Abstract
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, but none of these appear to factor in the interethnic variation in obesity. Emerging evidence is increasingly pointing to a link between reduced basal metabolism and ineffective brown adipose tissue (BAT) thermogenesis. In fact, BAT presence and function are strongly correlated with metabolic rates and directly influence obesity susceptibility. My colleagues and I recently theorized that ancestral exposure to cold necessitated the evolution of enhanced BAT thermogenesis, which, with today’s hypercaloric and sedentary lifestyle, becomes advantageous, because 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 further reconciles global evolutionary climatic exposures with obesity demographics to understand the genetic basis for the obesity pandemic, and new insights from the most recent studies are provided, including those assessing archaic human admixture. Key genetic variants influencing BAT thermogenesis are outlined 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.
Highlights
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Emerging evidence is increasingly pointing to a link between reduced basal metabolism and ineffective brown adipose tissue (BAT) thermogenesis
Nonshivering thermogenesis (NST) is a form of adaptive thermogenesis that facilitates rewarming from torpor or hibernation and/or maintains homoeothermic endothermy, which is defined as the ability to raise and maintain core body temperature above and beyond that derived from the external environment [18]
Summary
Nonshivering thermogenesis (NST) is a form of adaptive thermogenesis that facilitates rewarming from torpor or hibernation and/or maintains homoeothermic endothermy, which is defined as the ability to raise and maintain core body temperature above and beyond that derived from the external environment [18]. Because fish do not possess BAT and are generally not endothermic, a nonthermogenic role for ancient UCP1 has been postulated; it is possible this gene may have provided a localized thermogenic role, such as in cranial endothermy in specialized heater cells within the brains of certain fish species [21]. In line with this argument, cold exposure results in increased brain UCP1 expression in the common carp [22], though more direct evidence for thermogenic properties of UCP1 in fish is required. An energy wastage variant of ADRB3 that promotes lipolysis and NST has been found only in humans, supporting the notion that the common ancestor of nonhuman primates and hominids who lived in Africa had not required energy wastage alleles that augmented thermogenesis [32]
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