Efficacy of glimepiride on insulin resistance, adipocytokines, and atherosclerosis

Abstract

: Background : Plasma adiponectin levels increase after the administration of glimepiride. This unique effects would also be expected to improve other adipocytokines and have antiatherosclerotic action in patients with metabolic syndrome. Methods : Thirty-four patients with type 2 diabetes mellitus who were administrated glibenclamide were randomly divided into two groups. In 20 patients glibenclamide was changed to glimepiride (GP group), and the administration of glibenclamide (GB group) was continued in 14 patients. Twelve patients receiving insulin therapy (INS group) were enrolled for comparison. The levels of plasma adiponectin, high sensitive-CRP, TNF-! , interleukin-6, homeostasis model assessment-insulin resistance (HOMA-IR), brachial-ankle pulse wave velocity (baPWV) and augmentation index (AI) were measured before and 28 weeks after the therapy. Results: HOMA-IR in the GP group was significantly decreased compared to the GB group. Plasma adiponectin levels were significantly increased in the GP group but not in the other groups. TNF-! , interleukin-6 and high sensitive-CRP levels were significantly decreased in the GP group, but not in the other groups. The baPWV and AI levels did not change in either the GB or the INS group, but were significantly decreased in the GP group. Conclusions Glimepiride appears to improve insulin resistance and atherosclerotic disorders. J. Med. Invest. 53:87-94, February, 2006

Relationship between job strain and radial arterial wave reflection in middle-aged male workers

“…All workers were engaged in daytime desk work. Subjects on medication for hypertension, dyslipidemia, or diabetes mellitus (n = 111) were excluded, to avoid the effect of these medications on arterial stiffness and wave reflection (Nichols and Singh, 2002;Koshiba et al, 2006;Efrati et al, 2007). Subjects with a history or presence of CVD (n = 5) were also excluded because arterial wave reflection may be affected by reduced cardiac function (Schofield et al, 2007).…”

Reduced Cell Proliferation and Neuroblast Differentiation in the Dentate Gyrus of High Fat Diet-Fed Mice are Ameliorated by Metformin and Glimepiride Treatment

“…Metformin hydrochloride decreases hepatic glucose production, decreases the intestinal absorption of glucose, and improves insulin sensitivity by increasing peripheral glucose uptake and utilization [16,17]. In addition, glimepiride is a sulfonylurea that stimulates the release of insulin from pancreatic beta cells and induces the increased activity of intracellular insulin receptors [18]. Glimepiride may offer some advantages when used in combination with metformin due to its more prominent extrapancreatic activity and more favorable safety profile compared with other sulfonylureas [18][19][20][21].…”

“…In addition, glimepiride is a sulfonylurea that stimulates the release of insulin from pancreatic beta cells and induces the increased activity of intracellular insulin receptors [18]. Glimepiride may offer some advantages when used in combination with metformin due to its more prominent extrapancreatic activity and more favorable safety profile compared with other sulfonylureas [18][19][20][21]. Some pharmacy sells metformin-glimepiride tablets, which resulted in significantly greater reductions in glycated hemoglobin (HbA1c) and fasting plasma glucose compared with metformin ?…”

Sulfonylureas in the modern strategy of therapy of type 2 diabetes

“…Было показано также, что на фоне приема Амарила повыша-ется продукция адипонектина и снижается уровень фактора не-кроза опухолей -TNF-α [51], что сопровождается снижением индекса HOMA-IR (Homeostasis Model Assesment of Insulinresistance), за счет снижения ингибирующего влияния TNF-α на ак-тивность тирозинкиназы инсулинового рецептора и секрецию адипонектина адипоцитами. Недавно было показано непосред-ственное связывание препарата с PPARG и повышение транс-крипционной активности гена PPAR-γ, что сопровождалось изменением уровня мРНК генов-мишеней для лептина и ади-понектина [52].…”

“…Амарил, в отличие от глибенкламида, не проявляет селективности к SUR 2A и SUR 2В, поскольку в его структуре отсутствует бензамидная группировка, благо-даря чему не выявлено его отрицательного влияния на коронар-ный кровоток и сосудистый тонус ни в экспериментах in vitro, ни в опытах in vivo [56,57]. В последнее время появились данные о кардиопротективном и антиатерогенном действии препарата: в исследовании Koshiba K. et al [51] было отмечено снижение таких маркеров кардиоваскулярного риска, как IL-6, CRP, TNF-α у больных, получавших Амарил в ходе 28-недельного сравнительного исследования с глибенкламидом. Антиатеро-склеротический эффект препарата проявляется также в поло-жительном влиянии на липидный обмен [58] и в повышении продукции NO эндотелием [59].…”