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The impact of early human migration on brown adipose tissue evolution and its relevance to the modern obesity pandemic

Sellayah, D. (2019) The impact of early human migration on brown adipose tissue evolution and its relevance to the modern obesity pandemic. Journal of the Endocrine Society, 3 (2). pp. 372-386. ISSN 2472-1972

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To link to this item DOI: 10.1210/js.2018-00363

Abstract/Summary

Genetic factors are believed to be primarily responsible for obesity, however, an understanding of how genes for obesity have become so prevalent in modern society has proved elusive. Several theories have attempted to explain the genetic basis for obesity, however none of these appear to factor in the inter-ethnic variation in obesity. Emerging evidence is increasingly pointing to a link between reduced basal metabolism and ineffective brown adipose tissue (BAT) thermogenesis. In fact, brown adipose tissue presence and function is strongly correlated with metabolic rates and directly influences obesity susceptibility. We recently theorized that ancestral exposure to cold necessitated the evolution of enhanced brown adipose tissue thermogenesis, which with today’s hypercaloric and sedentary lifestyle becomes advantageous as thermogenesis is energetically wasteful, raising basal metabolism and burning excess calories. The opposite may be true for the descendants of heat-adapted populations. This review serves to further reconcile global evolutionary climatic exposures with obesity demographics to understand the genetic basis for the obesity pandemic, providing new insights from the most recent studies including those assessing archaic human admixture. Here we outline key genetic variants influencing BAT thermogenesis that have also been linked with climatic exposure to cold and appear to support the theory that evolutionary factors relevant to climate may have shaped the modern obesity pandemic.

Item Type:Article
Refereed:Yes
Divisions:Faculty of Life Sciences > School of Biological Sciences > Biomedical Sciences
ID Code:81238
Publisher:Oxford University Press

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