Abstract
Obesity rates are rapidly increasing worldwide and facilitate the development of many related disease states, such as cardiovascular disease, the metabolic syndrome, type 2 diabetes mellitus, and various types of cancer. Variation in metabolically important genes can have a great impact on a population's susceptibility to becoming obese and/or developing related complications. The adipokines adiponectin and leptin, as well as the leptin receptor, are major players in the regulation of body energy homeostasis and fat storage. This paper summarizes the findings of single nucleotide polymorphisms in these three genes and their effect on obesity and metabolic disease risk. Additionally, studies of gene-nutrient interactions involving adiponectin, leptin, and the leptin receptor are highlighted to emphasize the critical role of diet in susceptible populations.
Highlights
Obesity is the result of an imbalance in energy homeostasis and is characterized by increased adipose tissue mass, chronic low-grade inflammation, insulin resistance, and endothelial dysfunction
Obesity is a major risk factor for type 2 diabetes mellitus (T2DM), cardiovascular disease (CVD), and several types of cancer [1,2,3], and lies at the core of a cluster of metabolic abnormalities defined as the metabolic syndrome, which includes insulin resistance and hyperinsulinemia, hypertension, impaired glucose tolerance, and T2DM [4]
The findings revealed that participants in the lowest median of plasma (n-3) PUFA and LCPUFA with the GG genotype of the rs3790433 single nucleotide polymorphisms (SNPs) were at higher risk for hyperinsulinemia and insulin resistance, whereas in individuals with the same genotype but high plasma (n-3) PUFA and LCPUFA the risk of developing hyperinsulinemia and insulin resistance was effectively eliminated
Summary
Obesity is the result of an imbalance in energy homeostasis and is characterized by increased adipose tissue mass, chronic low-grade inflammation, insulin resistance, and endothelial dysfunction. Adipose tissue plays multiple important roles in body weight regulation and energy homeostasis. Adipose tissue is an active endocrine organ, secreting many cytokines, chemokines, and hormone-like factors. These molecules, which are produced and secreted primarily by adipocytes, are known as adipokines [7]. Genetic variation in adipokine genes has been shown to modulate circulating adipokine levels and could predispose carriers of single nucleotide polymorphisms (SNPs) to developing obesity or other metabolic illnesses in which adipokines play a prominent role, or alternatively, provide them some protection against disease. Studying the impact of such gene polymorphisms in human populations can provide insight into the roles specific adipokines play in obesity and related pathologies. Due to the profound effect that diet can have on weight gain and regulation, the recent literature on nutrient-gene interaction studies involving adipokines and dietary factors will be highlighted
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