23-03-2015, 09:52 PM
Here's an excellent study on adipose (fat), adipose tissue acts as its own steroid hormone organ, that's pretty cool, And the predominant activity of adipose tissue, comes from the reduction of inactive cortisone to active cortisol.
Pathways of adipose tissue androgen metabolism in women: depot differences and modulation by adipogenesis
A SURVEY OF THE LITERATURE on adipose tissue steroid conversions indicated that several isoforms of steroidogenic and steroid-inactivating enzymes can be detected in adipose tissue (3). Specifically, as many as 15 steroidogenic and steroid-inactivating enzyme mRNAs/activities have been detected to date in human adipose tissue, including aromatase, 3β-hydroxysteroid dehydrogenase (HSD) type 1, 3α-HSD type 3 [aldo-keto reductase 1C2 (AKR1C2)], 11β-HSD type 1 and type 2, 17β-HSD types 2, 3, and 5 (AKR1C3), 20α-HSD (AKR1C1), 7α-hydroxylase, 17α-hydroxylase, 5α-reductase, steroid sulfatase, and UDP-glucuronosyltransferase 2B15 (3–7, 11, 38). The capacity of peripheral tissues to synthesize and inactivate androgens/estrogens has been termed intracrinology (21, 22). Thus, in addition to its widely recognized endocrine chracteristics (20), adipose tissue also functions as an intracrine organ with respect to steroid hormones.
One of the steroidogenic enzymes expressed in adipose tissue, 11β-HSD-1, has attracted much scientific attention in recent years. Expression and activity of 11β-HSD-1 was demonstrated in fat cells from breast, omental, and subcutaneous adipose tissue (8, 42). Studies have found that the predominant activity in adipose tissue was the reduction of inactive cortisone to active cortisol (8, 19). Using cell cultures and transgenic mouse model studies by Bujalska et al. (9) and Masuzaki et al. (24) led to the demonstration that increased local cortisol production by 11β-HSD-1 may be one of the causal factors in the etiology of visceral obesity. These studies on local cortisol metabolism in fat have dramatically emphasized the importance of steroidogenic enzyme expression in the etiology of visceral obesity and related metabolic complications (9, 24). The impact of other steroidogenic enzymes that could modulate in a similar manner the exposure of abdominal adipocytes to active steroids, namely androgens and estrogens, remains to be established. In addition, regional adipose tissue depot differences in steroid-converting enzymes have not been examined for most of the enzymes identified in adipose tissue.
http://ajpendo.physiology.org/content/296/2/E244
11β-HSD-1 is influenced by Licorice Root
Pathways of adipose tissue androgen metabolism in women: depot differences and modulation by adipogenesis
A SURVEY OF THE LITERATURE on adipose tissue steroid conversions indicated that several isoforms of steroidogenic and steroid-inactivating enzymes can be detected in adipose tissue (3). Specifically, as many as 15 steroidogenic and steroid-inactivating enzyme mRNAs/activities have been detected to date in human adipose tissue, including aromatase, 3β-hydroxysteroid dehydrogenase (HSD) type 1, 3α-HSD type 3 [aldo-keto reductase 1C2 (AKR1C2)], 11β-HSD type 1 and type 2, 17β-HSD types 2, 3, and 5 (AKR1C3), 20α-HSD (AKR1C1), 7α-hydroxylase, 17α-hydroxylase, 5α-reductase, steroid sulfatase, and UDP-glucuronosyltransferase 2B15 (3–7, 11, 38). The capacity of peripheral tissues to synthesize and inactivate androgens/estrogens has been termed intracrinology (21, 22). Thus, in addition to its widely recognized endocrine chracteristics (20), adipose tissue also functions as an intracrine organ with respect to steroid hormones.
One of the steroidogenic enzymes expressed in adipose tissue, 11β-HSD-1, has attracted much scientific attention in recent years. Expression and activity of 11β-HSD-1 was demonstrated in fat cells from breast, omental, and subcutaneous adipose tissue (8, 42). Studies have found that the predominant activity in adipose tissue was the reduction of inactive cortisone to active cortisol (8, 19). Using cell cultures and transgenic mouse model studies by Bujalska et al. (9) and Masuzaki et al. (24) led to the demonstration that increased local cortisol production by 11β-HSD-1 may be one of the causal factors in the etiology of visceral obesity. These studies on local cortisol metabolism in fat have dramatically emphasized the importance of steroidogenic enzyme expression in the etiology of visceral obesity and related metabolic complications (9, 24). The impact of other steroidogenic enzymes that could modulate in a similar manner the exposure of abdominal adipocytes to active steroids, namely androgens and estrogens, remains to be established. In addition, regional adipose tissue depot differences in steroid-converting enzymes have not been examined for most of the enzymes identified in adipose tissue.
http://ajpendo.physiology.org/content/296/2/E244
11β-HSD-1 is influenced by Licorice Root