Mechanisms of obesity-associated insulin resistance: many choices on the menu.

By M. Qatanani, Mitchell A. Lazar. Genes & Development, 2007

837 citations recorded by the source corpus.

Obesity-associated insulin resistance is a major risk factor for type 2 diabetes and cardiovascular disease. In the past decade, a large number of endocrine, inflammatory, neural, and cell-intrinsic pathways have been shown to be dysregulated in obesity. Although it is possible that one of these factors plays a dominant role, many of these factors are interdependent, and it is likely that their dynamic interplay underlies the pathophysiology of insulin resistance. Understanding the biology of these systems will inform the search for interventions that specifically prevent or treat insulin resistance and its associated pathologies.

Subfields: Endocrine and Autonomic Systems, Epidemiology, Physiology

View Paper: https://www.semanticscholar.org/paper/f05ddbe16b6f7aa654ccccc5b603a166c2ee01f2

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In Endocrine and Autonomic Systems

In Epidemiology

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Citations in the corpus

Adipose Tissue Distribution, Inflammation and Its Metabolic Consequences, Including Diabetes and Cardiovascular Disease (2020, background): “Thus, adipose tissue functions as an energy balance “hub” that integrates and services the energy requirements of diverse organ systems, such as the liver, skeletal and heart muscle, pancreas, and brain (64).”
Adipocyte-derived Th2 cytokines and myeloid PPARdelta regulate macrophage polarization and insulin sensitivity. (2008, background): “Within this microenvironment, adipocytes secrete adipokines, including leptin, adiponectin, and resistin, to control systemic lipid and glucose metabolism (Qatanani and Lazar, 2007; Rosen and Spiegelman, 2006).”
Regulatory Mechanisms for Adipose Tissue M1 and M2 Macrophages in Diet-Induced Obese Mice (2009, background): “3 besity and insulin resistance are closely associated with a state of low-grade inflammation in adipose tissue, where resident macrophages play important roles (1-9).”
Alternative M2 activation of Kupffer cells by PPARdelta ameliorates obesity-induced insulin resistance. (2008, background): “The infiltration and activation of macrophages in metabolic tissues are key events in the pathogenesis of diet-induced obesity and insulin resistance (Qatanani and Lazar, 2007).”
Pathogenesis of Type 2 Diabetes Mellitus (2015, background): “(E) The cell-extrinsic modulators such as endocrine and inflammatory signals can intensified IR [57].”
INFLAMMATION AND LIPID SIGNALING IN THE ETIOLOGY OF INSULIN RESISTANCE (2012, neutral): “The etiology of insulin resistance has been intensely studied (Qatanani and Lazar, 2007; Shulman, 2000), and it is now recognized that chronic tissue inflammation is an important cause of obesity-induced insulin resistance (Attie and Scherer, 2009; Lumeng and Saltiel, 2011; Olefsky and Glass, 2010;…”