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Journal ArticleDOI

Mechanisms linking obesity to insulin resistance and type 2 diabetes

Steven E. Kahn, +2 more
- 14 Dec 2006 - 
- Vol. 444, Iss: 7121, pp 840-846
TLDR
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.
Abstract
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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Citations
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Journal ArticleDOI

Changes in gut microbiota control metabolic endotoxemia-induced inflammation in high-fat diet-induced obesity and diabetes in mice

TL;DR: It is found that changes of gut microbiota induced by an antibiotic treatment reduced metabolic endotoxemia and the cecal content of LPS in both high-fat–fed and ob/ob mice, demonstrating that changes in gut microbiota controls metabolic endotoxinemia, inflammation, and associated disorders by a mechanism that could increase intestinal permeability.
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Dynamics of fat cell turnover in humans

TL;DR: It is shown that adipocyte number is a major determinant for the fat mass in adults, however, the number of fat cells stays constant in adulthood in lean and obese individuals, even after marked weight loss, indicating that thenumber of adipocytes is set during childhood and adolescence.
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Pathophysiology of Human Visceral Obesity: An Update

TL;DR: In clinical practice, measuring waist circumference in addition to the body mass index could be helpful for the identification and management of a subgroup of overweight or obese patients at high cardiometabolic risk.
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TL;DR: The GLOBOCAN 2002 database was first made available in September 2005 and presented estimates for 2002, based on the most recent incidence, mortality, and survival data available at IARC, but more recent figures may be available directly from local sources.
References
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Journal ArticleDOI

Global Prevalence of Diabetes: Estimates for the year 2000 and projections for 2030

TL;DR: Findings indicate that the "diabetes epidemic" will continue even if levels of obesity remain constant, and given the increasing prevalence of obesity, it is likely that these figures provide an underestimate of future diabetes prevalence.
Journal ArticleDOI

Role of Insulin Resistance in Human Disease

TL;DR: The possibility is raised that resistance to insulin-stimulated glucose uptake and hyperinsulinemia are involved in the etiology and clinical course of three major related diseases— NIDDM, hypertension, and CAD.
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Obesity is associated with macrophage accumulation in adipose tissue

TL;DR: Transcript expression in perigonadal adipose tissue from groups of mice in which adiposity varied due to sex, diet, and the obesity-related mutations agouti (Ay) and obese (Lepob) found that the expression of 1,304 transcripts correlated significantly with body mass.
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Central nervous system control of food intake

TL;DR: A model is described that delineates the roles of individual hormonal and neuropeptide signalling pathways in the control of food intake and the means by which obesity can arise from inherited or acquired defects in their function.
Journal ArticleDOI

Chronic inflammation in fat plays a crucial role in the development of obesity-related insulin resistance.

TL;DR: It is proposed that obesity-related insulin resistance is, at least in part, a chronic inflammatory disease initiated in adipose tissue, and that macrophage-related inflammatory activities may contribute to the pathogenesis of obesity-induced insulin resistance.
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