Drugs online research references
Gastroenterology. 2001 Apr;120(5):1263-70.
Prevention of pancreatic cancer induction in hamsters by metformin.
Schneider MB, Matsuzaki H, Haorah J, Ulrich A, Standop J, Ding XZ, Adrian TE, Pour PM.
The Eppley Institute for Research in Cancer and Allied Diseases, University of Nebraska Medical Center, Omaha, Nebraska 68198-6805, USA.
BACKGROUND AND AIMS: Our previous study suggested that the known promotional effect of a high fat diet, which in hamsters induces peripheral insulin resistance, is related to a compensatory proliferation of islet cells. The present study was to examine whether the prevention of islet cell proliferation can inhibit the promotional effect of a high-fat diet in pancreatic carcinogenesis. METHODS: Two groups of high fat-fed hamsters were used. One group received Metformin in drinking water for life (HF+Met group), and the other group served as a control (HF group). At the time when the normalization of the plasma insulin level was expected, all hamsters were treated with the pancreatic carcinogen, N-nitrosobis-(2-oxopropyl)amine, and the experiment was terminated 42 weeks later. RESULTS: Although 50% of the hamsters in the high-fat group developed malignant lesions, none was found in the HF+Met group (P < 0.05). Also, significantly more hyperplastic and premalignant lesions, most of which were found within the islets, were detected in the high-fat group (8.6 lesions/hamster) than in the HF+Met group (1.8 lesions/hamster). CONCLUSIONS: The results lend further support on the significant role of islet cells in pancreatic carcinogenesis and may explain the association between pancreatic cancer and obesity, which is usually associated with peripheral insulin resistance.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11266389&dopt=Abstract
Can Med Assoc J. 1983 Jan 1;128(1):24-6.
The status of metformin in Canada.
Lucis OJ.
During the 1970s two biguanide drugs, phenformin and metformin, were used to control hyperglycemia. Phenformin was phased out of the Canadian market because it carried an unacceptable risk of causing lactic acidosis, but metformin remains available. All documented cases of lactic acidosis associated with metformin administration, which are rare, have occurred abroad in patients who were taking the drug in spite of having contraindications to its use. The two drugs are metabolized differently, phenformin being deactivated and concentrated in the liver, and metformin being excreted rapidly, unchanged, by the kidneys. In properly selected diabetic patients therapeutic doses of metformin do not raise the blood levels of intermediary metabolites enough to induce ketoacidosis or lactic acidosis. The safety of the drug is supported by the clinical experience over about 56,000 patient-years in Canada.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=6847752&dopt=Abstract
Diabetes Care. 1990 Jan;13(1):1-8.
Effect of metformin on carbohydrate and lipoprotein metabolism in NIDDM patients.
Wu MS, Johnston P, Sheu WH, Hollenbeck CB, Jeng CY, Goldfine ID, Chen YD, Reaven GM.
Department of Medicine, Stanford University School of Medicine, San Francisco, California.
The effect of metformin treatment on various aspects of carbohydrate and lipoprotein metabolism has been defined in 12 patients with non-insulin-dependent diabetes mellitus (NIDDM). Patients were studied before and after approximately 4 mo of metformin therapy. Treatment was initiated with a single dose of 500 mg/day, increased at weekly intervals, and maintained at a final dose of 2.5 g/day (given at divided intervals) for the last 3 mo of the treatment program. Results demonstrated that both fasting and postprandial glucose concentrations were significantly lower after metformin administration, with the greatest change seen after meals. As a result, the total incremental plasma glucose response above basal measured from 0800 to 1600 after metformin was less than 25% of that seen initially. The improvement in ambient plasma glucose concentration in association with metformin occurred despite a modest but statistically significant decrease in circulating plasma insulin concentration. In addition, insulin-stimulated glucose uptake measured during hyperinsulinemic clamp studies was similar before and after metformin treatment. Furthermore, changes in insulin binding and insulin internalization by isolated monocytes did not correlate with the improvement in glycemic control. Thus, the ability of metformin to lower plasma glucose concentration in NIDDM does not appear to be secondary to an improvement in insulin action. Finally, metformin treatment was associated with a significant (P less than 0.01) decrease in plasma triglyceride concentration and an increase in plasma high-density lipoprotein cholesterol concentration. These results indicate that metformin treatment of patients with NIDDM led to an improvement in both glycemic control and lipoprotein metabolism.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=2404714&dopt=Abstract
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