Nandrolone enhances glucose disposal

As I have been saying at steirodology, progesterone agonists enhance glucose disposal.......and ER agonsists decrease it.
Thanks for the study........I was looking for that one.

Fonz

Fonz, so are you saying things like Test and Dbol lower glucose disposal? Im not questioning, just trying to understand this.

Posted by: iced

Fonz, so are you saying things like Test and Dbol lower glucose disposal? Im not questioning, just trying to understand this.

In essence...yes.

Increased estrogen is directly linked to a reduction in Glucose Disposal.

Fonz

quote:

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Increased estrogen is directly linked to a reduction in Glucose Disposal.

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It is actually a bit more complex than that. Estrogen exerts a biphasic effect in that a deficiency of estrogen causes insulin resistance (1), estrogen at levels asociated with early pregnancy improve insulin sensitivity, while very high levels, like those found in late pregnancy lower insulin sensitivity (2). Another study sums it up thusly:

"There is extensive experimental evidence that sex steroids and insulin interact in their actions on tissues. At physiological levels, testosterone and oestradiol are thought to be involved in maintaining normal insulin sensitivity. However, outside this 'physiological window' these steroids may promote insulin resistance." (3)

Synthetic progestins, on the other hand promote insulin resistance (4). To quote from a study in humans,

"Insulin resistance is prevalent in healthy postmenopausal women. A moderate dose of estrogen appears to increase insulin sensitivity but higher doses may attenuate this benefit and progestins may cause a decrease in insulin sensitivity." (5)

Progesterone has the same effect as synthetic progestins:

"It was concluded that particularly E2 plays an important role in the maintenance of normal insulin sensitivity while P alone seems to be followed by insulin resistance, both effects apparently mainly by regulation of glucose uptake in muscle."(6)

Perhaps the best studied cases of progestin induced insulin resistance come from studies of oral contraceptives:

"Associated with progesterone and the synthetic progestins used in oral contraceptives is a dose-dependent impairment of carbohydrate metabolism." (7)

(1) Mol Cell Endocrinol 2002 Jul 31;193(1-2):7-12

Effect of estrogen deficiency in the male: the ArKO mouse model.

(2) Life Sci 2002 Feb 22;70(14):1621-30

Effect of treatment with different doses of 17-beta-estradiol on the insulin receptor.

Gonzalez C, Alonso A, Grueso NA, Esteban MM, Fernandez S, Patterson AM.

(3) Clin Sci (Lond) 2002 Feb;102(2):151-66

Sex steroids and insulin resistance.

Livingstone C, Collison M.

(4) J Reprod Med 1999 Feb;44(2 Suppl):180-4

Progestogens and cardiovascular disease. A critical review.

Clarkson TB.

(5) Fertil Steril 1993 Oct;60(4):664-7

A possible bimodal effect of estrogen on insulin sensitivity in postmenopausal women and the attenuating effect of added progestin.

Lindheim SR, Presser SC, Ditkoff EC, Vijod MA, Stanczyk FZ, Lobo RA

(6) Acta Physiol Scand 1993 Sep;149(1):91-7

The effects of oestrogen and progesterone on insulin sensitivity in female rats.

Kumagai S, Holmang A, Bjorntorp P.

(7) Am J Obstet Gynecol 1993 Mar;168(3 Pt 2):1041-7

Effects of desogestrel on carbohydrate metabolism.

Shoupe D.

I realize its more complicated than that...but its because nandrolone increases glucose disposal that people lose fat
on it. This most likely is due to the fact that its a PR agonist.
Testosterone on the other hand(W/o any type of enti-estrogens) will increase estrogen levels(via the increased estrogen produced from the aromatase enzyme).....which will cause glucose disposal to be reduced.

Fonz

Seriously Fonz, progesterone agonists have the opposite effect: they induce insulin resistance. I just presented numerous examples. In men, progestins are seldom used, so there are not the hundreds of studies like in women. The most common progestin used in men is probably Megestrol acetate. It is used to increase appetite and help with weight gain in AIDS and cancer patients. Insulin resistance is a well recognized side effect:

Severe hyperglycemia in an HIV clinic: preexisting versus drug-associated diabetes mellitus.

J Acquir Immune Defic Syndr Hum Retrovirol. 1998 Jan 1;17(1):46-50. Unique Identifier : AIDSLINE MED/98097258
Kilby JM; Tabereaux PB; Department of Medicine, University of Alabama at Birmingham,; 35294-2050, USA.

--------------------------------------------------------------------------------
Abstract: We determined the frequency and clinical nature of severe hyperglycemia in a university clinic for HIV-1-infected patients. The medical records of 1392 adult HIV-infected patients were reviewed for cases of severe hyperglycemia, defined as two or more serum glucose values >250 mg/dl or diabetes treatment during clinic care. Demographic information, family histories of diabetes mellitus, body weights, CD4+ lymphocyte counts, and use of corticosteroids, megestrol acetate, pentamidine, or didanosine were recorded for subjects meeting the case definition. Comparisons were made between preexisting diabetic (group 1) and incident hyperglycemic cases (group 2). Less than 2% of the total clinic population experienced severe hyperglycemia: 12 in group 1 and 13 in group 2. Group 2 had lower body weights (mean, 70.6 kg versus 90.0 kg; p < 0.05) and more advanced HIV disease (mean CD4 count, 79/mm3 versus 550/mm3; p < 0.05) than group 1. Group 2 cases had evidence of drug-associated hyperglycemia; four cases demonstrated hyperglycemia coinciding with large fluctuations in weight during megestrol therapy. Among megestrol recipients, cases did not differ from noncases in demographics, weight, or CD4 count. Severe hyperglycemia is uncommon in adult HIV-infected patients. Approximately one half of these patients have preexisting diabetic conditions; many of the remainder may have drug-induced hyperglycemia,especially as a result of corticosteroids or megestrol acetate.

I'd put the blame moslty on the cortico-steroids. Specially prednisone IMO.(Most widely used cortico-steroid).

But if PR agonists cause insulin resistance, how do people lose fat on nadrolone cycles?

Fonz

Androgens have so many other lipolytic effects, like elevating IGF-1, either locally or hepatically, increasing hormone sensitive lipase, and decreasing lipoprotein lipase, that these effects most likely swamp any adipogenic effects from decreased insulin sensitivity.

It's been noted in many studies and reviews that AAS in general can induce insulin resistance, yet most burn fat.

"More recent studies indicate that glucose intolerance, insulin resistance, increased cardiovascular disease risk profiles,... accompany anabolic steroid intake" (1)

(1) Med Toxicol Adverse Drug Exp 1989 Jul-Aug;4(4):254-71

Adverse effects of anabolic steroids.

Hickson RC, Ball KL, Falduto MT.

Not having the brain that you guys have but still having two cents. Wouldn't insulin resistance lead to greater body fat disposal due to the fact that your body will have to turn to its own stores for energy since it can't access the glucose in the blood (due to the insulin resistance)?

0

Wouldn't insulin resistance lead to greater body fat disposal due to the fact that your body will have to turn to its own stores for energy since it can't access the glucose in the blood (due to the insulin resistance)?

Generally the body is able to compensate to a large degree for the decreased ability to take up glucose in muscle by simply secreting more insulin. It is this elevated insulin that makes a person fat. Insulin increases the activity of lipoprotein lipase, the body's primary fat storage enzyme (it allows for fat to leave the blood and enter fat cells).

I wanted to get back to this to note how hard it is to draw conclusions from any one study at this point. The study quoted from below is quite recent, from 2002

https://academic.oup.com/jcem/article/87/1/136/2846816

The authors had this to say:

"The effects of T on insulin sensitivity remain controversial; some studies have suggested that physiological T replacement improves insulin sensitivity in middle-aged men with low T levels (17, 18, 19). In contrast, administration of supraphysiological doses of T to castrated male rats (20) and of anabolic steroids to women (21) and power lifters (22) has been shown to induce insulin resistance, suggesting that the relationship between circulating T concentrations and insulin sensitivity is complex."

"The effects of T administration on glucose metabolism and insulin sensitivity remain poorly understood. Total T levels are inversely related to insulin concentrations in several cross-sectional studies (39, 42, 43, 44, 45). Fasting insulin levels are higher and T and SHBG values are lower in men with type 2 diabetes mellitus (39). Haffner et al. ( 39) reported that lower T levels were correlated with a higher waist/hip ratio and lower nonoxidative, whole body glucose disposal in men. Administration of exogenous androgens has been reported to induce glucose intolerance and hyperinsulinemia in some studies (20, 21, 22), but other studies found no significant changes in glucose tolerance or insulin concentrations with administration of T or 19-nor-T to men even at pharmacological doses (46). A marked lowering of T levels in the male rat by surgical castration as well as the administration of supraphysiological doses of T induces insulin resistance (20). This suggests that the relationship between T levels and insulin sensitivity might be curvilinear. Our study failed to find any significant changes in SI, SG, and AIRG in any treatment group over a wide range of serum T concentrations. Our data differ from those of Marin (17, 18, 19, 47), who reported improvements in insulin sensitivity, blood glucose, and blood pressure after T supplementation in middle-aged men who had visceral obesity and low T levels. In contrast to the studies by Marin et al. (17, 18, 19, 47), the subjects in our study were younger and had significantly lower fat mass. Marin et al. used euglycemic-hyperinsulinemic clamp, whereas we used frequently sampled iv glucose tolerance test to assess insulin sensitivity; we do not know whether the differences in methodology could have contributed to the observed differences in outcomes. We cannot exclude the possibility that in middle-aged men with midsegment obesity, T might decrease whole body and intraabdominal fat and thereby improve insulin sensitivity."

So some studies are finding no change, improvements, and deteriorations in insulin sensitivity to androgen administration.

The best we can hope to do is speculate, since these experts have no explanation.

The case of deca is interesting and I will speculate. JGUNS abstract noted that it was only basal (non insulin stimulated) glucose uptake that was enhanced with Deca. This means in the absence of a glucose challenge, when no insulin secretion was stimulated, glucose uptake was increased. Under the influence of a glucose load, evidently there was no enhancement of glucose uptake.

This may be related to a Deca induced increase in free IGF-1, which acts like insulin (1). This elevated free IGF-1 may be enhancing basal glucose uptake. On the other hand, when glucose is administered, this extra IGF-1 could cause the pancreas to respond with a lower insulin output (since the IGF-1 is acting like insulin already present). So with a glucose challenge, insulin output is less, but glucose uptake is normal (because the IGF is compensating for the lowered insulin secretion).

(1) J Clin Endocrinol Metab 1993 Sep;77(3):776-9

Testosterone administration increases insulin-like growth factor-I levels in normal men.

Hobbs CJ, Plymate SR, Rosen CJ, Adler RA.

well, nandi, according to what you just said, it sounds like deca would be an optimal anabolic to run concurrently with HGH and slin. throw an oral in there with some T. susp and that sounds like a great IGF-1 cocktail!
the deca, t. susp, and orals have shown to elivate igf-1 production, and of course the use of slin to extend the life and block igfbp.

on a side note, ive always thought i did better on low carbs with deca, now i know why.

Would this be the selfsame hepatic igf-1 we are referring to?

jb

Posted by: big_byrd52

well, nandi, according to what you just said, it sounds like deca would be an optimal anabolic to run concurrently with HGH and slin. throw an oral in there with some T. susp and that sounds like a great IGF-1 cocktail!
the deca, t. susp, and orals have shown to elivate igf-1 production, and of course the use of slin to extend the life and block igfbp.

on a side note, ive always thought i did better on low carbs with deca, now i know why.

Would this be the selfsame hepatic igf-1 we are referring to?

Well as that rat study showed where they blocked hepatic IGF-1 production, it's not needed for growth. That was my point in our other discussion jb. The authors pointed out that what it IS good for is regulating glucose and fat metabolism. I never denied that, in fact I pointed it out!" In conclusion, liver-derived or endocrine IGF-I is not required for post-natal statural growth, but seems to be of vital importance for normal carbohydrate and lipid metabolism." (1)Also as pointed out in this article, 20% of the circulating IGF-1 is secreted from muscles and makes its way into the circulation. Nandrolone has been shown in a couple of studies to increase muscle derived IGF-1, so that is probably contributing here as well.Big_byrd, it is a long standing bodybuilding myth that oral AAS act on the liver somehow to make IGF-1. There is no evidence for that. (1) Horm Res 2001;55 Suppl 2:18-21 Metabolic functions of liver-derived (endocrine) insulin-like growth factor I.Isaksson OG, Jansson JO, Sjogren K, Ohlsson C.