The aim of this work was to study the relationship between excess body weight and the risks of hypertension and diabetes in the population of northeastern China. Subsections of a cross-sectional survey in Da Qing City were used to assess the relationship of excess weight to risk factors for coronary heart disease (CHD). A 6-year prospective study also assessed the probability of developing Type 2 diabetes. A total of 2856 adults (25-70 years of age) were assessed cross-sectionally and 629 non-diabetic subjects of similar age were followed-up for 6 years. Blood pressure, plasma fasting glucose, triglycerides, high-density lipoporotein (HDL) cholesterol and fibrinogen levels were measured as well as weight, height and waist and hip circumferences. About 45% of adults had a body mass index (BMI) of > or =25.0. Risk factors increased with increasing BMI from a baseline value of 21.0: at a BMI of 23.0-24.9, the risk of hypertension and hypertriglyceridaemia doubled; the risk increased threefold at a BMI of 25.0-26.9. The prevalence of Type 2 diabetes increased progressively in women within the normal BMI range and in men from a BMI of 25.0. Type 2 diabetes was four times as common if the BMI was >27.0. Increasing waist measurements predicted 10-fold increases in hypertension and a three-to-five times increased risk of diabetes. Suitable waist cut-off points were 85cm for men and 80cm for women, with statistical analysis showing waist as the more dominant predictor of risk than age, waist-to-hip ratios or BMIs. Hence, small increases in BMI, and particularly in waist circumference, predict a substantial increase in the risk of diabetes and risk for CHD, especially hypertension, in Chinese adults.

BackgroundDyslipidemia and lipotoxicity-induced insulin resistance, inflammation and oxidative stress are the key pathogeneses of renal damage in type 2 diabetes. Increasing evidence shows that whole-body low dose radiation (LDR) plays a critical role in attenuating insulin resistance, inflammation and oxidative stress.ObjectiveThe aims of the present study were to investigate whether LDR can prevent type 2 diabetes-induced renal damage and the underlying mechanisms.MethodsMice were fed with a high-fat diet (HFD, 40% of calories from fat) for 12 weeks to induce obesity followed by a single intraperitoneal injection of streptozotocin (STZ, 50 mg/kg) to develop a type 2 diabetic mouse model. The mice were exposed to LDR at different doses (25, 50 and 75 mGy) for 4 or 8 weeks along with HFD treatment. At each time-point, the kidney weight, renal function, blood glucose level and insulin resistance were examined. The pathological changes, renal lipid profiles, inflammation, oxidative stress and fibrosis were also measured.ResultsHFD/STZ-induced type 2 diabetic mice exhibited severe pathological changes in the kidney and renal dysfunction. Exposure of the mice to LDR for 4 weeks, especially at 50 and 75 mGy, significantly improved lipid profiles, insulin sensitivity and protein kinase B activation, meanwhile, attenuated inflammation and oxidative stress in the diabetic kidney. The LDR-induced anti-oxidative effect was associated with up-regulation of renal nuclear factor E2-related factor-2 (Nrf-2) expression and function. However, the above beneficial effects were weakened once LDR treatment was extended to 8 weeks.ConclusionThese results suggest that LDR exposure significantly prevented type 2 diabetes-induced kidney injury characterized by renal dysfunction and pathological changes. The protective mechanisms of LDR are complicated but may be mainly attributed to the attenuation of dyslipidemia and the subsequent lipotoxicity-induced insulin resistance, inflammation and oxidative stress.

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Repetitive exposure of diabetic mice to low-dose radiation (LDR) at 25 mGy could significantly attenuate diabetes-induced renal inflammation, oxidative damage, remodeling, and dysfunction, for which, however, the underlying mechanism remained unknown. The present study explored the effects of LDR on the expression and function of Akt and Nrf2 in the kidney of diabetic mice. C57BL/6J mice were used to induce type 1 diabetes with multiple low-dose streptozotocin. Diabetic and age-matched control mice were irradiated with whole body X-rays at either single 25 mGy and 75 mGy or accumulated 75 mGy (25 mGy daily for 3 days) and then sacrificed at 1–12 h for examining renal Akt phosphorylation and Nrf2 expression and function. We found that 75 mGy of X-rays can stimulate Akt signaling pathway and upregulate Nrf2 expression and function in diabetic kidneys; single exposure of 25 mGy did not, but three exposures to 25 mGy of X-rays could offer a similar effect as single exposure to 75 mGy on the stimulation of Akt phosphorylation and the upregulation of Nrf2 expression and transcription function. These results suggest that single 75 mGy or multiple 25 mGy of X-rays can stimulate Akt phosphorylation and upregulate Nrf2 expression and function, which may explain the prevention of LDR against the diabetic nephropathy mentioned above.