Adipose tissue is viewed as a dynamic fuel reserve mobilized during food deprivation with the release of fatty acids (FFA) for oxidation. From the other site the accumulation of FFA in circulation produces the endothelial dysfunction, oversecretion of insulin and lipotoxicit. Adipose cells are derived from pluripotent stem cells, and the process of adipogenesis involves a complex communication network between various transcription factors, some of which are sensors for nutrients ( carbohydrates, fatty acids, proteins) its metabolites and hormones. These nuclear receptors bind to specific target sequences in the promoter regions, and control the transcription of specific genes. Integrators of homeostatic control of nutrient intake and energy production are: for energy and glucose metabolism the peroxisome proliferator-activated receptors gamma , carbohydrate-response-element-binding protein (ChREBP) and Forkhead transcription factors (FOXO); for fatty acid, trigliceryde and lipoprotein metabolism: PPARalpha, beta, and gama; hepatocyte nuclear factor 4 alfa (HNF4), sterol regulatory element binding proteins (SREBPs); for reverse cholesterol transport and cholesterol absorbtion and xenobiotic metabolism: the liver X receptors (LXRs) and liver receptor homolog-1 (LRH-1), farnesol X receptor (FXR), pregnane X receptor (PXR), steroid and xenobiotic receptor (SXR); and for aminoacids and protein: the mammalian target for rapamycin (mTOR). Most nuclear receptors are active as monomers, dimers or heterodimers with retinoid X receptor/retinoic acid receptors, vitamin D receptor (VDR) and the others. The induction by the exogenous stimuli the CCAAT/enhancer binding proteins (C/EBP-beta,-delta,-alfa ) allows the cross – talk among these factors. The phosphorylation of corepressors ( NcoR; SMRT, RIP)/ coactivators (PGC-1,-2; p300/CBP, p/CIP and others) is an integral part of regulation of gene expression by regulation of NAD-dependent histone deacetylase recruitment and chromatin remodeling. Thus the AMP/ATP ratio as well as the nutrient supply regulate the the mTOR –dependent mitochondrial morphogenesis thus regulate the adipose tissue differentiation and insulin sensing leptin production. Caloric restriction as well as resveratrol induce sirtuins, the longevity genes.This results in inhibition of adipose tissue mass, inhibition of inflammatory cytokine production and augmentation of adiponectin release. Thus nutrient and energy supply as well as epigenetic modification of DNA supply - induced changes in the elegant cooperation of transcriptional factor activity results in the imbalance in metabolism. Polymorphism of HNF-4 in the induction of diabetes type MODY, or FOXO gene polymorphism leading to the carbohydrate-diet dependent development of obesity. It is the one of the genetically based mechanisms resulting in metabolic changes followed by appearance of metabolic disorders generating risk of cardiovascular disease.

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