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The understanding of genetic factors involved in the risk for obesity has identified genes that are closely linked to obesity related diseases. A single gene effect versus multiple genes effect may indicate either the interaction unique to various environments that regulate abnormal molecular or cellular events responsible for obesity with several hypotheses proposed in relation to the development of obesity. The understanding of the development of adipogenesis has been the focus of the global community with obesity genetics, epigenetic regulatory mechanisms and transcription factors important to the world-wide obesity epidemic with increased risk for adiposity. The search for specific genes that are sensitive to nutritional regulation, oxidative stress, inflammation, endocrine disease, lipid/ glucose metabolism, insulin resistance and Alzheimer’s disease has been the focus of the current obesity epidemic in various developed countries. Epigenetics is now considered as an important mechanism for the development of obesity and can result from changes in cellular chromatin structure without alterations in DNA sequence, including DNA methylation, histone modifications and chromatin remodelling. Epigenetic modifications induced by unhealthy diets and the environment effect nuclear/mitochondria interactions and implicate nuclear receptors such as Sirt 1 as a single gene effect with interactions with microRNA and transcription factors such as p53 that regulate cellular and immune events with effects on cellular lipid metabolism and energy expenditure that induce senescence with poor DNA repair. Epigenetic modifications in various communities are now closely involved in NAFLD associated with excess transfer of fat to the adipose tissue and the induction of obesity in developed countries. The failure of various anti-obese drugs has encouraged the use of nutrigenomic diets that reverse senescence and assist in the early nutritional intervention that reverses NAFLD with reduced adiposity.
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