Effects of Bee Bread Extract on Fasting Glycaemia and Irs-1 Gene Expression in a Streptozotocin-Nicotinamide Model of Diabetes in Male Rats
M. Bello *
Department of Chemical Pathology, School of Medical Laboratory Sciences, Usmanu Danfodiyo University, Sokoto, Nigeria.
U. Wali
Department of Chemical Pathology, School of Medical Laboratory Sciences, Usmanu Danfodiyo University, Sokoto, Nigeria.
Z. U. Umar
Department of Physiology, College of Health Sciences, Usmanu Danfodiyo University, Sokoto, Nigeria.
A. S. Mainasara
Department of Chemical Pathology and Immunology, College of Health Sciences, Usmanu Danfodiyo University, Sokoto, Nigeria.
*Author to whom correspondence should be addressed.
Abstract
Background and Objective: Bee bread contains nutrients and phytochemicals that may influence metabolic homeostasis, but its effects on insulin-signalling-related outcomes in experimental diabetes remain incompletely characterised. This study evaluated the effects of ethanolic bee bread extract on fasting blood glucose (FBG), serum insulin, glucagon, an assay-derived serum GLUT4 concentration, pancreatic histology, and skeletal-muscle insulin receptor substrate-1 (IRS-1) gene expression in a streptozotocin-nicotinamide model of diabetes in male rats.
Methods: Twenty-seven rats were included in the efficacy experiment and allocated to six groups: non-diabetic control (n = 5), untreated diabetic control (n = 4), metformin 100 mg/kg (n = 4), and bee bread extract at 150 mg/kg (n = 5), 300 mg/kg (n = 4), or 600 mg/kg (n = 5). Treatments were administered orally once daily for 3 weeks. A separate eight-animal acute oral toxicity observation preceded the efficacy experiment. IRS-1 expression was assessed by RT-qPCR and expressed relative to GAPDH using the 2^-DeltaDeltaCt method.
Results: Mean FBG increased from 10.13 +/- 0.31 to 18.84 +/- 0.68 mmol/L in untreated diabetic rats, whereas final FBG was 5.71 +/- 0.47 mmol/L with metformin and 5.78 +/- 0.43, 5.20 +/- 0.50, and 4.84 +/- 0.31 mmol/L with 150, 300, and 600 mg/kg bee bread, respectively. Serum insulin remained similar among groups. Glucagon was higher in untreated diabetic rats (67.49 +/- 1.72 ng/mL) than in the non-diabetic group (29.71 +/- 1.41 ng/mL) and was lower in all bee-bread groups (39.73 +/- 0.63 to 33.94 +/- 1.50 ng/mL). The serum GLUT4 assay concentration was lowest in untreated diabetic rats (0.49 +/- 0.08 ng/L) and higher after bee bread treatment (1.70 +/- 0.11 to 3.04 +/- 0.04 ng/L). Relative IRS-1 expression was 0.50 in untreated diabetic rats and 1.10, 1.18, and 1.31 in the 150, 300, and 600 mg/kg groups, respectively. Pancreatic histology showed no major qualitative architectural differences across groups.
Conclusion: Bee bread administration was associated with lower fasting glycaemia and glucagon, higher assay-derived GLUT4 concentrations, and higher skeletal-muscle IRS-1 expression in this experimental model. These findings support an association with altered insulin-signalling-related outcomes but do not establish IRS-1 upregulation as the causal mediator of the glycaemic response.
Keywords: Bee bread, diabetes mellitus, fasting blood glucose, glucagon, GLUT4, IRS-1, RT-qPCR