Drugs online research references
Fertil Steril. 1996 May;65(5):946-9.
Can metformin reduce insulin resistance in polycystic ovary syndrome?
Acbay O, Gundogdu S.
Department of Internal Medicine, Cerrahpasa Medical Faculty of Istanbul University, Turkey.
OBJECTIVE: To examine whether metformin is able to reduce insulin resistance in polycystic ovary syndrome (PCOS). DESIGN: Single-blind study comprising two successive periods of treatment: 8 weeks of placebo and 10 weeks of metformin (orally, 850 mg twice daily). SETTING: Clinic of endocrinology and metabolism of Cerrahpasa Medical Faculty at Istanbul University, Istanbul, Turkey. PATIENTS: Sixteen insulin-resistant women with PCOS. INTERVENTIONS: Insulin sensitivity (with an IV insulin tolerance test), plasma glucose and insulin levels during an oral glucose tolerance test (OGTT), serum androgens, and lipids were measured at baseline and after each treatment period. RESULTS: Insulin sensitivity, the mean fasting serum levels of glucose, insulin, total cholesterol, triglyceride, low-density lipoprotein cholesterol, high-density lipoprotein cholesterol, total T, free T, androstenedione, DHEAS, and LH:FSH ratio, and the areas under the curve for plasma glucose and insulin during OGTT were not changed by either placebo or metformin treatment. CONCLUSION: Metformin does not decrease insulin resistance in PCOS. This finding suggests that cellular mechanism of insulin resistance in PCOS is different from other common insulin-resistant states such as non-insulin dependent diabetes mellitus and obesity.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8612854&dopt=Abstract
Postgrad Med J. 1996 Jun;72(848):352-4.
Metformin treatment in NIDDM patients with mild renal impairment.
Connolly V, Kesson CM.
Diabetes Centre, Victoria Infirmary NHS Trust, Glasgow, UK.
Metformin is contraindicated in patients with renal failure because of the risk of lactic acidosis. This study assessed the complications of metformin treatment in patients with non-insulin-dependent diabetes mellitis with normal and raised serum creatinine. Subjects using metformin with serum creatinine above the upper reference range (120 mu mol/l) were identified (n = 17) from a hospital diabetes register; those with abnormal liver function, cardiac failure, peripheral vascular disease or recent severe illness were excluded. Reference plasma lactate levels were established, mean 1.742 mu mol/l (SD 0.819) using age-matched non-diabetic subjects. Age-matched patients treated with metformin with normal serum creatinine levels formed the control group (n = 24). Details of gastrointestinal disturbance were recorded, and plasma lactic acid and vitamin B12 levels measured. The median total daily dose of metformin in both groups was 1700 mg. The mean plasma lactate in subjects with serum creatinine 80-120 mu mol/l (2.640 mmol/l (SD 1.434) p < 0.02) was higher than non-diabetic control levels while diabetic subjects with serum creatinine 120-160 mumol/l had a mean of 2.272 mmol/l (SD 0.763) p < 0.05. There was no significant difference between the two groups taking metformin, nor any significant difference in the reporting of gastrointestinal symptoms between the groups on metformin (11.76% vs 12.5%). Plasma lactic acid levels are higher in diabetic subjects taking metformin compared with healthy volunteers but, within the diabetic groups, the small elevation of serum creatinine was not associated with higher plasma lactate levels.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8758014&dopt=Abstract
Minerva Endocrinol. 1996 Sep;21(3):101-10.
[Comparison of two treatment models in type-II diabetic patients with poor metabolic control: Preformed combination of glibenclamide 2,5 mg + metformin 400 mg or mono-therapy with sulfonylurea at maximal doses? An evaluation at six months]
[Article in Italian]
D'Argenzio R, Cavallo P, Merante D, Morelli A.
Centro Antidiabetico, Caserta.
Both glibenclamide and metformin have been used alone or in association for many years. In the treatment of type 2 or non-insulin-dependent diabetes (NIDDM). Glibenclamide stimulates insulin release by pancreatic beta cells (pancreatic attachment point), while metformin acts at a peripheral level by increasing glucose absorption in muscular, fatty and hepatic tissues, thus considerably reducing insulin resistance (extra-pancreatic attachment point). The aim of this study was to evaluate the therapeutic efficacy of the pre-formed association of glibenclamide 2.5 mg+metformin 400 mg (treatment group 1) compared to treatment with glibenclamide 5 mg alone (treatment group 2) at almost double therapeutic doses compared to those contained in the association. A total of 40 NIDDM patients were examined (24 females and 16 males) with a mean age of 55.86 years, a mean duration of disease of 9.37 years, generally obese or overweight. From the final results of the study it was found that the associative therapy of glibenclamide 2.5 mg+metformin 400 mg was very advantageous, leading to a significant improvement in the glycometabolic control (HbA1c and fasting plasma glucose) compared to patients treated using single drug therapy who maintained almost stable control of the disease.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=9072666&dopt=Abstract
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