Follow-up to hhajdo's Interesting Point


Community Veteran, DO /
Follow-up to hhadjo's Interesting Point

I am referring to the info you just presented, on another (now closed) thread, regarding estrogens' possible lipolytic properties. That is VERY interesting!

I am wondering, however, how it can be that when I raise my patients' T levels, but control estrogen, they increase their lean-to-fat ratio. I see this all the time. Obviously this, like the "what actually causes prostatic disease?" debate, is a very complicated one, with multiple factors at interplay. Let's keep our eyes open for more info on this important and interesting subject.

I don't think there is any doubt, though, that increased estrogen leads to a redistribution of fat deposits, into a more "feminine" pattern.
Man I am going to have to bump this. I have my own ideas relating to this matter, but I would like to have some more responces befor I jump into it.
I really don't see how estrogen can be it decreases glucose disposal.

Progesterone on the other hand increases glucose disposal.

Hence why people tend to lose fat on Anabolic Androgenic Steroids (AAS) that are PR agonists...i.e. Deca and Anadrol.

All other things remaining equal of course. :)

That was Nandi12's post...

An increase of lean to fat ratio is expected since androgens promote muscle gain & fat loss...

As for the estrogen and its lipolytic properties, that's not something I've researched a lot.

Its lipolytic effect is thought to be caused by suppression of lipoprotein lipase...

Increasing your estradiol from too low to normal range can result in increased insulin sensitivity (Estrogen deficient men are usually insulin resistant.), while increasing it above normal range can cause insulin resistance...

..."One of the findings demonstrating the action of estrogen on adipose tissue is that female rodents who undergo ovariectomy become obese (7, 8). One can imagine that lack of estrogen brought about by ovariectomy accounts for this change. In fact, this hypothesis was confirmed by the fact that replacement of estrogen in these ovariectomy animals abrogated the obesity. Administration of estrogen reduces food intake (9, 10) and increases ambulatory activity (11).

A line of evidence has been reported that strongly suggests the involvement of estrogen in lipid metabolism in the adipose tissue. Estrogen replacement to ovariectomy animals resulted in decreased lipoprotein lipase (LPL)1 enzyme activity and mRNA in the adipose tissue (12-16). It has been also shown in humans that estrogen suppresses LPL activity in plasma (17) and the adipose tissue as well (18).

...Clinical observations have demonstrated that serum triglyceride levels increase in postmenopausal women and that the level of LPL activity is reduced by estrogen treatment (14)....

..."The aromatase-deficient man described by Morishima et al. (9) had abnormalities of carbohydrate and lipid metabolism (61). The insulin resistance and the elevated levels of serum cholesterol, low-density lipoprotein (LDL)-cholesterol triglycerides, and a low concentration of high-density lipoprotein-cholesterol (Table 10) gradually returned to the normal range after the administration of low-dose conjugated estrogen replacement therapy..."

It can also increase the rate of proliferation in preadipocytes in vitro...

..."This study demonstrates that the local E2 concentration within adipose tissue may represent one potential mechanism for the regulation of regional adipose tissue accumulation in human preadipocytes by altering the rate of proliferation and, hence, number in a gender- and site-specific pattern..."

Elevated estrogen can also lead to increased GH which has lipolytic properties...

I'll PM Nandi to come over....
Last edited:
Here are two more closely related pathways in addition. Reduced food intake and increased adipocyte response to NorEpi.
Int J Obes Relat Metab Disord 2002 Aug;26(8):1103-9

Estrogen receptor beta is involved in the anorectic action of estrogen.

OBJECTIVE: Estrogen has been implicated in feeding behavior and adiposity. This study was undertaken to elucidate the mechanism underlying the anti-obesity and anorectic action of estrogen and the role of estrogen receptor (ER) in the central nervous system. METHODS AND RESULTS: Ovariectomy in 8-week-old female Wistar rats induced hyperphagia along with an increase in body weight and abdominal fat accumulation compared to control sham-operated rats. These changes were fully reversed by subcutaneous replacement of estradiol and were abrogated by pair-feeding. Then, the effects of intracerebroventricular infusion of estradiol, alone or in combination with antisense oligodeoxynucleotides (ODN), for ER in ovariectomized rats were examined. The estradiol group showed 10-20% lower daily food intake, and after the 2-week infusion period a 14% reduction in body weight with a similar reduction in abdominal fat compared to the vehicle group. The inhibitory effect of estradiol on food intake and body weight was blocked by co-administration of ER-beta antisense ODN, whereas ER-alpha antisense ODN did not show any influence. CONCLUSION: These results indicate that ER-beta in the central nervous system is involved in the anorectic action of estrogen.
and NorEpi
Am J Physiol 1991 Jan;260(1 Pt 2):R47-51

Role of sympathetic nerves in effects of estradiol on rat white adipose tissue.

Two experiments examined the role of the sympathetic nerves in estradiol-induced fat pad weight losses in ovariectomized (OVX) rats. Rats were OVX, and the retroperitoneal white adipose tissue (RWAT) was unilaterally denervated 4 wk later. After 14 days of treatment with estradiol benzoate (EB, 2 micrograms/day), the intact pads lost 23% more weight than the denervated pads. There was no effect of denervation on fat pad weight or on cytosol estrogen receptor concentration in RWAT in the animals treated with sesame oil vehicle. These data suggest that the sympathetic nerves play a role in estrogen-induced reductions in fat pad weight but not via changes in adipose tissue cytosol estrogen receptors. A second experiment examined whether estradiol-induced fat pad weight losses are accompanied by increased norepinephrine (NE) turnover, an index of sympathetic activity, in adipose tissue. Rats were OVX and treated with EB or sesame oil vehicle. NE turnover was assessed by measuring the decline of tissue NE over time after injection of alpha-methyl-p-tyrosine, an inhibitor of tyrosine hydroxylase activity and thus NE biosynthesis. NE turnover in RWAT, but not heart, was significantly greater in animals treated with EB, suggesting that estradiol decreases fat pad weight in part by increasing sympathetic nervous system activity. It is possible that estradiol acts in the brain to regulate the activity of the sympathetic nerves to white adipose tissue and peripherally to alter adipose tissue responsiveness to catecholamines.
I've always understood progesterone makes you fat.
J Endocrinol 1981 Aug;90(2):285-94

Effect of progesterone on lipid metabolism in the intact rat.

Females rats implanted with progesterone gained weight more rapidly than control animals and had an increased proportion of total body fat. Restriction of food intake to control levels demonstrated that the weight changes was not dependent on increased energy intake. Serum concentrations of cholesterol, phospholipid and non-esterified fatty acid were raised in hormone-treated rats but triglyceride levels were normal. Endogenous production of triglyceride was also unchanged. Total postheparin lipoprotein lipase activity was increased in the plasma of progesterone-treated rats largely due to increased release of the extrahepatic protamine sulphate-labile fraction. The basal rate of lipogenesis was also increased in adipocytes isolated from hormone-treated rats as was the insulin-stimulated rate of oxidation of[1-14 C]glucose. Basal and adrenaline-stimulated rates of fat cell lipolysis were, however, unchanged by treatment with progesterone.
Thanks nox, - it's good to see you here...

Am J Human Biol 1999;11(2):209-224 Related Articles, Links

Hormonal changes during puberty and their relationship to fat distribution.

Roemmich JN, Rogol AD.

University of Virginia Health Sciences Center, Department of Pediatrics, Charlottesville, Virginia 22908.

In adults, abdominal visceral adiposity is related to an increased risk of cardiovascular diseases, Type 2 diabetes mellitus, and stroke. The antecedents of these conditions likely begin with the alterations in body fat distribution during childhood and adolescence. The sexually dimorphic alterations in fat distribution are influenced by sex differences in hormone concentrations, anatomical differences in the number and density of specific hormone receptors, capillary blood flow, and the activity of enzymes promoting lipid synthesis or degradation. Hormones influencing the amount and regional distribution of adipose tissue during puberty include cortisol, insulin, growth hormone, and the sex steroids. Cortisol and insulin promote fat deposition while the sex steroids and GH stimulate lipolysis. An overly sensitive hypothalamic-pituitary-adrenal axis may exist in obesity and disrupt the balance between the lipogenic effects of cortisol and insulin and the lipolytic effects of sex steroids and growth hormone. Leptin is released from the adipocytes and may act as a metabolic signal to the hypothalamic areas controlling satiety, energy expenditure, and the regulation of cortisol, insulin, sex steroid and growth hormone release. The complex issues of the hormonal control of alterations in body fat distribution during puberty are developed and a working model is proposed. Am. J. Hum. Biol. 11:209-224, 1999. Copyright 1999 Wiley-Liss, Inc.


Metabolism 1997 Feb;46(2):179-85 Related Articles, Links

Evidence for sex steroid inhibition of lipoprotein lipase in men: comparison of abdominal and femoral adipose tissue.

Ramirez ME, McMurry MP, Wiebke GA, Felten KJ, Ren K, Meikle AW, Iverius PH.

Department of Internal Medicine, University of Utah, Salt Lake City, USA.

Plasma estradiol has been suggested to suppress adipose tissue lipoprotein lipase (LPL) activity in women. The present study explores the regulation of LPL by sex steroids in sedentary obese men (N = 24) at their usual weight. Femoral adipose tissue LPL activity, eluted with serum and heparin or extracted with detergent, showed significant inverse correlations with plasma levels of testosterone, bioavailable testosterone, dihydrotestosterone, and estradiol. Both measures of femoral LPL activity were also correlated with the weight change occurring despite efforts to maintain a constant weight. Abdominal LPL activity showed significant but weaker inverse correlations with bioavailable testosterone only. Multivariate analysis of potential predictors for eluted femoral LPL activity showed that plasma testosterone, dihydrotestosterone, and estradiol were interdependent, whereas the rate of weight change was an independent variable. In the regression equation, only bioavailable testosterone and weight change were retained, explaining 63% of the variability (R = .79, P = .0002).These results suggest that sex steroids suppress adipose tissue LPL activity in men, and more so in the thigh than in the abdomen, thereby possibly contributing to a central fat accumulation. The data are compatible with a model from male animals suggesting that testosterone effects on adipose tissue LPL are mediated by estradiol formed locally.


Int J Obes Relat Metab Disord 1996 Apr;20(4):291-302 Related Articles, Links

The regulation of adipose tissue distribution in humans.

Bjorntorp P.

Department of Heart and Lung Disease, Sahlgren's Hospital, University of Goteborg, Sweden.

The regulation of adipose tissue distribution is an important problem in view of the close epidemiological and metabolic associations between centralized fat accumulation and disease. With visceral fat accumulation multiple endocrine perturbations are found, including elevated cortisol and androgens in women, as well as low growth hormone (GH) and, in men, testosterone (T) secretion. These abnormalities probably derive from a hypersensitive hypothalamo-pituitary-adrenal axis, with hyperinsulinemia related to a marked insulin resistance as a consequence. These hormonal changes exert profound effects on adipose tissue metabolism and distribution. At the adipocyte level cortisol and insulin promote lipid accumulation by expressing lipoprotein lipase activity, while T, GH and probably estrogens exert opposite effects. The consequences will most likely be more expressed in visceral than subcutaneous adipose tissues because of a higher cellularity, innervation and blood flow.
...the functional effects of estrogens in women are similar to those of T in men. The mechanisms are, however, probably indirect because of the apparent absence of specific estrogen and progesterone receptors in human adipose tissue. This interpretation from the studies referred to above fits well with physiological, and clinical conditions with increased visceral fat mass, where the balance between the lipid accumulating hormone couple (cortisol and insulin) and the hormones which prevent lipid accumulation and instead activate lipid mobilization pathways (sex steroid hormones and GH) is shifted to the advantage of the former...

Last edited:
my personal experience is that when lowering estro levels with an Aromatase inhibitor (AI) while dieting, I have lost more adipose, especially in the estro patterned areas, than when I haven't used. This has also been accentuated moreso with the addition of test. So my conclusion, based on my results is that the higher androgen:estrogen ratio has increased fat loss greatly.
Fonz said:
I really don't see how estrogen can be it decreases glucose disposal.

Progesterone on the other hand increases glucose disposal.

Hence why people tend to lose fat on Anabolic Androgenic Steroids (AAS) that are PR agonists...i.e. Deca and Anadrol.

All other things remaining equal of course. :)

welcome fonz , is the original fonz from elite and parts unknown ?
DADAWG said:
welcome fonz , is the original fonz from elite and parts unknown ?

Yes, its the same Fonz from EF.:)

So many boards all over the place...hard to post in all. Don't have much time these days.

Fonz said:
Yes, its the same Fonz from EF.:)

So many boards all over the place...hard to post in all. Don't have much time these days.

a long time ago i hung around elite a lot but under a different name , trusted the wrong person with my board name [ oh well shit happens lol ] good to see you here bro , this place kicks ass even if they did let fantom in :p , be careful if you hang around very much you might just call this place home :D