Testosterone and Insulin Sensitivity.

Fertil Steril. 2006 Jul;86(1):136-44.

Effects of treatment with testosterone alone or in combination with estrogen on insulin sensitivity in postmenopausal women.

Zang H, Carlström K, Arner P, Hirschberg AL.

Department of Obstetrics and Gynecology, Karolinska University Hospital, Stockholm, Sweden.

OBJECTIVE: Little is known about metabolic effects of testosterone treatment in postmenopausal women. The aim of the study was to compare the treatment effects of testosterone, estrogen, and testosterone plus estrogen on insulin sensitivities, body compositions, and lipid profiles in healthy postmenopausal women. DESIGN: An open, randomized clinical study with parallel group comparison. SETTING: Women's health clinical research unit at a university hospital. PATIENT(S): Sixty-three naturally postmenopausal women participated in the study. INTERVENTION(S): The participants were randomly assigned to 3 months of treatment with testosterone undecanoate (40 mg every second day), estradiol valerate (2 mg daily), or the combination of both. MAIN OUTCOME MEASURE(S): Insulin sensitivity assessed by euglycemic hyperinsulinemic clamp, body composition, and serum lipids. RESULT(S): Insulin-induced glucose disposal was reduced by approximately 20% after treatment with testosterone alone, and after the combined treatment, but not by estrogen alone. Body weight, but not total body fat, increased significantly by about 1 kg in all groups. Lean body mass was significantly increased in the group of combined treatment and tended to be increased by testosterone alone. High-density lipoprotein (HDL)-cholesterol decreased significantly by testosterone treatment. In contrast, HDL-cholesterol increased, whereas low-density lipoprotein (LDL)-cholesterol and lipoprotein-(a) [Lp(a)] decreased with estradiol treatment. CONCLUSION(S): We conclude that 3 months of treatment with testosterone undecanoate in postmenopausal women induces insulin resistance and an adverse serum lipid profile but may increase lean body mass.

my slin levels have doubled after 8 weeks on 500 mg sust (weekly).

How was your diet?

Posted by: guijr

How was your diet?

usual.
the same before starting the cycle.
complex carbs,good proteins (fish,chicken and so on).
gui, clean your message box (please).

androgens decrease adiponectin expression by sequestering ARA70, a coactivator common to both the androgen receptor (AR) and peroxisome proliferator-activated receptor gamma.

J Biol Chem. 1999 Jun 4;274(23):16147-52.

Identification of ARA70 as a ligand-enhanced coactivator for the peroxisome proliferator-activated receptor gamma.

Heinlein CA, Ting HJ, Yeh S, Chang C.

George Whipple Laboratory for Cancer Research, Departments of Pathology, Urology, and Radiation Oncology, University of Rochester Medical Center, Rochester, New York, 14642, USA.

In an effort to understand transcriptional regulation by the peroxisome proliferator-activated receptor gamma (PPARgamma), we have investigated its potential interaction with coregulators and have identified ARA70 as a ligand-enhanced coactivator. ARA70 was initially described as a coactivator for the androgen receptor (AR) and is expressed in a range of tissues including adipose tissue (Yeh, S., and Chang, C. (1996) Proc. Natl. Acad. Sci. U. S. A. 93, 5517-5521). Here we show that ARA70 and PPARgamma specifically interact by coimmunoprecipitation and in a mammalian two-hybrid assay. PPARgamma and ARA70 interact in the absence of the PPARgamma ligand 15-deoxy-Delta12,14-prostaglandin J2, although the addition of exogenous ligand enhances this interaction. Similarly, in transient transfection of DU145 cells, cotransfection of PPARgamma and ARA70 induces transcription from reporter constructs driven by either three copies of an isolated PPAR response element or the natural promoter of the adipocyte fatty acid-binding protein 2 in the absence of exogenous 15-deoxy-Delta12,14-prostaglandin J2. However, this PPARgamma-ARA70 transactivation is enhanced by the addition of ligand. Thus, ARA70 can function as a ligand-enhanced coactivator of PPARgamma. Finally, we show that AR can squelch PPARgamma-ARA70 transactivation, which suggests that cross-talk may occur between PPARgamma- and AR-mediated responses in adipocytes. Last edited by oswaldosalcedo on 07-11-2007 at 04:33 PM

Posted by: oswaldosalcedo

usual.
the same before starting the cycle.
complex carbs,good proteins (fish,chicken and so on).
gui, clean your message box (please).

androgens decrease adiponectin expression by sequestering ARA70, a coactivator common to both the androgen receptor (AR) and peroxisome proliferator-activated receptor gamma.

J Biol Chem. 1999 Jun 4;274(23):16147-52.

Identification of ARA70 as a ligand-enhanced coactivator for the peroxisome proliferator-activated receptor gamma.

Heinlein CA, Ting HJ, Yeh S, Chang C.

George Whipple Laboratory for Cancer Research, Departments of Pathology, Urology, and Radiation Oncology, University of Rochester Medical Center, Rochester, New York, 14642, USA.

In an effort to understand transcriptional regulation by the peroxisome proliferator-activated receptor gamma (PPARgamma), we have investigated its potential interaction with coregulators and have identified ARA70 as a ligand-enhanced coactivator. ARA70 was initially described as a coactivator for the androgen receptor (AR) and is expressed in a range of tissues including adipose tissue (Yeh, S., and Chang, C. (1996) Proc. Natl. Acad. Sci. U. S. A. 93, 5517-5521). Here we show that ARA70 and PPARgamma specifically interact by coimmunoprecipitation and in a mammalian two-hybrid assay. PPARgamma and ARA70 interact in the absence of the PPARgamma ligand 15-deoxy-Delta12,14-prostaglandin J2, although the addition of exogenous ligand enhances this interaction. Similarly, in transient transfection of DU145 cells, cotransfection of PPARgamma and ARA70 induces transcription from reporter constructs driven by either three copies of an isolated PPAR response element or the natural promoter of the adipocyte fatty acid-binding protein 2 in the absence of exogenous 15-deoxy-Delta12,14-prostaglandin J2. However, this PPARgamma-ARA70 transactivation is enhanced by the addition of ligand. Thus, ARA70 can function as a ligand-enhanced coactivator of PPARgamma. Finally, we show that AR can squelch PPARgamma-ARA70 transactivation, which suggests that cross-talk may occur between PPARgamma- and AR-mediated responses in adipocytes.

Oswaldo it's now clear, thanks. Waiting for your pm.

This user's mailbox is currently full, and cannot be sent any messages until it is cleaned out. An email has been sent notifying the user of this. Please try your request at a later time.

today.

Biochem J. 2002 Feb 1;361(Pt 3):629-33.

Induction of Bach1 and ARA70 gene expression at an early stage of adipocyte differentiation of mouse 3t3-L1 cells.

Nishizuka M, Tsuchiya T, Nishihara T, Imagawa M.

Laboratory of Environmental Biochemistry, Graduate School of Pharmaceutical Sciences, Osaka University, 1-6 Yamada-Oka, Suita, Osaka 565-0871, Japan.

Using a subtraction method, we have isolated genes that are induced early in the differentiation of mouse 3T3-L1 preadipocyte cells into adipocytes. These include the genes encoding transcription factors and signalling proteins, as well as unknown genes. Bach1, a transcription factor, and ARA70, a cofactor, were rapidly induced during differentiation. The induction of these two genes was observed only in growth-arrested 3T3-L1 cells, and not in proliferating cells. In NIH-3T3 cells, no induction was observed under either set of conditions. These results strongly indicate that Bach1 and ARA70 have valuable roles at the onset of adipocyte differentiation.

Obesity is a contributory factor for many diseases, such as hypertension, heart disease and diabetes. Therefore further
insight into the molecular basis of obesity is needed. The differentiation of cells into adipocytes has been relatively well
characterized, and several transcription factors have been identified as master regulators of the differentiation process. The
peroxisome-proliferator-activated receptor gamma (PPARgamma) gene is expressed during adipogenesis and is known to activate adipocyte specific genes, and members of the CCAAT/enhancer binding protein (C/EBP) family have also been identified as master regulators.

Posted by: oswaldosalcedo

This user's mailbox is currently full, and cannot be sent any messages until it is cleaned out. An email has been sent notifying the user of this. Please try your request at a later time.

today.

Sorry, my bad, now I hope it's all clear.

J Clin Endocrinol Metab. 1994 Jul;79(1):265-71.

Induction of insulin resistance by androgens and estrogens.

Polderman KH, Gooren LJ, Asscheman H, Bakker A, Heine RJ.

Department of Internal Medicine, Free University Hospital, Amsterdam, The Netherlands.

Hyperinsulinemia is a common finding in hyperandrogenic women, during pregnancy, and in women using oral contraceptives. To test whether sex hormone treatment can induce insulin resistance in healthy subjects, we studied the effects of administration of testosterone to 13 female to male and of ethinyl estradiol to 18 male to female transsexuals. Utilization and production of glucose and levels of sex steroids were measured during a three-step hyperinsulinemic-euglycemic clamp before and after 4 months of hormone administration. Females were treated with im injections of testosterone esters (250 mg/2 weeks); males were treated with ethinyl estradiol alone (0.1 mg/day, orally) or a combination of ethinyl estradiol and cyproterone acetate (100 mg/day, orally). Similar insulin levels were achieved at each of the three steps of the clamp studies before and during hormone administration. During step 1 of each clamp, with insulin levels in the physiological range, glucose utilization decreased from 3.5 +/- 1.2 to 2.6 +/- 0.9 mmol/kg lean body mass (LBM).h in women treated with testosterone esters (P < 0.001) and from 3.2 +/- 0.7 to 2.5 +/- 0.5 mmol/kg lean body mass.h in men treated with ethinyl estradiol (P < 0.001). The effects of sex steroids during steps 2 and 3 of the clamp at higher (supraphysiological) insulin levels were less clear. Endogenous glucose production (measured by isotope dilution with tritiated glucose) was not affected by hormone administration, indicating that the observed changes in glucose requirement were determined by a diminished peripheral glucose uptake. We conclude that sex hormone administration, i.e. testosterone treatment in females and ethinyl estradiol treatment in males, can induce insulin resistance in healthy subjects.