[A cross-sectional survey on current status of type 2 diabetes mellitus with overweight or obesity in Guangdong province].

OBJECTIVE: To explore the glycemic control status and related risk factors of overweight or obesity patients with type 2 diabetes mellitus (T2DM) in Guangdong province. METHODS: The medical records of overweight or obesity patients with T2DM from 60 tertiary and secondary hospitals in Guangdong Province were collected by questionnaire and physical examination. And the clinical data were analyzed to explore the influencing factors of glycemic control. The HbA1c level was used to assess glycemic control. HbA1c < 7.0% indicated that glycemic control was up to standard. RESULTS: From August 2011 to March 2012, 5241 T2DM patients were recruited. The scope of current analysis was restricted to 4768 subjects with true data and deficiency no more than 5%. There were 2252 males and 2516 females. The age range was from 16 to 90 years, a median age 59.0 (50.0 - 69.0) years, onset age of diabetes 52.0 (44.0 - 60.0) years; a range of disease duration from 1 day to 42 years and a median of 5.0 (2.0 - 11.0) years. The median body mass index was 26.33(24.88 - 28.34) kg/m(2) and median waist circumference 93.0 (88.0 - 100.0) cm. Median HbA1c was 8.1% (6.9% - 10.1%) and only 26.2% patients reached the target level of HbA1c < 7.0%. Influencing factors of poor glycemic control were central obesity, high levels of resting heart rate, concurrent fatty liver and high intensity of treatment. And influencing factors of good glycemic control were regular exercises, smoking cessation, regular glycemic monitoring and good control of total cholesterol/triglyceride. CONCLUSION: A majority of Guangdong type 2 diabetics fail to achieve target values for glycemic control. There is an urgent need for comprehensive management for improving glycemic control.

SIRT1 interacts with metabolic transcriptional factors in the pancreas of insulin-resistant and calorie-restricted rats.

Sirtuin 1 (SIRT1) is one member of the silent information regulator 2 (Sir2)-like family of proteins involved in glucose homeostasis in mammals. It has been reported that SIRT1 modulates endocrine signaling of glucose and fat homeostasis by regulating transcription factors such as forkhead transcription factor 3a (FOXO3a), glucose transporter 4 (GLUT4), peroxisome proliferator-activated receptor gamma (PPARγ) and PPARγ coactivator (PGC-1α). However, it is still not clear how SIRT1 is involved in the development of insulin resistance. To determine the location and expression of SIRT1 and its target proteins in rats and analyze the interactions and functions of these proteins in insulin resistance. Forty-eight male Sprague-Dawley rats were randomly divided into four regimen groups: normal control (NC), calorie restriction (CR), high-fat (HFa), and high-fructose (HFr). Animals were fed for 12 weeks and blood samples collected from tail veins at weeks 2, 4, 6, 8 and 12 after fasting for 16 h. Baseline metabolic parameters such as fasting blood sugar, insulin, cholesterol and triglycerides were analyzed. A glucose tolerance test was carried out at the end of the study. Visceral fat, consisting of epididymis and perirenal fat, was isolated and weighed. The pancreas from each animal was also immediately removed. Immunohistochemical staining was performed to detect the locations of SIRT1, FOXO3a, GLUT4, PPARγ and PGC-1α in the ß-cell of the rat pancreas. Expression in the pancreas was analyzed by western blotting. Blood biochemical analysis indicated that the HFa and HFr groups were insulin-resistant. Immunohistochemical staining showed that GLUT4 was a nuclear protein. SIRT1, FOXO3a, PPARγ and PGC-1α were present in both the nucleus and the cytoplasm of ß-cells of pancreatic islets. The expression of SIRT1, GLUT4 and PGC-1α increased significantly in response to CR, but decreased in the HFr and HFa groups. FOXO3a was similar in the CR and the NC groups, whereas it declined in the HFa and HFr groups. PPARγ was elevated in the HFa group, but dropped in the CR and HFr groups. These data suggest that SIRT1 and its regulators are involved in the development of insulin resistance.