"Eating potatoes may increase the risk of type 2 diabetes and replacing them with whole grains may lower this risk, according to a study published online December 17 in Diabetes Care.
"Although potatoes are considered a vegeta"...
Mechanism of Action
The primary mode of action of GLUCOTROL (glipizide) in experimental animals appears to be the stimulation of insulin secretion from the beta cells of pancreatic islet tissue and is thus dependent on functioning beta cells in the pancreatic islets. In humans, GLUCOTROL (glipizide) appears to lower the blood glucose acutely by stimulating the release of insulin from the pancreas, an effect dependent upon functioning beta cells in the pancreatic islets. The mechanism by which GLUCOTROL (glipizide) lowers blood glucose during long-term administration has not been clearly established. In man, stimulation of insulin secretion by GLUCOTROL (glipizide) in response to a meal is undoubtedly of major importance. Fasting insulin levels are not elevated even on long-term GLUCOTROL (glipizide) administration, but the postprandial insulin response continues to be enhanced after at least 6 months of treatment. The insulinotropic response to a meal occurs within 30 minutes after an oral dose of GLUCOTROL (glipizide) in diabetic patients, but elevated insulin levels do not persist beyond the time of the meal challenge. Extrapancreatic effects may play a part in the mechanism of action of oral sulfonylurea hypoglycemic drugs.
Blood sugar control persists in some patients for up to 24 hours after a single dose of GLUCOTROL (glipizide) , even though plasma levels have declined to a small fraction of peak levels by that time (see Pharmacokinetics below).
Some patients fail to respond initially, or gradually lose their responsiveness to sulfonylurea drugs, including GLUCOTROL (glipizide) . Alternatively, GLUCOTROL (glipizide) may be effective in some patients who have not responded or have ceased to respond to other sulfonylureas.
Gastrointestinal absorption of GLUCOTROL (glipizide) in man is uniform, rapid, and essentially complete. Peak plasma concentrations occur 1-3 hours after a single oral dose. The half-life of elimination ranges from 2-4 hours in normal subjects, whether given intravenously or orally. The metabolic and excretory patterns are similar with the two routes of administration, indicating that first-pass metabolism is not significant. GLUCOTROL (glipizide) does not accumulate in plasma on repeated oral administration. Total absorption and disposition of an oral dose was unaffected by food in normal volunteers, but absorption was delayed by about 40 minutes. Thus, GLUCOTROL (glipizide) was more effective when administered about 30 minutes before, rather than with, a test meal in diabetic patients. Protein binding was studied in serum from volunteers who received either oral or intravenous GLUCOTROL (glipizide) and found to be 98-99% one hour after either route of administration. The apparent volume of distribution of GLUCOTROL (glipizide) after intravenous administration was 11 liters, indicative of localization within the extracellular fluid compartment. In mice, no GLUCOTROL (glipizide) or metabolites were detectable autoradiographically in the brain or spinal cord of males or females, nor in the fetuses of pregnant females. In another study, however, very small amounts of radioactivity were detected in the fetuses of rats given labelled drug.
The metabolism of GLUCOTROL (glipizide) is extensive and occurs mainly in the liver. The primary metabolites are inactive hydroxylation products and polar conjugates and are excreted mainly in the urine. Less than 10% unchanged GLUCOTROL (glipizide) is found in the urine.
Last reviewed on RxList: 4/4/2011
This monograph has been modified to include the generic and brand name in many instances.
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