Drugs online research references
Acta Diabetol. 1994 Apr;31(1):31-6.
Effects of glipizide on glucose metabolism and muscle content of the insulin-regulatable glucose transporter (GLUT 4) and glycogen synthase activity during hyperglycaemia in type 2 diabetic patients.
Schmitz O, Lund S, Bak JF, Orskov L, Andersen PH, Moller N, Rasmussen O, Christiansen JS, Pedersen O.
Medical Department M (Endocrinology and Diabetes), Aarhus Kommunehospital, Denmark.
To examine whether sulphonylureas influence hyperglycaemia-induced glucose disposal and suppression of hepatic glucose production (HGP) in type 2 diabetes mellitus, a 150-min hyperglycaemic (plasma glucose 14 mmol/l) clamp with concomitant somatostatin infusion was used in eight type 2 diabetic patients before and after 6 weeks of glipizide (GZ) therapy. During the clamp a small replacement dose of insulin was given (0.15 mU/kg per min). Isotopically determined glucose-induced glucose uptake was similar before and after GZ administration which led to improved glycaemic control (basal plasma glucose 12.2 +/- 1.3 vs 8.9 +/- 0.7 mmol/l; P < 0.01). Glucose-induced suppression of HGP was, however, more pronounced during GZ treatment (0.96 +/- 0.14 vs 1.44 +/- 0.20 mg/kg per min; P < 0.02). Following GZ treatment hyperglycaemia failed to stimulate glycogen synthase activity. Moreover, GZ resulted in a significant increase in the immunoreactive abundance of the insulin-regulatable glucose transport protein (GLUT 4) (P < 0.02). In conclusion, these results suggest that GZ therapy in type 2 diabetic patients enhances hepatic sensitivity to hyperglycaemia, while glucose-induced glucose uptake remains unaffected. In addition, GZ tends to normalize the activity of glycogen synthase and increases the content of GLUT 4 protein in skeletal muscle.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8043894&dopt=Abstract
Probl Endokrinol (Mosk). 1994 May-Jun;40(3):8-10.
[Atherogenic properties of oral sugar-reducing sulfonylurea derivatives]
[Article in Russian]
Maksumova MA, Sobenin IA, Balabolkin MI, Orekhov AN.
The authors have examined the effects of sulfonylurea drugs glibenclamide and glipizide and of their analogs manilil and minidiab on cholesterol levels in murine peritoneal macrophages. Both glibenclamide and glipizide had a direct atherogenic effect on cultured murine peritoneal macrophages. A similar effect was observed in vivo: blood sera of diabetics after a single intake of 5 mg of manilil or minidiab increased the atherogenic potential of cultured murine peritoneal macrophages.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8073011&dopt=Abstract
Br J Pharmacol. 1994 Jun;112(2):649-53.
Effects of glibenclamide on systemic and splanchnic haemodynamics in conscious rats.
Moreau R, Komeichi H, Kirstetter P, Yang S, Aupetit-Faisant B, Cailmail S, Lebrec D.
Laboratoire d'Hemodynamique Splanchnique, Unite de Recherches de Physiopathologie Hepatique, INSERM U-24, Hopital Beaujon, Clichy, France.
1. The effects of the sulphonylurea, glibenclamide (20 mg kg-1, i.v.), at a dose that blocks vascular potassium channels, on systemic and splanchnic haemodynamics (radioactive microspheres) were studied in conscious rats. 2. Glibenclamide significantly decreased cardiac index and hepatic artery blood flow while it significantly increased vascular resistance in systemic, portal and hepatic arterial territories. 3. In rats with suppressed cardiovascular reflexes, glibenclamide induced vasoconstriction in systemic, portal and hepatic arterial territories. 4. Intracerebroventricular administration of glibenclamide did not alter systemic or regional vascular tone. 5. Glibenclamide blunted the vasodilator effect of the potassium channel opener, diazoxide but not that of the L-type calcium channel blocker, nicardipine. 6. Another sulphonylurea, glipizide (20 mg kg-1, i.v.), induced significant systemic and splanchnic vasoconstriction. 7. Thus, the glibenclamide-induced blockade of vascular potassium channels caused a vasoconstriction in the systemic and splanchnic vascular beds. In these territories, therefore, the opening of glibenclamide-sensitive potassium channels might be responsible for a basal vasodilator tone.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8075883&dopt=Abstract
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