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Mechanisms of action of metformin with special reference to cardiovascular protection

Zilov A. V., Abdelaziz S. I., AlShammary A., Al Z. A., Amir A., Assaad K. S. H., Brand K., Elkafrawy N., Hassoun A. A. K., Jahed A., Jarrah N., Mrabeti S., Paruk I.
Diabetes/Metabolism Research and Reviews
Vol.35, Issue7, Num.e3173
Опубликовано: 2019
Тип ресурса: Обзор

DOI:10.1002/dmrr.3173

Аннотация:
Management guidelines continue to identify metformin as initial pharmacologic antidiabetic therapy of choice for people with type 2 diabetes without contraindications, despite recent randomized trials that have demonstrated significant improvements in cardiovascular outcomes with newer classes of antidiabetic therapies. The purpose of this review is to summarize the current state of knowledge of metformin's therapeutic actions on blood glucose and cardiovascular clinical evidence and to consider the mechanisms that underlie them. The effects of metformin on glycaemia occur mainly in the liver, but metformin-stimulated glucose disposal by the gut has emerged as an increasingly import site of action of metformin. Additionally, metformin induces increased secretion of GLP-1 from intestinal L-cells. Clinical cardiovascular protection with metformin is supported by three randomized outcomes trials (in newly diagnosed and late stage insulin-treated type 2 diabetes patients) and a wealth of o
Ключевые слова:
cardiovascular outcomes; hyperglycaemia; metformin; type 2 diabetes
antidiabetic agent; glucagon like peptide 1; glucose; incretin; metformin; antidiabetic agent; metformin; atherosclerosis; body fat distribution; body weight loss; cardiovascular risk; cardiovascular system; drug mechanism; endothelial progenitor cell; glucose blood level; heart protection; hemostasis; human; inflammation; information retrieval; intestine cell; intestine flora; non insulin dependent diabetes mellitus; oxidative stress; priority journal; Review; cardiovascular disease; non insulin dependent diabetes mellitus; prognosis; Cardiovascular Diseases; Diabetes Mellitus, Type 2; Humans; Hypoglycemic Agents; Metformin; Prognosis
Язык текста: Английский
ISSN: 1520-7560
Zilov A. V. Aleksej Vadimovich 1970-
Abdelaziz S. I.
AlShammary A.
Al Z. A. Zahrani A.
Amir A.
Assaad K. S. H. Khalil S.H.
Brand K.
Elkafrawy N.
Hassoun A. A. K.
Jahed A.
Jarrah N.
Mrabeti S.
Paruk I.
Зилов А. В. Алексей Вадимович 1970-
Абделазиз С. И.
АлШаммарy А.
Ал З. А. Захрани А.
Амир А.
Ассаад К. С. Х. Халил С.Х.
Бранд К.
Елкафраwy Н.
Хассоун А. А. К.
Йахед А.
Йаррах Н.
Мрабети С.
Парук И.
Mechanisms of action of metformin with special reference to cardiovascular protection
Текст визуальный непосредственный
Diabetes/Metabolism Research and Reviews
Wiley-Blackwell
Vol.35, Issue7 Num.e3173
2019
Обзор
cardiovascular outcomes hyperglycaemia metformin type 2 diabetes
antidiabetic agent glucagon like peptide 1 glucose incretin metformin antidiabetic agent metformin atherosclerosis body fat distribution body weight loss cardiovascular risk cardiovascular system drug mechanism endothelial progenitor cell glucose blood level heart protection hemostasis human inflammation information retrieval intestine cell intestine flora non insulin dependent diabetes mellitus oxidative stress priority journal Review cardiovascular disease non insulin dependent diabetes mellitus prognosis Cardiovascular Diseases Diabetes Mellitus, Type 2 Humans Hypoglycemic Agents Metformin Prognosis
Management guidelines continue to identify metformin as initial pharmacologic antidiabetic therapy of choice for people with type 2 diabetes without contraindications, despite recent randomized trials that have demonstrated significant improvements in cardiovascular outcomes with newer classes of antidiabetic therapies. The purpose of this review is to summarize the current state of knowledge of metformin's therapeutic actions on blood glucose and cardiovascular clinical evidence and to consider the mechanisms that underlie them. The effects of metformin on glycaemia occur mainly in the liver, but metformin-stimulated glucose disposal by the gut has emerged as an increasingly import site of action of metformin. Additionally, metformin induces increased secretion of GLP-1 from intestinal L-cells. Clinical cardiovascular protection with metformin is supported by three randomized outcomes trials (in newly diagnosed and late stage insulin-treated type 2 diabetes patients) and a wealth of o