Sunday, March 30, 2008
Treatment of Patients with Type 2 Diabetes Mellitus
The impaired glucose homeostasis whole number of type 2 diabetes is thinking to finish from defects in the metabolic processes that convert glucose to adenosine triphosphate (ATP) within pancreatic β-cells.
Normally, ATP inhibits ATP-sensitive K+ (KATP) channels, causing cell depolarisation and the porta of voltage-dependent Ca2+ channels.
The resulting influx of Ca2+ triggers exocytosis and insulin firing.
KATP channels comprise a pore of inwardly rectifying K+ distribution channel subunits encased by sulfonylurea complex body part (SUR) subunits with ATP-ase capability. Nateglinide binds competitively to SURs, thereby inhibiting KATP channels and stimulating insulin secernment.
The pharmacological plot of nateglinide is unique in several important respects.
Comparative in vitro studies indicate that nateglinide inhibits KATP channels more rapidly, and with a shorter period of activeness, than glibenclamide, glimepiride and repaglinide.
Nateglinide shows a greater stage of specialness for SUR1 over SUR2, as compared with glibenclamide and repaglinide (Figure 1). Animal studies suggest that nateglinide reduces the risk of sustained decrease of islet cell insulin compared with glibenclamide. Clinically, these benefits translate into a prompting anti-hyperglycaemic meaning at mealtimes, followed by a running game to basal insulin levels, a low risk of hypoglycaemia between meals and the avoidance of sustained pancreatic sex throughout the day.
In gain, nateglinide has little consequence on β-cell apoptosis, as compared with the stimulation associated with sulfonylureas.
This is a part of article Treatment of Patients with Type 2 Diabetes Mellitus Taken from "Generic Amaryl (Glimepiride) Information" Information Blog
Labels: pharmacology
