Why the study?
Dysfunction of brown adipose tissue may predispose to obesity and type 2 diabetes, and Ucp1-Ucp3 single nucleotide polymorphisms were recently associated with cardiometabolic disease risk.
Are uncoupling protein (Ucp) gene polymorphisms associated with an increased risk of cardiometabolic diseases?
Are uncoupling protein (Ucp) gene polymorphisms associated with an increased risk of cardiometabolic diseases?
Genetic variations in uncoupling protein (Ucp) genes may contribute to the pathogenesis of cardiometabolic diseases by affecting brown adipose tissue function and thermogenesis.
UCP polymorphisms show inconsistent CMD associations; leaves open their clinical utility for risk prediction pending standardized multi-ethnic studies.
The hereditary aspect of obesity is a major focus of modern medical genetics. The genetic background is known to determine a higher-than-average prevalence of obesity in certain regions, like Oceania. There is evidence that dysfunction of brown adipose tissue (BAT) may be a risk factor for obesity and type 2 diabetes (T2D). A significant number of studies in the field focus on the UCP family. The Ucp genes code for electron transport carriers. UCP1 (thermogenin) is the most abundant protein of the UCP superfamily and is expressed in BAT, contributing to its capability of generating heat. Single nucleotide polymorphisms (SNPs) of Ucp1-Ucp3 were recently associated with risk of cardiometabolic diseases. This review covers the main Ucp SNPs A-3826G, A-1766G, A-112C, Met229Leu, Ala64Thr (Ucp1), Ala55Val, G-866A (Ucp2), and C-55 T (Ucp3), which may be associated with the development of obesity, disturbance in lipid metabolism, T2D, and cardiovascular diseases.
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Pravednikova et al. (2020) studied this question.
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