Associations of estrogen and testosterone with insulin resistance in pre- and postmenopausal women with and without hormone therapy (original) (raw)
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The Journal of Clinical Endocrinology & Metabolism, 1999
Abnormalities of carbohydrate metabolism and insulin sensitivity have been reported in estrogen deficiency. Estrogen replacement appears to result in an improvement in these parameters, although progestagens may antagonize these effects. We have examined the effects of transdermal estradiol and oral norethisterone on insulin sensitivity using the hyperinsulinemic euglycemic clamp method by performing a randomized, double blind, placebo-controlled study in 22 healthy women after a surgically induced menopause. After baseline measurements, subjects were randomized to receive either transdermal 17-estradiol (50 g) or matching placebo patches for 6 weeks. The subjects were then further randomized to receive either estradiol in combination with oral norethisterone (1 mg) or a matching oral placebo preparation, crossing over after 6 weeks, with assessment of
American journal of physiology. Endocrinology and metabolism, 2018
The relationship between circulating estrogen levels and cardiometabolic risk factors such as insulin resistance is unclear in postmenopausal women. High estradiol (E) levels have been reported to predict increased risk of type 2 diabetes in this population. We aimed to examine associations among estrogen levels, adiposity measurements, and cardiometabolic risk variables including insulin resistance in postmenopausal women. One hundred-one healthy participants (mean ± SD: age 57 ± 4 yr, BMI 27.9 ± 4.8 kg/m) were included in the analysis. Fifteen plasma steroids or metabolites were measured by liquid chromatography-tandem mass spectrometry. Insulin sensitivity was assessed with a hyperinsulinemic-euglycemic clamp. Body composition and fat distribution were determined with hydrostatic weighing and computed tomography, respectively. Blood lipids and circulating cytokines were also measured. Circulating E was positively correlated with all adiposity indexes ( r = 0.62 to 0.42, P < 0....
The Journal of Clinical Endocrinology & Metabolism, 1997
Hyperandrogenicity in women is closely associated with insulin resistance and a risk factor for cardiovascular disease and noninsulindependent diabetes mellitus (NIDDM). Therefore, 25 postmenopausal women with NIDDM and sex hormone-binding globulin values less than 60 nmol/L, as an indicator of a moderate hyperandrogenicity, were treated with 2 mg 17--estradiol orally for 3 months in a double-blind, cross-over, placebo-controlled trial. During the last 16 days of active treatment, 1 mg norethisterone acetate was added for 10 days for endometrial protection. Blood glucose, glycosylated hemoglobin, insulin, c-peptide, lipoprotein profile, sex steroid hormones, GH, and insulin-like growth factor I (IGF-I) were measured, and insulin sensitivity was determined by
Fertility and Sterility, 2010
Objective: To determine whether insulin sensitizers lower androgen levels and whether androgen suppression improves insulin resistance in nondiabetic postmenopausal women. Design: Randomized, double-blind, placebo-controlled study. Setting: Clinical and Translational Research Center of a university hospital. Patient(s): Thirty-five postmenopausal women aged 50-79 years with insulin resistance and higher T levels. Intervention(s): Subjects were randomized to metformin plus leuprolide acetate (LA) placebo, LA plus metformin placebo, or LA placebo plus metformin placebo in a 1:1:1 fashion during a 12-week period. Main Outcome Measure(s): Insulin sensitivity (M) assessed by euglycemic-hyperinsulinemic clamp and free T by equilibrium dialysis. Result(s): In those randomized to metformin, free T decreased by 19% compared with placebo, along with an expected improvement in M. Total T also decreased significantly, whereas sex hormone-binding globulin (SHBG) did not change. In those randomized to LA, the percent change in M was not different from placebo, despite a 48% relative decrease in free T levels. Conclusion(s): These data are the first to establish a causal link between insulin resistance and T in postmenopausal women. They confirm that treatment of insulin resistance decreases T production in this population and demonstrate that pharmacologic lowering of T does not affect insulin resistance.
Effects of Hormone Replacement Therapy on Insulin Resistance in Postmenopausal Diabetic Women
Open Access Macedonian Journal of Medical Sciences, 2016
BACKGROUND: Insulin resistance (IR) is closely associated with diabetes mellitus. On the other hand, increased visceral fat in menopause is also associated with IR, which makes postmenopausal diabetic women in a big risk for cardiovascular diseases. There are conflicting reports about the effects on hormone replacement therapy (HRT) on IR. AIM: The aim of the study was to investigate the effects of HRT on IR. METHODS: A total of 40 postmenopausal women with type 2 diabetes were enrolled and followed for 12 months. Half of them were assigned to take HRT, while the other half made the control group. Fasting plasma glucose (FPG) and insulinemia were measured in both groups at baseline and after 12 months. IR was represented by Homeostatic model assessment for IR (HOMA-IR). RESULTS: HRT was associated with significant decrease in HOMA-IR, FPG and insulinemia in the examined group. There was no significant reduction in FPG and no significant increase in insulinemia levels and HOMA-IR values in control group after 12 months. CONCLUSION: HRT was associated with statistically signifficant increase of insulin sensitivity. Larger clinical trials will be necessary to understand whether HRT may improve insulin resistance and glucose homeostasis in women with diabetes, especially when given shortly after entering menopause.
Gonadotropins at menopause: the influence of obesity, insulin resistance, and estrogens
2001
Obese, postmenopausal women have lower FSH levels. To determine whether this is due to higher estrogen exposure, we compared feedback gonadotropin sensitivity and its relation to insulin resistance in four groups of obese and lean, postmenopausal women. Group one was treated with 400 mg troglitazone (TG) daily for two weeks; 150 clomiphene citrate (CC) was added daily for the second week. Group two received 150 mg CC daily for a week. Group three received 1000 mg metformin (MET) daily for two weeks, with 120 mg raloxifene (RAL) added during the second week. Group four received 120 mg RAL for a week. Before and after each period, a serum pool was obtained from samples taken every minute during a 10 ml interval. The women recruited for this study were categorized as obese or lean based on BMI Ն 29 or BMI Ͻ 29, respectively. Obese, menopausal women had lower FSH (45.5 IU/l) and LH (16.2 IU/l) values than those of lean (64.1 IU/l and 23.0 IU/l), but the obese menopausal women had higher leptin, DHEAS, glucose, insulin, and HOMA-IR levels. Log [FSH] was associated with BMI (r ϭ Ϫ0.53, P Ͻ 0.000001) and number of pregnancies (r ϭ Ϫ0.37, P ϭ 0.0009). TG treatment did not change HOMA-IR or gonadotropin levels, but DHEAS and androstenedione levels decreased significantly. CC alone or together with TG, diminished FSH (Ϫ7.9 and Ϫ9.2) and LH (Ϫ2.5 and Ϫ3.6) concentrations, with a greater reduction in lean women. MET reduced glucose and the HOMA-IR index without affecting gonadotropin or steroid levels. Conclusions: obese, menopausal women have lower FSH levels due to greater estrogen exposure, by mechanisms unrelated to insulin resistance.
The objective of the present srudy was to compare dre effects of various gesmgens on insuiin sensitivity in postrnenopausal \\'omen on hormone replacement therapy'(HRT). This prospective study enrolled 156 postrnenopausal women who had menopausal status for at least 6 months. Group I was treated with l7/i-estradiol (E2; 2 mg) plus norethisterone acetate (NETA; 1 mg); Group 2 was given Ez (2 mg) plus medroxlprogesterone acerate (MPA; 2-5 mg); Group 3 was given E2 (2 mg) plus dydrogesterone (DG; l0 mg); and Group 4 vras given Ez (2 mg) plus micronized progesterone (MP; tbO mg). Group 5 u'as the surgical menopausal group and rvas given only E2 (2 mg) continuously. All 156 subjects compleredrhe 3mondr follorv-up on thc uial. The patients were anallzed by using homeostatic model assessment (FIOlvlA) for insulin sensitir-iq' before treatment and 3 months after ueatment, comparing the effecrs of various HRT regimens on insulin sensitiriry. No significant differences were found in the baseline characterisrics of the patiens (p > 0.05), There were no significant differences in mean values of HOMA before HRT among the five groups (p > 0.05). There were statistically significant differences in mean values of HOMA only in Group I (E2+NETA) and Group 3 (E'+DG) after HRT (p > 0.0i). E3 + NETA and E2 + DG were found to improve insulin sensitiviry in postmenopausal women after 3 monrhs of treatmentJ s'hereas E' + MPA, E2 + MP and E2 only did not show such an effect in postnenopausal rvomen.