Abstract
The search for genetic risk factors in type-II diabetes has been hindered by a failure to consider dietary variables. Dietary nutrients impact metabolic disease risk and severity and are essential to maintaining metabolic health. Genetic variation between individuals confers differences in metabolism, which directly impacts response to diet. Most studies attempting to identify genetic risk factors in disease fail to incorporate dietary components, and thus are ill-equipped to capture the breadth of the genome’s impact on metabolism. Understanding how genetic background interacts with nutrients holds the key to predicting and preventing metabolic diseases through the implementation of personalized nutrition. Dysregulation of iron homeostasis is associated with type-II diabetes, but the link between dietary iron and metabolic dysfunction is poorly defined. High iron burden in adipose tissue induces insulin resistance, but the mechanisms underlying adipose iron accumulation remain unknown. Hepcidin controls dietary iron absorption and distribution in metabolic tissues, but it is unknown whether genetic variation influencing hepcidin expression modifies susceptibility to dietary iron-induced insulin resistance. This review highlights discoveries concerning the axis of iron homeostasis and adipose function and suggests that genetic variation underlying dietary iron metabolism is an understudied component of metabolic disease.
Highlights
Diet influences metabolism, but individuals vary in metabolic response to diet, leading to different long-term health outcomes
This review highlights discoveries concerning the axis of iron homeostasis and adipose function and suggests that genetic variation underlying dietary iron metabolism is an understudied component of metabolic disease
This review focuses on the role of iron in metabolic homeostasis and disease, and calls for researchers to incorporate dietary iron components when searching for genetic risk factors
Summary
But individuals vary in metabolic response to diet, leading to different long-term health outcomes. The term gene-environment interaction (GEI) is applied to phenomena where two genotypes respond differently to identical environmental inputs, and to when identical genotypes respond differently to different environmental inputs Put another way, genetic variation produces observable phenotypic differences under specific conditions, e.g., diet, temperature, or age [1]. Another study examined iron status in an elderly population (n = 1016), and found that 12.9% of individuals had clinically high levels of iron stores, despite normal levels of iron consumption [3]. These studies suggest there is substantial variation in iron homeostasis in human populations, and that GEI likely underlies individual response to dietary iron. This review focuses on the role of iron in metabolic homeostasis and disease, and calls for researchers to incorporate dietary iron components when searching for genetic risk factors
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