Objective To investigate the effects of low carbohydrate on body weight,glucose and lipid metabolism,sex hormones and conception of polycystic ovary syndrome (PCOS) with obese patients.Methods Sixty-four patients with PCOS and obesity and fertility were enrolled in this study from November 2015 to December 2016,and were randomly divided into low-carbohydrate diet group (study group) and control group.Before and after the intervention,the body weight,body fat composition analysis,reproductive endocrine hormone,glucose and lipid metabolism,menstrual cycle changes and conception were measured at 12 weeks after intervention.Results (1) After 12 weeks of treatment,the body weight,waist circumference,Body Mass Index(BMI)and visceral fat area of the study group were lower than those of the control group,the difference was statistically significant (P ＜ 0.05).(2) After 12 weeks of treatment,fasting blood glucose (FPG) of the two groups had no significant difference (P ＞ 0.05),while the 2 h postprandial blood glucose (PPG) of study group was significantly lower than the control group,the difference between the two groups was statistically significant (P ＜ 0.05).After treatment,the fasting insulin (FINS) of the study group and control groupwas respectively decreased by 48.8％ and 25.3％ compared with the baseline,the difference was statistically significant (P ＜ 0.05).(3) After treatment,the testosterone (T),free androgen index (FAI) and luteinizing hormone (LH) of the two groups decreased,compared to the control group,the study group decreased significantly (P ＜ 0.05).(4) The recovery rate of menstrual cycle and natural pregnancy rate in the study group were significantly better than those in the control group (P ＜ 0.05).Conclusions Low carbohydrate diet combined with metformin and moderate intensity exercise can effectively reduce weight,improve glucose,lipid metabolism and sex hormone levels,improve the natural pregnancy rate.

Mitochondrial unfolded protein response (UPR mt) is a protein-toxic stress response, which regulates the communication from mitochondria to the nucleus. It is activated when a large number of unfolded or misfolded proteins accumulate in the mitochondria. The activation of UPR mt increases the expression of a series of chaperones and proteases, and maintains the homeostasis and function of mitochondrial proteins. Mitochondria play an important role in maintaining cardiomyocyte homeostasis. The damage of myocardial mitochondria leads to the metabolic disorder of cells suffering from ischemia/reperfusion injury. It is the key mechanism of myocardial cell death. This article mainly reviews the regulatory pathway of UPR mt and the research progress of UPR mt in myocardial ischemia/reperfusion injury (MIRI), in order to provide new ideas for the treatment of MIRI.