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EFFECT OF CAMEL MILK ON THE ACTIVITIES OF ATPASES IN NORMAL AND STREPTOZOTOCIN-DIABETIC RATS
 
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Publication date: 2010-12-31
 
 
Pol. J. Food Nutr. Sci. 2010;60(4):375-380
 
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ABSTRACT
Diabetes mellitus is the world’s largest endocrine disorder resulting in multiple aetiologies, involving metabolic disorders of carbohydrate, fat and protein. All forms of diabetes are due to a decrease in the circulating concentration of insulin (insulin deficiency) and a decrease in the response of peripheral tissues to insulin i.e., insulin resistance. According to the World Health Organization projections, the prevalence of diabetes is likely to increase by 35% by the year 2025. In this study, the streptozotocin (STZ)-induced diabetic rats, the activities of membrane-bound adenosine triphosphatases (ATPases) are altered in erythrocytes and in tissues such as liver and kidney. Albino Wistar rats were rendered diabetic by a single intraperitoneal injection of STZ (40 mg/kg body weight). Diabetic rats exhibited significantly (p<0.05) increased levels of plasma glucose and decreased levels of plasma insulin. The activities of total ATPases, (Na++K+)-ATPase, Ca2+-ATPase and Mg2+-ATPase were significantly (p<0.05) decreased in diabetic control rats. Control and diabetic rats were treated with camel milk (250 mL/day) for a period of 45 days. A group of diabetic rats were also treated with glibenclamide (600 µg/kg body weight). After the treatment period, a significant (p<0.05) decrease in the levels of glucose and increase in the levels of plasma insulin and the activities of ATPases in erythrocytes and tissues were observed in diabetic rats treated with camel milk. A similar effect is also observed in the glibenclamide treated rats. But, control rats treated with camel milk did not show any significant (p<0.05) effect in any of the parameters studied. Our study shows that camel milk has the potential to restore the deranged activities of membrane-bound ATPases in STZ-diabetic rats. Further detailed investigation is necessary to find out its mechanism of action.
eISSN:2083-6007
ISSN:1230-0322
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