AIM To investigate the effect of nicotinamide riboside (NR) on mitochondrial fusion and fission in type 1 diabetic hearts and its underlying mechanisms.
METHODS Type 1 diabetic mellitus (DM) rat models were induced by streptozotocin (STZ) injection. The animals were randomly divided into four groups: Control (Con) group, Con+NR group, DM group, and DM+NR group. Blood glucose and body weight were measured. Intraperitoneal glucose tolerance test (IPGTT) was used to determine glucose metabolism. Cardiac functions were evaluated by echocardiography, cardiomyocyte apoptosis was determined by TUNEL assay and ROS was detected by DHE staining. Mitochondrial morphology was analyzed by transmission electron microscope and plasma triglyceride (TG) and total cholesterol (TC) were detected by automatic biochemical analyzer. Western blot was used to detect the expressions of mitochondrial fission and fusion-related proteins.
RESULTS Compared with those in control group, the blood glucose and blood lipid were significantly increased and the body weight was decreased in diabetic rats. Cardiac functions were impaired in diabetic rats (P<0.05, P<0.01) and the expression of Opa1 was significantly down-regulated (P<0.01). Cardiomyocyte apoptosis and oxidative stress were increased in diabetic hears and mitochondrial fission was significantly enhanced in diabetic hearts (P<0.01). NR treatment effectively improved cardiac functions in diabetic rats and reduced cardiomyocyte apoptosis and oxidative stress in diabetic hearts (P<0.05). Importantly, NR treatment increased Opa1 expression and promoted mitochondrial fusion in diabetic hearts (P<0.01).
CONCLUSION Nicotine ribose increases the expression of Opa1 and prevents mitochondrial fission in diabetic hearts. Nicotine ribose inhibits cardiomyocyte apoptosis and oxidative stress and improves cardiac functions in diabetic rats.
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