Singh Manish Kumar, Dwivedi Shailendra, Yadav Suraj Singh, Yadav Rajesh Singh, Khattri Sanjay
Department of Biochemistry, Government Medical College Badaun, Badaun, UP 243601 India.
2Department of Biochemistry, All India Institute of Medical Sciences, Jodhpur, 342005 India.
Indian J Clin Biochem. 2020 Apr;35(2):179-187. doi: 10.1007/s12291-019-00820-5. Epub 2019 Mar 25.
Chronic exposure to arsenic through drinking water and occupational exposure has been found to be associated with the diabetic symptoms. Earlier, we reported that arsenic induced enhanced oxidative stress, inflammation, dislipidemia and hepatotoxicity in mice have been protected by treatment with (amla). The present study has therefore been focused to investigate the efficacy of amla in mitigation of arsenic induced hyperglycemia in mice. Arsenic exposure (3 mg/kg b.w./day for 30 days) in mice altered glucose homeostasis and significantly decreases hepatic glucose regulatory enzyme, glucokinase (43%), glucose-6 phosphate dehydrogenase (38%), malic enzyme (60%) and significantly increases the level of glucose-6 phosphates (65%), phosphoenolpyruvate carboxykinase (43%), lactate, (59%) Na (6.8%) Cl (10.4%), anion gap (13.9%) and pancreatic (IL-1β, TNF-α) inflammation markers (52%, 53%) as compared to controls. Arsenic exposure also significantly decreased serum insulin (44%) and c-peptide protein (38%) in mice as compared to controls. Co-administration of arsenic and amla (500 mg/kg b.w./day for 30 days) balanced blood sugar level, hepatic glucose regulatory enzyme (glucokinase, glucose-6 phosphate dehydrogenase, malic enzyme (68%, 37%, 45%) and significantly decreases glucose-6 phosphatase (25%), phosphoenolpyruvate carboxykinase (22%), blood ion concentration and also lactate, Na, Cl and anion gap (20%, 4.6%, 6.7%, 5.2%), pancreatic (IL-1β, TNF-α) inflammation marker (21%, 24%) and significantly increased the serum insulin (57%) and c-peptide protein (31%) as compared to those treated with arsenic alone. Results of the present study suggests that the hypoglycemic and antioxidant property of amla could be responsible for its protective efficacy in arsenic induced hyperglycemia.
已发现通过饮用水长期接触砷以及职业接触砷与糖尿病症状有关。早些时候，我们报道过砷诱导的小鼠氧化应激增强、炎症、血脂异常和肝毒性通过（印度醋栗）治疗得到了缓解。因此，本研究着重于探究印度醋栗对减轻小鼠砷诱导的高血糖症的功效。小鼠暴露于砷（3毫克/千克体重/天，持续30天）会改变葡萄糖稳态，并显著降低肝脏葡萄糖调节酶、葡萄糖激酶（降低43%）、葡萄糖-6-磷酸脱氢酶（降低38%）、苹果酸酶（降低60%），并显著提高葡萄糖-6-磷酸（提高65%）、磷酸烯醇式丙酮酸羧激酶（提高43%）、乳酸（提高59%）、钠（提高6.8%）、氯（提高10.4%）、阴离子间隙（提高13.9%）以及胰腺（白细胞介素-1β、肿瘤坏死因子-α）炎症标志物（分别提高52%、53%），与对照组相比有显著差异。与对照组相比，砷暴露还显著降低了小鼠血清胰岛素（降低44%）和C肽蛋白（降低38%）。砷与印度醋栗共同给药（500毫克/千克体重/天，持续30天）使血糖水平、肝脏葡萄糖调节酶（葡萄糖激酶、葡萄糖-6-磷酸脱氢酶、苹果酸酶（分别提高68%、37%、45%）达到平衡，并显著降低葡萄糖-6-磷酸酶（降低25%）、磷酸烯醇式丙酮酸羧激酶（降低22%）、血液离子浓度以及乳酸、钠、氯和阴离子间隙（分别降低20%、4.6%、6.7%、5.2%）、胰腺（白细胞介素-1β、肿瘤坏死因子-α）炎症标志物（分别降低21%、24%），与单独用砷处理的小鼠相比，血清胰岛素显著提高（提高57%）和C肽蛋白（提高31%）。本研究结果表明，印度醋栗的降血糖和抗氧化特性可能是其对砷诱导的高血糖症具有保护功效的原因。
