Genetics of fat deposition

Adipose tissue distribution usually varies among men and women. In men, adipose tissue is known to accumulate in the abdominal region surrounding the visceral organs (android fat distribution) whereas, in women, the accumulation of adipose tissue generally occurs in the gluteal-femoral regions (gynoid fat distribution). In some cases, however, android distribution can be found in women and gynoid distribution can be found in men. The regulation of adipose tissue accumulation involves interaction of a variety of genetic and environmental factors. This review examines genetic factors that cause differential distribution of adipose tissue in different depots of the body, between men and women and between different ethnicities. Genome-wide association studies can be used to identify genetic associations with the distribution and accumulation of adipose tissue. Insight into adipose tissue accumulation and distribution mechanisms could lead to development of personalized interventions for people who develop increased fat mass

Steroid-converting enzymes in human adipose tissues and fat deposition with a focus on AKR1C enzymes

Adipocytes express various enzymes, such as aldo-keto reductases (AKR1C), 11β-hydroxysteroid dehydrogenase (11β-HSD), aromatase, 5α-reductases, 3β-HSD, and 17β-HSDs involved in steroid hormone metabolism in adipose tissues. Increased activity of AKR1C enzymes and their expression in mature adipocytes might indicate the association of these enzymes with subcutaneous adipose tissue deposition. The inactivation of androgens by AKR1C enzymes increases adipogenesis and fat mass, particularly subcutaneous fat. AKR1C also causes reduction of estrone, a weak estrogen, to produce 17β-estradiol, a potent estrogen and, in addition, it plays a role in progesterone metabolism. Functional impairments of adipose tissue and imbalance of steroid biosynthesis could lead to metabolic disturbances. In this review, we will focus on the enzymes involved in steroid metabolism and fat tissue deposition

Steroid-converting enzymes in human adipose tissues and fat deposition with a focus on AKR1C enzymes.

Adipocytes express various enzymes, such as aldo-keto reductases (AKR1C), 11β-hydroxysteroid dehydrogenase (11β-HSD), aromatase, 5α-reductases, 3β-HSD, and 17β-HSDs involved in steroid hormone metabolism in adipose tissues. Increased activity of AKR1C enzymes and their expression in mature adipocytes might indicate the association of these enzymes with subcutaneous adipose tissue deposition. The inactivation of androgens by AKR1C enzymes increases adipogenesis and fat mass, particularly subcutaneous fat. AKR1C also causes reduction of estrone, a weak estrogen, to produce 17β-estradiol, a potent estrogen and, in addition, it plays a role in progesterone metabolism. Functional impairments of adipose tissue and imbalance of steroid biosynthesis could lead to metabolic disturbances. In this review, we will focus on the enzymes involved in steroid metabolism and fat tissue deposition.info:eu-repo/semantics/publishe