Hi BN,
A quick thanks to Marcy, Ella, Hannah, Pom , Eloise (omg thanks
), Wendy, iaboy (no worries, post away), thank you again.........
I keep going back to
Leptin and how it can help benefit NBE. Additionally, "adipose" (fat) is also interwoven with a huge endocrine function, number #3 in my book. My apologies for the technical nature of this post, please plod along the best you can,
if you can grasp some of the basics of this (LEPTIN and adipose) you will undoubtedly be further along on how to adopt it into NBE. I will provide some of the broad strokes, (hopefully).
may the Boobie Force be with you.
Aromatization of Androgens by Human Abdominal and Breast Fat Tissue
Abstract
The ability of human abdominal, breast and axillary fat to convert androgens into estrogens was investigated by incubating labeled substrates in the presence of NADPH with a variety of cell preparations. The incubation products were subjected to phenolic partition, paper chromatography, methyl-ether formation, repeat chromatography and crystallization with cold carrier reference standards to constant specific activity.
Androstenedione was converted to estrone and, to a lesser extent, to 17β-estradiol by crude homogenates, minces, fat-free particulate fractions (1,000–100,000 × g) and isolated fat cells obtained from abdominal, breast or axillary fat. Testosterone was found to be aromatized as actively as androstenedione, but in this case more 17 β-estradiol was formed than estrone.
19-Hydroxyandrostenedione2 also served as substrate, giving results similar to those obtained with androstenedione. Fat tissue obtained from cancerous breasts was found to be as active as normal breast fat (1–4 pg/g fat/90 min) and within the range found for abdominal fat (1–27 pg/g fat/90 min). In each case in which
axillary fat was compared to breast fat from the same subject, the activity of the axillary fat was 5 to 10 times higher. The results indicate a possible role of adipose tissue as a significant extra-gonadal source of estrogens.[/b]
- See more at:
http://press.endocrine.org/doi/abs/10.12...Mhqtw.dpuf
From the study below:
Several steroidogenic enzymes are expressed in adipose tissue including cytochrome P450-dependent aro- matase, 3 -hydroxysteroid dehydrogenase (HSD), 3 HSD, 11 HSD1, 17 HSD, 7 -hydroxylase, 17 -hydroxylase, 5 - reductase, and UDP-glucuronosyltransferase 2B15 (71, 72). Given the mass of adipose tissue, the relative contribution of adipose tissue to whole body steroid metabolism is quite significant, with adipose tissue contributing up to 100% of circulating estrogen in postmenopausal women and 50% of circulating testosterone in premenopausal women.
Although the adrenal gland and gonads serve as the primary source of circulating steroid hormones, adipose tissue expresses a full arsenal of enzymes for activation, interconversion, and inactivation of steroid hormones.
http://www.iub.edu/~k662/articles/obesit...202004.pdf
Adipose Tissue as an Endocrine Organ
Adipose tissue is a complex, essential, and highly active metabolic and endocrine organ. Besides adipocytes, adipose tissue contains connective tissue matrix, nerve tissue, stromovascular cells, and immune cells. Together these components function as an integrated unit. Adipose tissue not only responds to afferent signals from traditional hormone systems and the central nervous system but also expresses and secretes factors with important endocrine functions. These factors include leptin, other cytokines, adiponectin, complement components, plasminogen activator inhibitor-1, proteins of the renin-angiotensin system, and resistin. Adipose tissue is also a major site for metabolism of sex steroids and glucocorticoids. The important endocrine function of adipose tissue is emphasized by the adverse metabolic consequences of both adipose tissue excess and deficiency. A better understanding of the endocrine function of adipose tissue will likely lead to more rational therapy for these increasingly prevalent disorders. This review presents an overview of the endocrine functions of adipose tissue. (J Clin Endocrinol Metab 89: 2548 –2556, 2004)
