Abstract
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 Emblica officinalis (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.