationships in thymoma bearing mice. Effects of dietary glucose and fructose

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