Shindea Urmila A, Sharma Geeta, Xu Yan J, Dhalla Naranjan S, Goyal Ramesh K
Department of Pharmacology, L.M. college of Pharmacy, P.O. Box 4011, Navrangpura, Ahmedabad 380 009, India.
J Trace Elem Med Biol. 2004;18(1):23-32. doi: 10.1016/j.jtemb.2004.03.002.
Although chromium is an essential element for carbohydrate and lipid metabolism, its effects in diabetic patients are still debated. We have studied the effect of 6 week treatment with chromium picolinate (8 microg/ml in drinking water) in streptozotocin (STZ)-induced type 1 and type 2 diabetic rat models. The mechanism of anti-diabetic action of chromium picolinate was studied using C2C12 myoblasts and 3T3-L1 adipocytes. Chromium picolinate significantly decreased the area under the curve over 120 min for glucose of both STZ-induced type 1 (40mg/kg, i.v. in adult rats) and type 2 (90 mg/kg, i.p. in 2 day old rat neonates) diabetic rats without any significant change in area under the curve over 120 min for insulin as compared to controls. The composite insulin sensitivity index and insulin sensitivity index (KITT) values of both type 1 and type 2 diabetic rats were increased significantly by chromium picolinate. Treatment with chromium picolinate produced a significant decrease in elevated cholesterol and triglyceride levels in both types of diabetic rats. In 3T3-L1 adipocytes, chromium picolinate (0-10 micromol) per se did not produce any effect, however, when co-incubated with insulin it significantly increased the intracellular triglyceride synthesis (EC50 = 363.7nmol/1). Similarly in C2C12 myoblasts, chromium picolinate alone did not produce any effect, however, it significantly increased insulin-induced transport of 14C-glucose. In conclusion, chromium picolinate significantly improves deranged carbohydrate and lipid metabolism of experimental chemically induced diabetes in rats. The mechanism of in vivo anti-diabetic action appears to be peripheral (skeletal muscle and adipose tissue) insulin enhancing action of chromium.
尽管铬是碳水化合物和脂质代谢的必需元素,但其对糖尿病患者的影响仍存在争议。我们研究了用吡啶甲酸铬(饮用水中浓度为8微克/毫升)对链脲佐菌素(STZ)诱导的1型和2型糖尿病大鼠模型进行6周治疗的效果。使用C2C12成肌细胞和3T3-L1脂肪细胞研究了吡啶甲酸铬的抗糖尿病作用机制。吡啶甲酸铬显著降低了STZ诱导的1型(成年大鼠静脉注射40毫克/千克)和2型(2日龄大鼠新生仔腹腔注射90毫克/千克)糖尿病大鼠120分钟内葡萄糖曲线下面积,与对照组相比,胰岛素120分钟内曲线下面积无显著变化。吡啶甲酸铬显著提高了1型和2型糖尿病大鼠的综合胰岛素敏感性指数和胰岛素敏感性指数(KITT)值。吡啶甲酸铬治疗使两种糖尿病大鼠升高的胆固醇和甘油三酯水平显著降低。在3T3-L1脂肪细胞中,吡啶甲酸铬(0 - 10微摩尔)本身没有任何作用,然而,当与胰岛素共同孵育时,它显著增加了细胞内甘油三酯的合成(半数有效浓度=363.7纳摩尔/升)。同样,在C2C12成肌细胞中,单独的吡啶甲酸铬没有任何作用,然而,它显著增加了胰岛素诱导的14C-葡萄糖转运。总之,吡啶甲酸铬显著改善了实验性化学诱导糖尿病大鼠紊乱的碳水化合物和脂质代谢。体内抗糖尿病作用机制似乎是铬对周围组织(骨骼肌和脂肪组织)的胰岛素增强作用。