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Evolutionary origins of insulin resistance: a behavioral switch hypothesis

DOI: 10.1186/1471-2148-7-61

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Abstract:

We propose a hypothesis that insulin resistance is a socio-ecological adaptation that mediates two phenotypic transitions, (i) a transition in reproductive strategy from "r" (large number of offspring with little investment in each) to "K" (smaller number of offspring with more investment in each) and (ii) a transition from "stronger to smarter" or "soldier to diplomat" i.e. from relatively more muscle dependent to brain dependent lifestyle. A common switch could have evolved for the two transitions since the appropriate environmental conditions for the two transitions are highly overlapping and interacting.Gestational insulin resistance diverts more energy through the placenta, resulting in increased investment per offspring. On the other hand, insulin resistance is associated with reduced ovulation. The insulin signaling pathway is also related to longevity. Insulin resistance diverts more nutrients to the brain as compared to muscle. Also, hyperinsulinemia has direct positive effects on cognitive functions of the brain. The hypothesis gets support from known patterns in human clinical data and recent research on the molecular interactions in the insulin signaling pathway. Further we state many predictions of the hypothesis that can be tested experimentally or epidemiologically.The hypothesis can bring about a significant change in the line of treatment as well as public health policies for the control of metabolic syndrome.The Insulin Resistance Syndrome (IRS), also called metabolic syndrome or syndrome X, consists of a cluster of conditions including hyperinsulinemia, insulin resistance, impaired glucose tolerance, type 2 diabetes, hypertension, atherosclerotic vascular disease and coronary artery disease [1,2]. Insulin resistance is a condition in which tissues exhibit reduced response to insulin. This is accompanied by increased insulin synthesis resulting in hyperinsulinemia which is thought to be a compensatory response to reduced insulin sensitivity. A prel

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