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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-ГЋвњ« 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.

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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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