| BackgroundType 2 diabetes mellitus (T2DM) is one of the ordinary endocrine diseases. With the development of economy and the richness of people's living, the incidence of T2DM increased quickly. The incidence of T2DM of our country is not high compared with developed country, but the absolute number of T2DM patients is very big for our big population. Being relatively short of medical resources, our country has to bear with the heavy economic burdens. Both genetic factors and living styles play key roles in the initiation and development of T2DM. Usually the onset of T2DM is slowing so that we can find out the patients in early time. So the alternation of unhealthy life styles and the suitable medical intervention may have an important significance to prevent T2DM and increase the quality of life of T2DM patients. ObjectFind out the epidemic characters of high risk group of T2DM and the relations between new diagnosed T2DM and the risk factors, such as dietary, nutrition, smoking, drinking, exercise and inheritance in Hubei province. So we can provide epidemic causes for the prevention of T2DM. Explore the important role of oxidative stress and antioxidant system in the initiation and development of type 2 diabetes mellitus induced by insulin resistance. Also, we will discuss whether oxidative stress can cause insulin resistance andβ-cell dysfunction by DNA oxidative damage in the development of CGI and new diagnosed T2DM subjects.MethodEvery subject was questioned who went to the diabetic clinic for the first time. According to the results of OGTT, all subjects were divided into NGT, CGT and T2DM group. The differences of subjects'characters, behavior and dietary customs were analyzed among three groups. The control group was similar to CGI and T2DM group with sex and age. The differences of oxidative stress, antioxidant systems, DNA oxidative damage, insulin resistance andβ-cell function appraised by HOMA were analyzed. The relationships between oxidative stress, antioxidant systems or DNA oxidative damage and insulin resistance were also discussed.Result(1)There was any difference of every dietary frequency among NGT (n = 32), CGI (n =73) and T2DM (n =259) groups in Hubei province. The diets of maximum frequency are vegetable and fish. Logistic regressive analysis provided evidences that the subjects had high risk of T2DM who had the symptoms of skin itching and bluured vision and were fond of alcohol and sweet. (2) The susceptible index (MDA) of oxidative stress in T2DM (n = 113) group was higher significantly than in CGI (n = 78, P < 0.05) and NGT (n = 92, P < 0.05) group; the total antioxidant capacity in T2DM group was lower significantly than in CGI (P < 0.05) and NGT (P < 0.05). The HOMA IR has significant difference among three groups (P < 0.05). HOMAβ-cell was higher significantly in NGT and GI versus T2DM individuals and no difference between NGT and IG. (3) The DNA oxidative damage appraised by SCGE was higher significantly in CGI (n = 6, P < 0.01) and T2DM (n = 16, P < 0.01) group than in NGT (n = 19) group. Related analysis suggested oxidative stress and DNA oxidative damage had positive correlation with insulin resistance and reverse correlation withβ-cell excreting functions. ConclusionType 2 diabetes mellitus mostly affect the middle age and old age peoples. But more and more younglings are suffering from this disease. The similar dietary custom and behavior suggest it's high time to carry out healthy guidance in Hubei province. Because every subject has different social, economics, living, dietary or inheritable factors, the differences of oxidative stress and antioxidant defense systems exit. The accumulation of ROS will induce DNA oxidative damage and weaken insulin signal pathway. So insulin resistance appears. Insulin resistance can makeβ-cell secrete excessive insulin to maintain normal plasma glucose. Also, the insulin resistance and DNA oxidative damage ofβ-cell itself can induceβ-cell dysfunction, lower anti-apoptosis. Oxidative stress may cause insulin resistance andβ-cell dysfunction by DNA oxidative damage in the initiation and development T2DM.
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