Effect of camel milk protein hydrolysates against hyperglycemia, hyperlipidemia, and associated oxidative stress in streptozotocin (STZ)-induced diabetic rats

• Published in: Journal of dairy science Vol. 104; no. 2; pp. 1304 - 1317
• Main Authors: Kilari, Bhanu Priya, Mudgil, Priti, Azimullah, Sheikh, Bansal, Nidhi, Ojha, Shreesh, Maqsood, Sajid
• Format: Journal Article
• Language: English
• Published: United States Elsevier Inc 01.02.2021
• Subjects: Animals; Antioxidants - therapeutic use; Blood Glucose - analysis; camel milk; Camelus - metabolism; diabetes mellitus; Diabetes Mellitus, Experimental - blood; Diabetes Mellitus, Experimental - drug therapy; Diabetes Mellitus, Experimental - pathology; hypoglycemia; Hypoglycemic Agents - therapeutic use; Hypolipidemic Agents - therapeutic use; Insulin-Secreting Cells - pathology; Lipid Peroxidation - drug effects; Liver - chemistry; Liver - pathology; Male; Malondialdehyde - metabolism; Milk - metabolism; Milk Proteins - therapeutic use; Oxidative Stress - drug effects; protein hydrolysates; Protein Hydrolysates - therapeutic use; Rats; streptozotocin; protein hydrolysates; diabetes mellitus; streptozotocin; camel milk; hypoglycemia
• ISSN: 0022-0302; 1525-3198
• DOI: 10.3168/jds.2020-19412

This study investigated the effect of camel milk protein hydrolysates (CMPH) at 100, 500 and 1,000 mg/kg of body weight (BW) for 8 wk on hyperglycemia, hyperlipidemia, and associated oxidative stress in streptozotocin-induced diabetic rats. Body weights and fasting blood glucose levels were observed after every week until 8 wk, and oral glucose tolerance test (OGTT) levels and biochemical parameters were evaluated after 8 wk in blood and serum samples. Antioxidant enzyme activity and lipid peroxidation in the liver were estimated, and histological examination of the liver and pancreatic tissues was also conducted. Results showed that CMPH at 500 mg/kg of BW [camel milk protein hydrolysate, mid-level dosage (CMPH-M)] exhibited potent hypoglycemic activity, as shown in the reduction in fasting blood glucose and OGTT levels. The hypolipidemic effect of CMPH was indicated by normalization of serum lipid levels. Significant improvement in activity of superoxide dismutase and catalase, and reduced glutathione levels were observed, along with the attenuation of malondialdehyde content in groups fed CMPH, especially CMPH-M, was observed. Decreased levels of liver function enzymes (aspartate aminotransferase and alanine aminotransferase) in the CMPH-M group was also noted. Histology of liver and pancreatic tissue displayed absence of lipid accumulation in hepatocytes and preservation of β-cells in the CMPH-M group compared with the diabetic control group. This is the first study to report anti-hyperglycemic and anti-hyperlipidemic effect of CMPH in an animal model system. This study indicates that CMPH can be suggested for its therapeutic benefits for hyperglycemia and hyperlipidemia, thus validating its use for better management of diabetes and associated comorbidities.