Introduction

For most of human evolution, the ability to store nutrients in the form of esterified lipids [triacylglycerols (TAG)] has constituted a survival advantage for times of famine and/or energy deficit. In more recent times, this "thrifty" fuel economy has been challenged by overconsumption of energy-dense foods and reduced physical activity, leading to dysfunction of major tissues and organs and alarming increases in the incidence of obesity-related diseases such as diabetes, hypertension, and cardiovascular disease. Skeletal muscle has received particular attention, because it is the major site of glucose disposal, accounting for approx 80% of glucose clearance in the postprandial state. With the recent advent and integration of tools of molecular biology and comprehensive

From: Contemporary Endocrinology: Type 2 Diabetes Mellitus: An Evidence-Based Approach to Practical Management Edited by: M. N. Feinglos and M. A. Bethel © Humana Press, Totowa, NJ

metabolic analysis, a review of mechanisms by which overconsumption of energy rich diets leads to insulin resistance in skeletal muscle seems warranted. Particular themes that will be highlighted in this chapter include: 1) Inter-organ communication networks among liver, adipose tissue, and muscle that contribute to muscle insulin resistance; 2) Critical evaluation of the idea that lipid-induced muscle insulin resistance occurs as a consequence of reduced fatty acid oxidation, leading to accumulation of toxic lipid-derived metabolites and TAG; 3) Discussion of an alternative and recently emergent concept that accumulation of lipid-derived metabolites that interfere with insulin action occurs due to an increase rather than a decrease in fatty acid oxidation in skeletal muscle.

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