Drugs online research references
Arzneimittelforschung. 1975 Apr;25(4):668-75.
[Proinsulin and insulin secretion in obese females before and after administration of metformin]
[Article in German]
Hausmann VL, Schubotz R.
In 49 normal and overweighty women the basal and reactive proinsulin and insulin level as well as serum cholesterol and triglycerides were determined before and after the application of N,N-dimethylbiguanide-hydrochloride (metformin, Glucophage retard-R). The proinsulin fraction of the basal total insulin is 70 percent in normal women. With increasing overweight the percentage of proinsulin decreases in favor of insulin. Stimulation with 100 g oral glucose, in analogy to the total insulin, significantly increased proinsulin levels, remaining, however, below the insulin levels. Accordingly the increased secretion of total insulin in overweighty persons consists mostly of insulin and to a lesser degree of proinsulin. Additionally there exists a significant correlation between the triglycerides and the degree of overweight. After 4 weeks application of 1.7 g metformin daily the weight reduction reached on an average 1.4 kg, after 16 weeks 5.2 kg. In relation to the weight reduction lower proinsulin and insulin levels were noticed before and after stimulation with glucose. Even those test persons who did not lose weight under metformin showed lower proinsulin and insulin levels. It might be that metformin leads to a slow-down in glucose absorption and as a consequence to a decrease of insulin secretion. Lower triglyceride values after treatment with metformin not only were a sign of weight reduction: biguanides also influence the fat metabolism independently of the carbohydrate metabolism. Additional to the reduction diet the treatment with metformin seems to be very appropriate for overweighty patients with hyperinsulinism and hypertriglyceridemia.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=1174086&dopt=Abstract
peds.uab.edu
Leptin's role in the regulation of food intake, energy expenditure and weight control are widely recognized, especially in rodents. Likewise, the potential regulation of leptin secretion by insulin (and vice versa) has been of particular interest insofar as these nutrient signals may have meaningful, even adverse (inter)actions, in diabetes. We used a freshly isolated rat adipose tissue culture model to examine the effect of insulin, metformin and glibenclamide on basal and steroid-stimulated leptin secretion. This model was selected because of its physiologic rates of leptin formation and preservation of potentially significant cell-cell interactions compared to isolated cells. The basal rate of leptin secretion was 3. 4+/-1.2 ng/100 mg tissue/24 h. The addition of 100 nM dexamethasone or 400 nM hydrocortisone stimulated leptin secretion by 3-4 fold over basal (no steroid). Insulin inhibited both basal and steroid-activated leptin secretion by 35-50%. This inhibition was present with either 1 mM pyruvate or 5 mM glucose as a substrate suggesting that glycolysis was not required. Metformin inhibited basal and dexamethasone-stimulated leptin secretion in a dose dependent manner (50% inhibition occurred at 1 mM metformin) while glibenclamide was ineffective. The effect of insulin on isolated fat cells versus fat tissue was tested in parallel. After 24 h in culture, insulin inhibited leptin secretion similarly in both adipose preparations. The addition of 200 nM (-)N6-(2-phenylisopropyl)-adenosine did not alter the results.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11068185&dopt=Abstract
zoo.uvm.edu
BACKGROUND: Measurement of glycated hemoglobin and hemoglobin A1c (HbA1c) is now well established as the best means of measuring overall glucose control in managing diabetes. Other glycated serum protein assays reflecting recent glycemic control, e.g., glycated albumin and glycated protein (fructosamine), have also been validated in clinical studies. Regardless of the method, the expense and inconvenience of laboratory testing of blood samples may contribute to the well-documented underutilization of clinical glycated protein assessment. Accordingly, a rapid, inexpensive fingerstick test of fructosamine has been developed. This study cross-sectionally and prospectively assesses the clinical validity of fingerstick fructosamine versus laboratory determination. METHODS: Fifty-one subjects (18 control, 33 with diabetes) participated in a cross-sectional study and 20 subjects with type 2 diabetes participated in a prospective, 6-week study with clinical intervention consisting of glipizide gits or metformin in mono- and combination therapy. Subjects had weekly laboratory determination of serum fructosamine, glycated hemoglobin, and fasting glucose; fingerstick fructosamine was obtained at each clinic visit. RESULTS: Fingerstick fructosamine was shown to correlate highly to laboratory fructosamine (r = 0.80, p < 0.001) and glycated hemoglobin (r = 0.81, p < 0.001). In the clinical intervention study subjects, significant decreases in fasting glucose (p < 0.001), laboratory fructosamine (p < 0.001), and fingerstick fructosamine (p < 0.001) were noted compared to baseline. The subject's self-test fingerstick fructosamine mirrored laboratory testing of fructosamine in detection of changes in clinical glucose control. CONCLUSIONS: This study demonstrates that fingerstick fructosamine correlates well to laboratory assessment of fructosamine and glycated hemoglobin. The patient self-test fructosamine provides the same clinical information as laboratory assessment.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11474829&dopt=Abstract
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