Type 2 diabetes is characterized by a decreased ability of insulin to facilitate glucose uptake into insulin sensitive tissue,i.e.,skeletal muscle.The mechanism behind this is at the moment unresolved.It has been sugg...Type 2 diabetes is characterized by a decreased ability of insulin to facilitate glucose uptake into insulin sensitive tissue,i.e.,skeletal muscle.The mechanism behind this is at the moment unresolved.It has been suggested that increased amount of lipids inside the skeletal muscle(intramuscular triglyceride,diacylglycerol and ceramides)will impair insulin action in skeletal muscle,but data are not consistent in the human literature.It has also been hypothesized that the impaired insulin sensitivity is due to a dysfunction in the mitochondria resulting in an impaired ability to oxidize lipids,but the majority of the literature is not supporting this hypothesis.Recently it has been suggested that the production of reactive oxygen species play an essential role in skeletal muscle insulin sensitivity.It is well accepted that physical activity(endurance,strength and high intensity training)improves insulin sensitivity in healthy humans and in patients with type 2 diabetes.Whether patients with type 2 diabetes have the same beneficial effects(same improvement)as control subjects,when it comes to regular physical activity in regard to mitochondrial function,is not established in the literature.This review will focus only on the effect of physical activity on skeletal muscle(mitochondrial function)in patients with type 2 diabetes.展开更多
Background: Impaired insulin sensitivity may partly arise from a dysregulated lipid metabolism in human skeletal muscle. This study investigates the expression levels of perilipin 2, 3, and 5, and four key lipases in ...Background: Impaired insulin sensitivity may partly arise from a dysregulated lipid metabolism in human skeletal muscle. This study investigates the expression levels of perilipin 2, 3, and 5, and four key lipases in human skeletal muscle from the subjects that exhibit a range from normal to very low insulin sensitivity. Methods: 25 middle aged male participants were matched for lean body mass and recruited into three groups;type 2 diabetes patients (T2D), impaired glucose tolerance (IGT), and healthy sedentary controls (CON) according to their glucose tolerance and VO2peak. A muscle biopsy was obtained from vastus lateralis, and a two-step sequential euglycaemic-hyperinsulinaemic clamp was performed. Muscle samples were analyzed by Western blot for expression of perilipin 2, 3, 5, adipose triglyceride lipase (ATGL), hormone-sensitive lipase (HSL), endothelial lipase (EL) and lipoprotein lipase (LPL). Results: Perilipin 3 expression was higher in T2D compared to CON. Perilipin 2 expression was higher in CON than T2D. We observed no difference in expression of perili pin 5, ATGL, HSL, EL or LPL between the groups. Conclusions: In the present study the muscle perilipin 3 expression and perilipin 2 expression varied markedly with insulin sensitivity. This difference in perilipin expression may indicate that the lipid droplet function and thus storage and release of fatty acid-vary with insulin sensitivity.展开更多
文摘Type 2 diabetes is characterized by a decreased ability of insulin to facilitate glucose uptake into insulin sensitive tissue,i.e.,skeletal muscle.The mechanism behind this is at the moment unresolved.It has been suggested that increased amount of lipids inside the skeletal muscle(intramuscular triglyceride,diacylglycerol and ceramides)will impair insulin action in skeletal muscle,but data are not consistent in the human literature.It has also been hypothesized that the impaired insulin sensitivity is due to a dysfunction in the mitochondria resulting in an impaired ability to oxidize lipids,but the majority of the literature is not supporting this hypothesis.Recently it has been suggested that the production of reactive oxygen species play an essential role in skeletal muscle insulin sensitivity.It is well accepted that physical activity(endurance,strength and high intensity training)improves insulin sensitivity in healthy humans and in patients with type 2 diabetes.Whether patients with type 2 diabetes have the same beneficial effects(same improvement)as control subjects,when it comes to regular physical activity in regard to mitochondrial function,is not established in the literature.This review will focus only on the effect of physical activity on skeletal muscle(mitochondrial function)in patients with type 2 diabetes.
基金Financial support from The 1991 Pharmacy Foundation,NOVO Nordic Foundation,Direktor Verner Richter and Hustrus foundation,the foundation of 1870,Direktor Jacob and Olga Madsens foundation,Aase and Ejnar Danielsens foundation and EU project EXGENESIS 005272 is gratefully acknowledged
文摘Background: Impaired insulin sensitivity may partly arise from a dysregulated lipid metabolism in human skeletal muscle. This study investigates the expression levels of perilipin 2, 3, and 5, and four key lipases in human skeletal muscle from the subjects that exhibit a range from normal to very low insulin sensitivity. Methods: 25 middle aged male participants were matched for lean body mass and recruited into three groups;type 2 diabetes patients (T2D), impaired glucose tolerance (IGT), and healthy sedentary controls (CON) according to their glucose tolerance and VO2peak. A muscle biopsy was obtained from vastus lateralis, and a two-step sequential euglycaemic-hyperinsulinaemic clamp was performed. Muscle samples were analyzed by Western blot for expression of perilipin 2, 3, 5, adipose triglyceride lipase (ATGL), hormone-sensitive lipase (HSL), endothelial lipase (EL) and lipoprotein lipase (LPL). Results: Perilipin 3 expression was higher in T2D compared to CON. Perilipin 2 expression was higher in CON than T2D. We observed no difference in expression of perili pin 5, ATGL, HSL, EL or LPL between the groups. Conclusions: In the present study the muscle perilipin 3 expression and perilipin 2 expression varied markedly with insulin sensitivity. This difference in perilipin expression may indicate that the lipid droplet function and thus storage and release of fatty acid-vary with insulin sensitivity.
