الفهرس 
Introduction and aim of the workOnly 14 pages are availabe for public view
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Abstract
Ovarian steroids as estradiol (E2) controls various of physiological function such as puberty, reproduction, and metabolic rate. Low estrogen levels have been associated with a higher prevalence of obesity. A promising strategy for obesity control involves the formation of beige adipocytes, referred to as the browning of white adipose tissue (WAT).
Several factors have been identified as crucial for the formation of brown fat cells, including PGC1α, CIDEA, PRDM16, and PPar1α. PRDM16 serves as the master regulator of brown adipogenesis, stimulating the differentiation of Myf5-positive myogenic precursor cells into brown fat cells. Increasing PRDM16 expression leads to elevated expression of BAT-selective genes in beige fat cells. PGC1α, a master regulator of mitochondrial biogenesis and oxidative metabolism, induces UCP1 expression, playing a role in brown fat development and thermogenic function. CIDEA contributes to energy homeostasis, with varied expression patterns in human and mouse adipose tissues. Peroxisome proliferator-activator receptors (PPARs), a superfamily of nuclear transcription factors, regulate lipid metabolism. PPar1-α, the first genetic sensor for fat, is linked to fatty acid oxidation, especially in the liver. Estrogen has been found to impact PPar1-α, inhibiting its activation on obesity and lipid metabolism.