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BACKGROUND: Insulin resistance is probably the key factor in the pathogenesis of polycystic ovary syndrome, and thus insulin sensitization can be a beneficial treatment. We tried to investigate effects of long-term therapy with metformin in polycystic ovary syndrome on steroid levels, ovarian steroidogenesis and on insulin resistance and secretion. We also tried to find predictors of the successful therapy (in terms of improvement of menstrual cyclicity). METHODS AND RESULTS: 24 oligo/amenorhoeic women with polycystic ovary syndrome were included into the study. Basal blood samples were taken for the determination of testosterone, estradiol, androstenedione, dehydroepiandrosterone, dehydroepiandrosterone-sulphate, 17OH progesterone, 17OH pregnenonole, sex-hormone binding globulin and cortisol. Gonadoliberin (GnRH) analogue test was performed with estimation of the same steroids and LH. Oral glucose tolerance test was done with dextrose, and with estimation of glucose, insulin, and C peptide. HOMA model assessment was used for calculation of insulin resistance and insulin secretion. All examinations were done before and after 27 +/- 4 weeks (average +/- standard deviation) of therapy with metformin 1000 mg/day. Significant improvement in menstrual cyclicity was observed in 58% of women. No significant change in basal steroid levels was found. A trend towards decline in insulin resistance and secretion was detected. Significant decrease in the mean stimulated testosterone level (from 1.74 to 1.54 nmol/l, 95% CI 1.42-2.08 and 1.21-1.87; p < 0.05), 17OH progesterone level (from 3.32 to 2.37, 95% CI 1.42-2.08 and 1.21-1.87; p < 0.05), LH (from 9.1 to 4.8 IU/l, 95% CI 6.4-12.8 and 3.4-6.8; p < 0.05), and estradiol level (from 0.91 to 0.43 nmol/l, 95% CI 0.69-1.19 and 0.38-0.65; p < 0.01) were detected. The best prediction of the improvement in menstrual cyclicity after metformin was achieved with the combination of basal 17OH progesterone, androstendione, testosterone and SHBG. This model correctly classified 86.7% of subjects. CONCLUSIONS: Long-term therapy with metformin led to the improvement in menstrual cyclicity, without significant change in basal steroid levels or parameters of insulin resistance.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11789058&dopt=Abstract
Clin Exp Hypertens. 1999 Apr;21(3):199-211.
Troglitazone and metformin, but not glibenclamide, decrease blood pressure in Otsuka Long Evans Tokushima Fatty rats.
Kosegawa I, Chen S, Awata T, Negishi K, Katayama S.
The Fourth Department of Medicine, Saitama Medical School, Japan.
To determine whether hypoglycemic agents such as sulfonylureas, biguanides and the newly developed insulin sensitizers such as troglitazone, have hypotensive effects in an animal model of non-insulin-dependent diabetes mellitus associated with insulin resistance, male Otsuka Long Evans Tokushima Fatty (OLETF) rats aged 12 weeks were administered following hypoglycemic agents or vehicle by gavage for 26 weeks; glibenclamide (5 mg/kg/day), metformin (100 mg/kg/day) and troglitazone (70 mg/kg/day). The gain in body weight was similar in the different groups. At 36 weeks of age, troglitazone significantly decreased fasting plasma glucose levels when compared to controls. The area under the curve (AUC) for insulin during glucose loading (2 g/kg, i.p.) was 50% lower in the group treated with troglitazone. Serum triglyceride levels in troglitazone-treated rats were also significantly lower than in the glibenclamide-treated group. Plasma membrane GLUT4 protein content was significantly augmented by a factor of 1.48-fold (p<0.02) in the glibenclamide-treated group and tended to be increased 1.32 times by administration of metformin (p=0.06). The systolic blood pressure increased with age in controls and the glibenclamide-treated group. In contrast, treatment with either metformin or troglitazone significantly decreased systolic blood pressure after the age of 29 weeks. Plasma norepinephrine and epinephrine concentrations did not show a significant decrease in the treated group when compared with the control group. These results suggest that metformin and troglitazone, but not glibenclamide, lower blood pressure in an animal model of insulin resistance, providing further evidence of the beneficial effect of insulin sensitizing hypoglycemic agents on blood pressure.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10225476&dopt=Abstract
Br J Pharmacol. 1995 Aug;115(7):1182-7.
Effects of metformin treatment on glucose transporter proteins in subcellular fractions of skeletal muscle in (fa/fa) Zucker rats.
Rouru J, Koulu M, Peltonen J, Santti E, Hanninen V, Pesonen U, Huupponen R.
Department of Pharmacology, University of Turku, Finland.
1. The present study was designed to clarify the cellular mechanism through which the antihyperglycaemic drug, metformin, exerts its effects. For this purpose the contents of glucose transporter protein isoforms GLUT1 and GLUT4 were measured in plasma membrane and intracellular membrane fractions of skeletal muscle obtained from genetically obese, insulin-resistant Zucker rats. 2. Hindlimb muscles were dissected from metformin-treated (300 mg kg-1 day-1, p.o., for 12 days) and control rats in basal treatment state, and after acute stimulation with insulin (22 u kg-1, i.p.). Since metformin treatment reduces food intake, we also used a pair-fed control group to investigate the effects of altered insulinaemia per se. Glucose transporter levels were analysed by Western blot and slot blot-techniques. In addition, 2-deoxy-[14C]-glucose uptake in isolated muscle strips was evaluated. 3. No changes were noted in the contents of GLUT1 proteins in any of the subcellular fractions after metformin treatment. The contents of GLUT4 in subcellular fractions were not altered in the basal treatment state. After acute insulin exposure the content of GLUT4 in the intracellular membrane fraction declined significantly in the metformin-treated group, while no significant effect was seen in the plasma membrane fraction. In agreement with these results, metformin treatment did not alter 2-deoxyglucose uptake into isolated muscle strips. 4. In conclusion, the present study does not support the concept that metformin would enhance translocation of glucose transporter proteins from the intracellular compartment to the plasma membrane in skeletal muscle in vivo.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=7582542&dopt=Abstract
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