Progesterone levels associated with proteinuria in male diabetes mellitus patients: A cross-sectional retrospective study.

INTRODUCTION: The relationship between progesterone (P) and diabetic nephropathy (DKD) is unclear. Herein, we investigated the relationship between progesterone and DKD in men and postmenopausal women with type 2 diabetes mellitus. MATERIALS AND METHODS: We recruited 3,556 male and postmenopausal female patients and obtained the dominance ratio (OR) and corresponding 95% confidence intervals (CIs) associated with progesterone by logistic regression analysis after adjusting for potentially confounding variants. RESULTS: We found that progesterone levels were significantly lower in the massive proteinuria and microproteinuria groups compared with the non-DKD group for male patients. Also, microproteinuria and massive proteinuria prevalence were higher in the first (lowest) progesterone quartile than in the second to fourth quartiles. After adjusting for confounders, compared with the first (lowest) progesterone quartile group, the OR for the second to fourth quartiles in the male microproteinuria subgroup, were: Q2: 0.846 (95% CI: 0.581-1.233, P = 0.385); Q3: 0.667 (95% CI: 0.45-0988, P = 0.044); Q4: 0.597 (95% CI: 0.393-0.907, P = 0.016). In the male massive proteinuria subgroup, the OR for the third quartile group was 0.418 (95% CI: 0.201-0.867, P = 0.019). In contrast, no significant association was detected between progesterone and DKD prevalence in the female group. CONCLUSIONS: Progesterone levels were negatively associated with DKD incidence in hospitalized male patients with type 2 diabetes mellitus.

Effect of Aspirin on the Expression of Hepatocyte NF-kappaB and Serum TNF-alpha in Streptozotocin-Induced Type 2 Diabetic Rats

Aspirin is a kind of anti-inflammatory drug and may be used to reverse hyperglycemia, hyperinsulinemia, and dyslipidemia by improving insulin resistance. We hypothesized that aspirin improves insulin resistance in type 2 diabetes by inhibiting hepatic nuclear factor kappa-beta (NF-kappaB) activation and serum tumor necrosis factor-alpha (TNF-alpha). Adult male Wistar rats were randomly divided into four groups: control, untreated diabetic, diabetic treated with metformin (100 mg/kg/day), and diabetic treated with aspirin (120 mg/kg/day). Diabetes was induced by high-fat feeding and a low dose of streptozotocin (30 mg/kg). After treatment, plasma glucose, insulin, lipids, free fatty acids (FFAs) concentrations and serum TNF-alpha were determined. The expression of NF-kappaB in hepatocytes was analyzed by immunohistochemistry and western blot. The results showed administration of aspirin caused no significant lowering in fasting glucose level but significant reduction of hepatic NF-kappaB expression and serum TNF-alpha level with improved insulin resistance compared to the diabetic group. The relevant analysis showed positive correlation between the expression of homeostasis model assessment-insulin resistance (HOMA-IR) and NF-kappaB (r = 0.799, P < 0.01); HOMA-IR and serum TNF-alpha (r = 0.790, P < 0.01). It is concluded that aspirin improves insulin resistance by inhibiting hepatic NF-kappaB activation and TNF-alpha level in streptozotocin-induced type 2 diabetic rats.