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Association between ACE gene I/D polymorphism and the risk of overweight/obesity remains controversial. We investigated the possible relationship between ACE gene I/D polymorphism and obesity in Chinese type 2 diabetes mellitus (T2DM) patients. In this study, obesity was defined as a body mass index (BMI) value ≥ 25 kg/m 2 and subjects were classified into 4 groups (lean, normal, overweight, and obese). PCR (polymerase chain reaction) was used to detect the ACE gene I/D polymorphism in T2DM patients. Metabolic measurements including blood glucose, lipid profile, and blood pressure were obtained. Frequencies of the ACE genotypes (DD, ID, and II) were not significant among the 4 groups of BMI-defined patients ( P = 0.679) while ACE II carriers showed higher systolic blood pressure (SBP) and pulse pressure (PP) (all P < 0.050). Hyperglycemia, hypertension, and dyslipidemia in these T2DM patients were found to be significantly associated with BMI. In conclusion, the relationship of ACE gene I/D polymorphism with obesity is insignificant in Chinese patients with T2DM. SBP and PP might be higher in the ACE II carriers than in the DD and ID carriers., Competing Interests: The authors declare that no competing interests exist.

Objective . The aim of this study was to investigate the changes of regulatory T cells (Treg), interleukin-6 (IL-6), IL-10, transforming growth factor- β (TGF- β ), and tumor necrosis factor-alpha (TNF- α ) in patients with type 2 diabetes mellitus (T2DM). Methods . We performed a comprehensive search up to July 2016 for all clinical studies about the changes of Treg, IL-6, IL-10, IL-17, TGF- β , and TNF- α in T2DM patients versus healthy controls. Results . A total of 91 articles (5642 cases and 7378 controls) were included for this meta-analysis. Compared with the controls (all p < 0.001), the patients had increased serum levels of IL-6, TGF- β , and TNF- α but decreased the percentage of peripheral CD4 + CD25 + Foxp3 + Treg and serum IL-10 level. Furthermore, the percentage of peripheral CD4 + CD25 + Foxp3 + Treg ( p < 0.001) and serum IL-10 level ( p = 0.033) were significantly lower in the patients with complication and in the patients without complication, respectively. No significant changes about the percentage of CD4 + CD25 + Treg ( p = 0.360) and serum IL-17 level ( p = 0.459) were found in T2DM patients. Conclusions . T2DM patients have decreased the percentage of peripheral CD4 + CD25 + Foxp3 + Treg and levels of serum IL-10 but elevated serum levels of IL-6, TGF- β , and TNF- α . Presence of diabetic complications further lowers the peripheral CD4 + CD25 + Foxp3 + Treg number.

Purpose: The objective of this study is to investigate the effect of dual blockage of renin-angiotensin system (RAS) on renal kallikrein expression and inflammatory response in diabetic nephropathy (DN)., Methods: Rats were randomly divided into 5 groups with 10 rats in each group: normal control; DN model induced by high fat and high sucrose diets; and DN treated with either benazepril 10 mg/kg/d, irbesartan 30 mg/kg/d, or both. After 8-week treatment, we examined changes in the kidney histopathology, function and immunohistochemical stain of kallikrein, macrophage marker CD68, and profibrotic markers transforming growth factor- (TGF-) β and α-smooth muscle action (SMA)., Results: DN rats showed enlarged kidneys with glomerulosclerosis, interstitial chronic inflammation and fibrosis, and proteinuria. All the pathological damage and functional impairments were improved after the RAS blockades (all P < 0.05). Compared with monotherapy, combined treatment further alleviated the kidney impairments in parallel to increased tubular immunoreactivity for kallikrein and decreased immunopositive cells for CD68, TGF-β, and α-SMA., Conclusion: The renoprotective effects of the dual RAS blockade in diabetic nephropathy may be attributed to improved tubular kallikrein expression and interstitial inflammatory response.