The hypoglycemic action of vitamin K1 could have an indirect effect by inhibiting early-onset diabetic nephropathy triggered by high blood glucose. Interleukin-10 levels were increased in renal tissues, suggesting the ability of vitamin K1 to trigger antiinflammatory state. Vitamin K1 inhibited renal inflammation by reducing nuclear factor-Î✫ and inducible nitric oxide synthase. Vitamin K1 also reduced oxidative stress and protected renal physiology by modulating Ca(2+) and Na(+)/K(+)-ATPases. Treatment of diabetic rats with vitamin K1 resulted in a decrease in blood glucose and prevented microalbuminuria. Urea, uric acid, creatinine, albumin and insulin levels were also estimated. At the end of the study, animals were sacrificed and kidney was dissected out and analysed for free radicals, antioxidants, aldose reductase, membrane ATPases, histopathology evaluation and expression of pro- and anti-inflammatory cytokines. Blood glucose was monitored once a month. Male Wistar rats were administered with 35 mg/kg STZ and after 3 days were treated with vitamin K1 (5 mg/kg, twice a week) for 3 months. ![]() The aim of this study was to determine whether the hypoglycemic action of vitamin K1 could inhibit early-onset diabetic nephropathy in a streptozotocin- induced rat kidney. Recently we demonstrated that vitamin K1 (5 mg/kg) protects against streptozotocin- induced type 1 diabetes and diabetic cataract. ![]() Vitamin K is increasingly being recognized for its antioxidant and antiinflammatory properties. Vitamin K is a potent regulator of vascular dynamics and prevents vascular calcification. Sai Varsha, M K N Raman, Thiagarajan Manikandan, R Dhanasekaran, G Hypoglycemic action of vitamin K1 protects against early-onset diabetic nephropathy in streptozotocin- induced rats.
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