Drugs online research references
Biochem Med Metab Biol. 1992 Apr;47(2):124-32.
Effect of chronic metformin treatment of hepatic and muscle glycogen metabolism in KK mice.
Reddi AS, Jyothirmayi GN.
Department of Medicine, New Jersey Medical School, University of Medicine and Dentistry of New Jersey, Newark 07103-2757.
Noninsulin-dependent diabetic KK mice, aged 90-100 days, with hyperinsulinemia and insulin resistance were treated with either metformin (N = 13) or water (control, N = 10) orally at a concentration of 50 mg/kg twice daily for 28 weeks. Age-matched nondiabetic Swiss Webster (SW) mice were also similarly treated. Liver and skeletal muscle glycogen synthase and phosphorylase enzymes were determined in all groups of mice. Both enzymes were significantly lower in control KK than in control SW mice. Metformin did not influence either of these enzymes in nondiabetic SW mice. However, it significantly increased the active form of glycogen synthase (a form) in both the liver and muscle of KK mice. Metformin also increased the active form of phosphorylase (a form) in the liver but not in the muscle of these mice. Hepatic glycogen content was similar in both control and metformin-treated KK mice. However, the muscle glycogen content was significantly higher in metformin-treated than in control KK mice. These data suggest that metformin preferentially stimulates glycogen synthesis in skeletal muscle, and this seems to be responsible for the observed improvement in fasting glucose and glucose response to an oral glucose load in KK mice.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=1515171&dopt=Abstract
Am Fam Physician. 1995 Nov 15;52(7):2075-8.
Oral hypoglycemic agents in type II diabetes mellitus.
Lubbos H, Miller JL, Rose LI.
Medical College of Pennsylvania, Philadelphia, USA.
The patient with type II, or non-insulin-dependent, diabetes mellitus (NIDDM) is characterized by obesity and insulin resistance, with resultant hyperinsulinemia and hyperglycemia. Sulfonylureas are the chief therapy for patients with NIDDM; for a limited time, these agents stimulate increased insulin secretion. With chronic administration, sulfonylureas improve the diabetic patient's insulin activity by increasing cellular insulin receptors and reducing insulin postreceptor defects. Metformin, a drug in the biguanide class, is now approved for use in the United States. This drug does not stimulate insulin release but works by lowering glucose in peripheral tissues. It can be used alone or in combination with a sulfonylurea. With sulfonylureas and metformin, therapy for the patient with NIDDM can be more effectively tailored.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=7484707&dopt=Abstract
Angiology. 1995 May;46(5):401-8.
The effects of metformin on the capillary permeability to albumin in women patients with cyclic edema.
Valensi P, Behar A, Andre P, Wiernsperger N, Attali JR.
Service d'Endocrinologie-Diabetologie-Nutrition, Hopital Jean Verdier, Universite Paris-Nord, France.
An experimental work has suggested the efficacy of metformin, an oral antidiabetic agent, on capillary permeability. This agent has been tested in 10 women patients with cyclic edema, 7 of them being obese. The capillary permeability to albumin studied by an isotope test derived from Landis's method was initially increased. After a mean of six-weeks of treatment the albumin retention and an index demonstrating the interstitial protein elimination through the lymph route were significantly improved. Concomitantly, the swelling feelings were reduced in 8 cases and the lower limb edema had decreased or disappeared in 8 of 9 patients who initially presented these symptoms. The effects of metformin are beneficial and have been observed to be independent of glycemic change. The results suggest a special effect of this agent on the microcirculation. Nevertheless, a controlled study is required.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=7741323&dopt=Abstract
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