Abstract
Epidemiology survey indicated that cigarette smoking is a risk factor of diabetes. However, the precise mechanisms remain to be clarified. In this study, we found that smoking caused metabolic malfunctions on pancreas and liver in experimental animal model. These were indicated by hyperglycemia, increased serum hemoglobin A1c level and decreased insulin secretion, inhibition of liver glycogen synthase (LGS), and hepatic glycogen synthesis. Mechanistic studies revealed that all these alterations were caused by the inflammatory reaction and reactive oxygen species (ROS) induced by the smoking. Melatonin treatment significantly preserved the functions of both pancreas and liver by reducing β cell apoptosis, CD68‐cell infiltration, ROS production, and caspase‐3 expression. The siRNA‐knockdown model identified that the protective effects of melatonin were mediated by melatonin receptor‐2 (MT2). This study uncovered potentially underlying mechanisms related to the association between smoking and diabetes. In addition, it is, for first time, to report that melatonin effectively protects against smoking‐induced glucose metabolic alterations and the signal transduction pathway of melatonin is mainly mediated by its MT2 receptor. These observations provide solid evidence for the clinically use of melatonin to reduce smoking‐related diabetes, and the therapeutic regimens are absent currently.
Highlights
Cigarette smoking is an unhealthy lifestyle habit
Diabetes appears to be heavily influenced by smoking,[1] and clinical epidemiology surveys involving homeostasis model assessment demonstrates that smoking may interfere with blood glucose balance.[2]
Insulin histochemical staining showed that the β cell area was significantly decreased in the islets of smoking rats, whereas the β cell area was increased in the islets of smoking+melatonin rats (Figure 1D,E, P < .05)
Summary
Cigarette smoking is an unhealthy lifestyle habit. Diabetes is of multifactorial origin and is associated with environmental factors and lifestyle. Diabetes appears to be heavily influenced by smoking,[1] and clinical epidemiology surveys involving homeostasis model assessment demonstrates that smoking may interfere with blood glucose balance.[2] the mechanisms underlying the effects of smoking on hyperglycemia and β cell function have not yet been investigated. The effects of melatonin on glucose metabolism have not been thoroughly examined To resolve these issues, we evaluated pancreatic insulin secretion and hepatic glycogen accumulation in the smoking rat model, and investigated the mechanism underlying the pathogenesis of hyperglycemia. The findings provide novel insight into the potential therapeutic utility of melatonin in glucose regulation
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