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medicine.nodak.edu
We have recently demonstrated that adult rat ventricular myocytes maintained in a high glucose (HG) culture medium exhibit abnormalities in excitation-contraction coupling similar to myocytes from diabetic rats. Metformin, an insulin-sensitizing biguanide, enhances peripheral insulin action and lowers blood pressure in hyperinsulinemic animals, but its direct impact on cardiac function is not fully understood. To examine the role of metformin on HG-induced cardiac dysfunction at the cellular level, normal adult ventricular myocytes were cultured for 1 day in a serum-free insulin-containing medium with either normal glucose (5.5 mmol/l glucose) or HG (25.5 mmol/l glucose) in the presence or absence of metformin or the sulfonylurea glyburide. Mechanical properties were evaluated using a high-speed video-edge detection system, and intracellular Ca2+ transients were recorded in fura-2-loaded myocytes. As previously reported, culturing myocytes in HG depresses peak shortening, prolongs time to 90% relengthening, and slows Ca2+ transient decay. Culturing cells with metformin (50 micromol/l) prevented the HG-induced abnormalities in relaxation without ameliorating depressed peak-shortening amplitudes. Incubation of the cells with metformin also prevented slower intracellular Ca2+ clearing induced by HG. However, the HG-induced relaxation defects were not improved by glyburide (50-300 micromol/l). Interestingly, metformin also improved HG-induced relaxation abnormalities in the absence of insulin, whereas it failed to protect against HG in the presence of the tyrosine kinase inhibitor genistein (50 micromol/l). These data demonstrate that, unlike glyburide, metformin provides cardioprotection against HG-induced abnormalities in myocyte relaxation, perhaps through tyrosine kinase-dependent changes in intracellular Ca2+ handling, independent of its insulin sensitizing action.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10512374&dopt=Abstract
Diabete Metab. 1991 Jan-Feb;17(1):19-28.
Do metformin and phenformin potentiate differently B-cell response to high glucose? An in vitro study on isolated rat pancreas.
Gregorio F, Ambrosi F, Cristallini S, Marchetti P, Navalesi R, Brunetti P, Filipponi P.
Instituti di Clinia Medica I, Universita di Perugia, Italy.
The study investigated the effects of metformin and phenformin, at "therapeutic" concentrations, on the pancreatic A-, B- and D- cell response to glucose using the isolated perfused rat pancreas model. Changes in the rate of pancreatic lactate output after these biguanides were also evaluated. Metformin--at 1.5 micrograms/ml--and phenformin--at 100 ng/ml--were separately infused both at 160 mg/dl and 300 mg/dl glucose levels. Neither metformin nor phenformin affected glucagon or somatostatin secretion during these two metabolic stimuli with glucose, nor did they significantly influence insulin response to the lower glucose stimulus. Both metformin and phenformin enhanced insulin response to 300 mg/dl glucose infusion and increased the second phase of the B-cell secretory profile but only phenformin significantly enhanced the pancreatic lactate output rate during the 300 mg/dl glucose infusion. Infusion with dichloroacetate (a stimulator of the mitochondrial pyruvate oxidation) or with verapamil (a calcium antagonist) alone did not modify the insulin response to high glucose concentrations. During metformin infusion dichloroacetate neither modified metformin's effects on B-cell response to high glucose nor did it affect the pancreatic lactate output rate. On the other hand dichloroacetate opposed phenformin's effects on the B-cell response to high glucose and reversed the rise in the pancreatic lactate output rate. Verapamil inhibited the effect of metformin on the B-cell response to high glucose but failed to affect phenformin's influence on high-glucose induced insulin release. These data suggest both metformin and phenformin potentiate--at least in rats--the late phase of insulin secretory response to high glucose. However metformin seems to influence pancreatic B-cell activity mainly by facilitating the trans-membrane calcium ion influx responsible for the second phase of insulin release. Phenformin's influence seems indirect since it increases pancreatic lactate production which mediates the enhanced B-cell response to glucose.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=1678360&dopt=Abstract
Diabetes Educ. 2001 Sep-Oct;27(5):669-77.
Patient perceptions of prandial oral therapy for type 2 diabetes.
Bonneville M, Colgin J, Nalesnick JA, Perez J, Wentz L.
Novo Nordisk Pharmaceuticals, Inc, 100 College Road West, Princeton, NJ 08540-7810, USA.
PURPOSE: This survey was conducted to assess patient perceptions of glycemic control, convenience, and flexibility of a prescribed prandial oral therapy for type 2 diabetes mellitus. METHODS: Questionnaires distributed by physicians yielded baseline responses from 3696 patients who were beginning repaglinide treatment. Data were analyzed from 1233 respondents who also completed follow-up questionnaires after 4 weeks of treatment. RESULTS: Among respondents, 60% were taking repaglinide with other antidiabetic agents in combination therapy; 59% were taking metformin, and 24% were taking troglitazone. Most respondents (84%) indicated that they were "satisfied" or "very satisfied" with repaglinide therapy, 92% wished to continue its use, and 60% believed that the treatment had improved their attitude toward taking antidiabetic medication. Patients perceived that fasting blood glucose levels were reduced during treatment, as was the incidence of hyperglycemia. Corresponding changes in perceived frequency of hypoglycemia during repaglinide treatment were minimal. CONCLUSIONS: Patient perceptions of prandial oral therapy with repaglinide were predominantly positive, due mostly to the perception that glucose control was achieved, with minimal perception of any increase in hypoglycemic episodes.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12212016&dopt=Abstract
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