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PubMed2000

[Antidiabetic drug at every meal. Repaglinide is especially recommended for slender type 2 diabetic patients].

Repaglinide is the first stimulator of insulin secretion from the new meglitinide family. Via specific binding to the ATP-sensitive potassium channel of the beta cell membrane, it stimulates the rapid release of insulin. In preclinical studies, the insulin-stimulating effect of repaglinide has been found to be 10 to 20 times more potent than that of glibenclamide. Repaglinide is rapidly absorbed and has a short action, which makes it particularly well suited for the regulation of prandial blood glucose and meal-related dose adjustment. Since repaglinide is eliminated almost exclusively by non-renal routes, it can be used without danger in patients with moderately reduced renal function. Repaglinide is a suitable agent for first-line monotherapy in patients whose glucose metabolism cannot be optimally controlled by increasing physical activity and appropriate dietary measures. Repaglinide is clearly superior to glibenclamide in reducing postprandial hyperglycemia, and has a lower hypoglycemia risk than all the sulphonylureas. The flexibility of repaglinide makes it possible for good oral meal-related treatment.

Blood Glucose↗
PubMed2000

Acceleration of the development of diabetes in obese diabetic (db/db) mice by nicotinamide: a comparison with its antidiabetic effects in non-obese diabetic mice.

Destruction of pancreatic beta cells has been implicted in the progression to hyperglycemia in type 1 diabetes. While there is evidence of beta-cell loss in type 2 diabetes, its contribution to the development of the diabetic state is undecided. Nicotinamide has defensive effects against toxic insults to the pancreatic islets and confers protection in both human and animal models of type 1 diabetes, but its effects on type 2 diabetes are less well documented. This report describes a comparison of the outcome of chronic oral administration of nicotinamide on the development of diabetes in obese diabetic (db/db) and non-obese diabetic (NOD) mice models of type 2 and type 1 diabetes, respectively. Nicotinamide was administered in the diet (5 g/kg diet) for 12 (db/db) or 24 (NOD) weeks. Over the 12 weeks of the study, control diabetic (db/db) mice became progressively more hyperglycemic and glycosuric, while serum and pancreatic insulin levels decreased compared with those on day 0. In mice treated with nicotinamide, there was a pronounced acceleration in the development of hyperglycemia and glycosuria, as well as a decrease in pancreatic insulin levels, compared with time-matched controls. In addition, the morphology of the pancreatic islets of nicotinamide-treated diabetic (db/db) mice showed an enhanced islet disorganization. By comparison, in NOD mice, nicotinamide prevented the decline in serum and pancreatic insulin levels and maintained normal islet architecture and insulin content. Our data shows that in contrast to its preventative effects on the development of autoimmune diabetes in NOD mice, chronic nicotinamide administration to obese diabetic (db/db) mice markedly accelerated the progression of diabetes. The results of our study caution against the use of nicotinamide in insulin-resistant states, such as type 2 diabetes.

Animals↗
PubMed2000

The molecular mechanism of the insulin-mimetic/sensitizing activity of the antidiabetic sulfonylurea drug Amaryl.

The hypoglycemic sulfonylurea drugs cause reduction of blood glucose predominantly via stimulation of insulin release from pancreatic beta cells. In addition, during long-term treatment, an insulin-independent blood glucose-decreasing mechanism is assumed to operate. This may include insulin-sensitizing and insulin-mimetic activity in muscle and adipose tissue. This review summarizes our current knowledge about the putative modes of action of the sulfonylurea compound, Amaryl, in pancreatic beta cells and, in particular, peripheral target cells that form the molecular basis for its characteristic pharmacological and clinical profile. The analysis was performed in comparison with the conventional and the "golden standard" sulfonylurea, glibenclamide. I conclude: (I) The blood glucose decrease provoked by Amaryl can be explained by a combination of stimulation of insulin release from the pancreas and direct enhancement, as well as potentiation of the insulin response of glucose utilization in peripheral tissues only. (II) The underlying molecular mechanisms seemed to rely on beta cells on a sulfonylurea receptor protein, SURX, associated with the ATP-sensitive potassium channel (K(ATP)) and different from SUR1 for glibenclamide, and in muscle and adipose cells on: (a) the increased production of diacylglycerol and activation of protein kinase C; (b) the enhanced expression of glucose transporter isoforms; and (c) the insulin receptor-independent activation of the insulin receptor substrate/phosphatidylinositol-3-kinase pathway. (III) The latter mechanism involved a nonreceptor tyrosine kinase and a number of components, such as caveolin and glycosylphosphatidylinositol structures, which are assembled in caveolae/detergent-insoluble glycolipid-enriched rafts of the target cell plasma membrane. Since hyperinsulinism and permanent K(ATP) closure are supposed to negatively affect the pathogenesis and therapy of non-insulin-dependent diabetes mellitus, the demonstrated higher insulin-independent blood glucose-lowering activity of Amaryl may be therapeutically relevant.

Amino Acid Sequence↗
PubMed2001

Antidiabetic activity of a polyherbal preparation (tincture of panchparna) in normal and diabetic rats.

The present work was executed to evaluate the anti-diabetic potency of a polyherbal formulation, and its influence on derangement in the metabolism of glucose and cholesterol and changes in sodium levels in serum and urine in normal and alloxan induced diabetic rats. Serum glucose and serum cholesterol levels were found to be increased in diabetic animals. Serum sodium and urinary sodium, hepatic glycogen levels are found to be decreased in diabetic state. Treatment with the polyherbal formulation (1.0 ml/kg body wt) for 30 days in diabetic animals has shown decrease in serum glucose and serum cholesterol levels in comparison to control animals, whereas in normal treated animals, the formulation does not effect the serum glucose and serum cholesterol levels. Serum sodium and urinary sodium levels were increased in both diabetic treated and the control animals. Hepatic glycogen levels were increased in diabetic treated animals, but there was no change in the control treated animals.

Animals↗