Impacts of Dietary Chrysophyllum albidum Fruit Pulp on Brain Cholinesterase Function in High-Fat Diet/Streptozotocin-Induced Diabetic Rats

Seun Funmilola Akomolafe, Sunday Idowu Oyeleye, Ifeoluwa Adebayo Odeniyi, Iyabo Folake Oladapo, Ayodele Jacob Akinyemi, Folake Lucy Oyetayo, Olubunmi Bolanle Ajayi


Epidemiologic studies have shown strong correlations between Alzheimer’s disease and diabetes mellitus. The exact mechanism through which this happens remains unclear. However, the dependence on glucose for brain function has been proposed as one possible mechanism. Hence, this study investigated the neuroprotective potential of Chrysophyllum albidum fruit pulp (CAPP) with hypoglycaemic properties in diabetic rats induced with high-fat diet/streptozotocin (STZ). The animals were grouped into seven units as follows: control, STZ-induced, STZ + metformin (positive control), STZ + 5% CAPP, STZ + 10% CAPP, control + 5% CAPP and control + 10% CAPP and each group was made up of six rats. The animals were first placed on normal diet (non-diabetic groups) and high fat diet (diabetic groups) for a fortnight, respectively before induction with STZ and were treated with diets containing 5 and 10% CAPP for 14 days. After the experiment, the rat brain cholinesterase and antioxidant activities were determined. The results revealed that acetylcholinesterase (AChE), butylcholinesterase (BuChE), arginase, adenosine deaminase (ADA) and antioxidant activities were altered in STZ-diabetic group in comparison to the control. However, a significant decrease at p < 0.05 was found in the activities of AChE, BuChE, arginase and ADA. In addition, there was a concomitant rise in the levels of antioxidant in all the groups administered supplemented diets and the group treated with metformin in comparison to the STZ-diabetic group. Conclusively, we can suggest that the fruit pulp prevents neurological damage in diabetic rats via anticholinesterase activity and improvement of brain antioxidant status.

Keywords: Chrysophyllum albidum; Diabetes; Metformin; Cognitive function; Neuromodulation.

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