Leonid E Fridlyand1, Louis H Philipson. 1. Department of Medicine, University of Chicago, MC-1027, 5841 S. Maryland Avenue, Chicago, IL 60637, USA.
Abstract
UNLABELLED: Type 2 diabetes mellitus (T2D) is approaching epidemic proportions globally. However, some human populations, such as Western-Europeans, have a lower prevalence compared with urban or westernized groups with origins in warmer climates. To explain this conspicuous trend we have developed a hypothesis suggesting that pressure for survival on ancestral Western-Europeans (or on other human populations) in extremely cold climates could lead to selection for a combination of specific genes or alleles, which we have named cold climate genes, promoting adaptation to these condition. The possible molecular basis for the effects of these genes could lead to decreasing susceptibility to T2D. The possible candidates for cold climate genes have been evaluated from three areas: the uncoupling proteins, maternally-transmitted mitochondrial genes, and mitochondrial biogenesis. CONCLUSIONS/SIGNIFICANCE: The possible existence of cold climate genes can lead to both increased thermogenesis and decreased prevalence of T2D. This may help explain the variations in prevalence of T2D in different ethnic groups. This consideration suggests testable experimental approaches towards prevention and therapies for T2D.
UNLABELLED: Type 2 diabetes mellitus (T2D) is approaching epidemic proportions globally. However, some human populations, such as Western-Europeans, have a lower prevalence compared with urban or westernized groups with origins in warmer climates. To explain this conspicuous trend we have developed a hypothesis suggesting that pressure for survival on ancestral Western-Europeans (or on other human populations) in extremely cold climates could lead to selection for a combination of specific genes or alleles, which we have named cold climate genes, promoting adaptation to these condition. The possible molecular basis for the effects of these genes could lead to decreasing susceptibility to T2D. The possible candidates for cold climate genes have been evaluated from three areas: the uncoupling proteins, maternally-transmitted mitochondrial genes, and mitochondrial biogenesis. CONCLUSIONS/SIGNIFICANCE: The possible existence of cold climate genes can lead to both increased thermogenesis and decreased prevalence of T2D. This may help explain the variations in prevalence of T2D in different ethnic groups. This consideration suggests testable experimental approaches towards prevention and therapies for T2D.
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