Mesenteric estrogen dependent adipogenesis protein (MEDAG)

Mesenteric estrogen dependent adipogenesis protein (MEDAG) is a cytoplasmic protein that acts as a key regulator of fat cell (adipocyte) differentiation and metabolic function, promoting lipid accumulation and glucose uptake in mature adipocytes[1][2][4]. MEDAG upregulates crucial transcription factors involved in adipogenesis, such as peroxisome proliferator-activated receptor gamma (PPARG), and modulates the expression of genes involved in lipid metabolism (e.g., fatty acid-binding protein 2, CD36, lipoprotein lipase)[2][4]. MEDAG is predominantly expressed in visceral fat depots and expression is strongly induced at early stages of adipocyte differentiation; it is also hormonally regulated, including by estradiol which reduces MEDAG expression in mesenteric adipose tissue[2]. Beyond its metabolic role, MEDAG has emerged as a possible biomarker and therapeutic target in type 2 diabetes due to its link to insulin resistance, as well as a prognostic marker in cancers such as papillary thyroid microcarcinoma, where elevated expression is associated with lymph node metastasis and poorer prognosis[2][4].

Other names

AWMS3C13orf33MEDA4hAWMS3MEDA-4FLJ14834Activated in W/Wv mouse stomach 3 homologMesenteric estrogen-dependent adipose 4mesenteric estrogen-dependent adipose 4activated in W/Wv mouse stomach 3 homologmesenteric estrogen-dependent adipogenesis protein