Endocrine Abstracts

Diabetes mellitus, a chronic metabolic disorder, adversely affects organs such as the heart, liver, and kidneys over time. Malaria, caused by Plasmodium species transmitted by infected mosquitoes, is a life-threatening disease and has been reported to be more prevalent in diabetic individuals in Nigeria. This study investigated the biochemical and immune alterations in mice subjected to co-morbid diabetes and Plasmodium berghei NK65 infection. Fifty-four male BALB/c mice were divided into eight groups: Group 1 (Normal Control), Group 2 (Malaria only), Group 3 (Diabetes only), Group 4 (Diabetes + Malaria), Group 5 (Malaria + Artemether-Lumefantrine [AL]), Group 6 (Diabetes + Metformin [MTF]), Group 7 (Diabetes + Malaria + MTF), and Group 8 (Diabetes + Malaria + MTF + AL). Diabetes was induced using streptozotocin (40 mg/kg for five consecutive days), and malaria was established by inoculating mice with P. berghei. Treatments included metformin (200 mg/kg body weight) for diabetes and artemether-lumefantrine (1.14/6.86 mg/kg) for malaria. The results indicated a significant reduction in body weights of infected groups compared to treated groups. Fasting blood glucose and parasitemia levels were significantly elevated (P<0.05) in co-morbid mice (Group 4) compared to single-condition groups (Groups 2 and 3). Creatinine levels significantly decreased in treated groups compared to untreated controls, while no significant differences were observed in urea concentrations or median TNF-α levels across groups. However, interleukin-6 (IL-6) levels were significantly elevated (P=0.046) in co-morbid mice compared to the Normal Control. This study highlights the increased susceptibility of diabetic mice to P. berghei infection and reveals that metformin lacks prophylactic efficacy against malaria. These findings emphasize the need for targeted therapeutic strategies in managing diabetes-malaria co-morbidities.