Insulin resistance in Chileans of European and indigenous descent: evidence for an ethnicity x environment interaction

欧洲裔和土著智利人的胰岛素抵抗:种族与环境交互作用的证据

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Abstract

BACKGROUND: Effects of urbanisation on diabetes risk appear to be greater in indigenous populations worldwide than in populations of European origin, but the reasons are unclear. This cross-sectional study aimed to determine whether the effects of environment (Rural vs. Urban), adiposity, fitness and lifestyle variables on insulin resistance differed between individuals of indigenous Mapuche origin compared to those of European origin in Chile. METHODOLOGY/PRINCIPAL FINDINGS: 123 Rural Mapuche, 124 Urban Mapuche, 91 Rural European and 134 Urban European Chilean adults had blood taken for determination of HOMA-estimated insulin resistance (HOMA(IR)) and underwent assessment of physical activity/sedentary behaviour (using accelerometry), cardiorespiratory fitness, dietary intake and body composition. General linear models were used to determine interactions with ethnicity for key variables. There was a significant "ethnicity x environment" interaction for HOMA(IR) (Mean±SD; Rural Mapuche: 1.65±2.03, Urban Mapuche: 4.90±3.05, Rural European: 0.82±0.61, Urban European: 1.55±1.34, p((interaction)) = 0.0003), such that the effect of urbanisation on HOMA(IR) was greater in Mapuches than Europeans. In addition, there were significant interactions (all p<0.004) with ethnicity for effects of adiposity, sedentary time and physical activity on HOMA(IR,) with greater effects seen in Mapuches compared to Europeans, an observation that persisted after adjustment for potential confounders. CONCLUSIONS/SIGNIFICANCE: Urbanisation, adiposity, physical activity and sedentary behaviour influence insulin resistance to a greater extent in Chilean Mapuches than Chileans of European descent. These findings have implications for the design and implementation of lifestyle strategies to reduce metabolic risk in different ethnic groups, and for understanding of the mechanisms underpinning human insulin resistance.

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