Drugs online research references
Teratology. 1994 Apr;49(4):260-6.
Effects of the biguanide class of oral hypoglycemic agents on mouse embryogenesis.
Denno KM, Sadler TW.
Department of Cell Biology and Anatomy, School of Medicine, University of North Carolina at Chapel Hill 27599.
The incidence of birth defects among offspring of mothers with non-insulin dependent diabetes mellitus (NIDDM) is 2-3-fold higher than among infants of non diabetics. Since mothers with NIDDM are frequently given oral hypoglycemic agents, including sulphonylureas and biguanides, to control their disease and since these agents have been associated with the occurrence of congenital malformations in humans and animals, the embryotoxic effects of the most commonly employed biguanides, metformin and phenformin, were evaluated in whole embryo culture. Neurulating mouse embryos were exposed to therapeutic concentrations (metformin 500-2,550 mg per day; phenformin 50-400 mg per day, respectively) of the compounds for 24-48 h. Concentrations of metformin in culture ranged from 0.15 to 1.8 mg/ml and phenformin from 2.5 x 10(-5) to 0.4 mg/ml. Cultures were terminated and scored for gross morphological alterations and total protein content. Metformin produced no alterations in embryonic growth and no major malformations. Approximately 10% of all embryos exposed to metformin regardless of dose, exhibited open cranial neuropores after 24 h of culture. However, this anomaly appeared to represent a delay in closure as opposed to an overt defect, since no embryos exposed to the highest concentration of the drug and cultured for 48 h showed open neural tubes. In contrast, phenformin produced dose dependent changes in incidence of malformations, protein content, and embryolethality. Malformations included neural tube closure defects, craniofacial hypoplasia, and reduction in size of the first and second visceral arches. Doses above 0.1 mg/ml produced embryolethality and all embryos were killed at the 0.4 mg/ml concentration.(ABSTRACT TRUNCATED AT 250 WORDS)
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8073364&dopt=Abstract
J Cardiovasc Pharmacol Ther. 1998 Oct;3(4):319-326.
Effects of Metformin on Collagen Glycation and Diastolic Dysfunction in Diabetic Myocardium.
Jyothirmayi GN, Soni BJ, Masurekar M, Lyons M, Regan TJ.
Department of Medicine, UMDNJ-New Jersey Medical School, Newark, New Jersey, USA
BACKGROUND: Collagen accumulation in the myocardial interstitium of diabetic animals is considered to promote diastolic stiffness through advanced glycosylation. Because in vitro data suggest that metformin can modify glycosylation, this study was undertaken in a canine diabetic model 4 months in duration. METHODS AND RESULTS: Untreated diabetics (group II) and diabetics treated with metformin alone (group III) or with insulin (group IV) were compared in the basal state and during volume infusion. Basal hemoglobin A(1c), heart rate, aortic pressure, and ejection fraction were comparable. Left ventricular end-diastolic pressure was significantly increased in the untreated diabetics of group II, associated with a reduced end-diastolic volume. By contrast these parameters in the metformin-treated diabetics of group III were comparable with those in the normals of group I. Similarly in group IV end-diastolic volume was higher than that in group II, but filling pressure, although lower, was not significantly so. Calculation of left ventricular chamber stiffness in the basal state indicated a higher level for group II compared with controls and the treatment groups. During the systemic infusion of dextran, the untreated diabetics of group II had the largest end-diastolic pressure increase and the smallest rise of end-diastolic volume of the treatment groups, consistent with a significantly greater chamber stiffness. Myocardial collagen concentration was increased in group II with an interstitial distribution on morphological exam. Levels of collagen-linked advanced glycosylation end products isolated from the left ventricular were significantly greater in group II than in group I. Treatment with metformin prevented the increment observed in the untreated diabetic but had no effect on the elevated collagen concentration. CONCLUSIONS: Untreated diabetics exhibited increased diastolic chamber stiffness associated with collagen-linked glycation in myocardium compared with control animals. Chronic metformin use prevented the abnormalities of function and composition.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10684514&dopt=Abstract [PubMed - as supplied by publisher]
J Clin Pharmacol. 2002 Jan;42(1):89-94.
Insulin-metformin combination therapy in obese patients with type 2 diabetes.
Jaber LA, Nowak SN, Slaughter RR.
Wayne State University, Detroit, Michigan 48201, USA.
The aim of the study was to evaluate the effects of insulin-metformin combination therapy compared to insulin monotherapyin obese, insulin-requiring patients with type 2 diabetes mellitus. Eighteen patients uncontrolled on > or = 70 U/day of insulin monotherapy were investigated in this prospective, open-label study. Patients continued their previous insulin and dietary regimens for 4 weeks, after which metformin was added with doses titrated to achieve a fasting plasma glucose (FPG) < 7.8 mmol/l or until the maximum daily dose was reached. Insulin-metformin combination therapy was continued for an additional 8 weeks. Insulin-metformin combination therapy resulted in a significant decrease in glycated hemoglobin values with a final mean reduction of 1.5% +/- 1.2% (p = 0.001). FPG decreased significantly (p < 0.005) by week 4 of insulin-metformin therapy, but the change was not statistically significant by week 12, and daily insulin requirements were significantly reduced during combination therapy (p < 0.05). These results suggest that in obese patients with type 2 diabetes mellitus receiving > or = 70 U of daily insulin, the addition of metformin leads to improved glycemic control with lower daily doses of insulin and without adverse effects.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11808829&dopt=Abstract
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