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Obesity and insulin resistance in humans: A dose-response study☆

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TLDR
In this paper, the authors examined insulin-mediated glucose metabolism (euglycemic insulin clamp at plasma insulin concentration of 100 microU/mL) and glucose-stimulated insulin secretion (hyperglycemic clamp) in 42 obese subjects (ideal body weight [IBW], 158 +/- 4%) with normal glucose tolerance and in 36 normal weight (IBW, 102% +/- 1%) age-matched controls.
Abstract
Insulin-mediated glucose metabolism (euglycemic insulin clamp at plasma insulin concentration of 100 microU/mL) and glucose-stimulated insulin secretion (hyperglycemic clamp) were examined in 42 obese subjects (ideal body weight [IBW], 158 +/- 4%) with normal glucose tolerance and in 36 normal weight (IBW, 102% +/- 1%) age-matched controls. In 10 obese and eight control subjects, insulin was infused at six rates to increase plasma insulin concentration by approximately 10, 20, 40, 80, 2,000, and 20,000 microU/mL. Throughout the physiologic range of plasma insulin concentrations, both the increase in total body glucose uptake and the suppression of hepatic glucose production (HGP) were significantly impaired in the obese group (P less than .001 to .01). At the two highest plasma insulin concentrations, inhibition of HGP and the stimulation of glucose disposal were similar in both the obese and control groups. Insulin secretion during the hyperglycemic (+/- 125 mg/dL) clamp was twofold greater in obese subjects than in controls (P less than .01) and was inversely related to the rate of glucose uptake during the insulin clamp (r = -.438, P less than .05), but was still unable to normalize glucose disposal (P less than .05). In conclusion, our results indicate that insulin resistance is a common accompaniment of obesity and can be overcome at supraphysiological insulin concentrations. Both in the basal state and following a hyperglycemic stimulus obese people display hyperinsulinemia, which correlates with the degree of insulin resistance. However, endogenous hyperinsulinemia fails to fully compensate for the insulin resistance.

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Insulin Resistance: A Multifaceted Syndrome Responsible for NIDDM, Obesity, Hypertension, Dyslipidemia, and Atherosclerotic Cardiovascular Disease

TL;DR: In summary, insulin resistance appears to be a syndrome that is associated with a clustering of metabolic disorders, including non-insulin-dependent diabetes mellitus, obesity, hypertension, lipid abnormalities, and atherosclerotic cardiovascular disease.
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Pathogenesis of NIDDM: A balanced overview

TL;DR: Information concerning the loss of first-phase insulin secretion, altered pulsatility of insulin release, and enhanced proinsulin-insulin secretory ratio is discussed as it pertains to altered β-cell function in NIDDM.
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Skeletal Muscle Insulin Resistance Is the Primary Defect in Type 2 Diabetes

TL;DR: This work focuses on recent advances about the time of onset, as well as the mechanism, of the skeletal muscle insulin resistance and the euglycemic insulin clamp technique.
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Abdominal Obesity and the Metabolic Syndrome: Contribution to Global Cardiometabolic Risk

TL;DR: Although waist circumference is a better marker of abdominal fat accumulation than the body mass index, an elevated waistline alone is not sufficient to diagnose visceral obesity and it is proposed that an elevated fasting triglyceride concentration could represent a simple clinical marker of excess visceral/ectopic fat.
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Current approaches for assessing insulin sensitivity and resistance in vivo: advantages, limitations, and appropriate usage.

TL;DR: The merits, limitations, and appropriate use of current in vivo measures of insulin sensitivity/resistance, including the quantitative insulin sensitivity check index, are highlighted.
References
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Journal ArticleDOI

Immunoassay of Endogenous Plasma Insulin in Man

TL;DR: For years investigators have sought an assay for insulin which would combine virtually absolute specificity with a high degree of sensitivity, sufficiently exquisite for measurement of the minute insulin concentrations usually present in the circulation as mentioned in this paper.
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The Effect of Insulin on the Disposal of Intravenous Glucose: Results from Indirect Calorimetry and Hepatic and Femoral Venous Catheterization

TL;DR: The results suggest that the ability of higher doses of insulin to further stimulate glucose metabolism is primarily the result of increased glucose storage by peripheral tissues, most likely muscle.
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Effects of insulin on peripheral and splanchnic glucose metabolism in noninsulin-dependent (type II) diabetes mellitus.

TL;DR: The results emphasize the importance of the peripheral tissues in the disposal of infused glucose and indicate that muscle is the most important site of the insulin resistance in NIDD.
Journal ArticleDOI

Insulin resistance, insulin insensitivity, and insulin unresponsiveness ; a necessary distinction

TL;DR: With more precise use of these terms and a more complete understanding of insulin action, it will be possible to begin to segregate the roles of the various prereceptor, receptor and postreceptor factors that are involved in producing the differing patterns of metabolism observed in disease.
Journal ArticleDOI

Dose-response characteristics for effects of insulin on production and utilization of glucose in man

TL;DR: The above dose-response relationships indicate that in man glucose production is more sensitive to changes in plasma insulin concentration than is glucose utilization; both hepatic and peripheral tissues may contain "spare" insulin receptors; and relatively minor changes in Plasma insulin concentration or insulin receptor function can cause appreciable alterations in glucose metabolism.
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In conclusion, our results indicate that insulin resistance is a common accompaniment of obesity and can be overcome at supraphysiological insulin concentrations.