Abstract

Objective: This study aimed to evaluate the antidiabetic and antidepressant effects of banana peel flakes in streptozotocin-induced diabetic rats.
 Methods: Twenty-five male Wistar rats were classified into five groups with different treatments. Groups I to IV were diabetic rats model groups that consumed only standard diet, standard diet containing 5%, 10%, and 20% of banana peel flakes, respectively. While group V was a healthy control group fed a standard diet. Immunohistochemistry staining was measured to examine serotonin expression in the colon and pancreas.
 Results: The diabetic rats treated with 20% banana peel flakes had a lower blood glucose concentration (p<0.05) compared with diabetic control and showed a shorter duration of immobility time (p<0.05) than the healthy control. Additionally, compared with diabetic control, the diabetic rats treated with 5% banana peel flakes showed higher serotonin expression (p<0.05) in the colon. In contrast, serotonin expression in the pancreas did not show any significant difference (p>0.05).
 Conclusion: The present study disclosed that the banana peel flakes provided an antidepressant effect in the diabetic rats model, which might occur through the mechanism of controlling blood glucose concentration.

Highlights

  • Patients with diabetes have a higher risk of depressive disorders compared with those who suffer from other diseases [1, 2], depressed individuals are more vulnerable to metabolic disorders such as diabetes [3]

  • The body weight of the diabetic control group was significantly reduced compared to banana peel flakes-treated diabetic rats (p

  • We demonstrated that the consumption of banana peel flakes for three weeks period was associated with blood glucose concentration and immobility time scores in rats

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Summary

Introduction

Patients with diabetes have a higher risk of depressive disorders compared with those who suffer from other diseases [1, 2], depressed individuals are more vulnerable to metabolic disorders such as diabetes [3]. Around 90% of tryptophan is available [8], and about 3% of tryptophan catabolism becomes serotonin, while the rest will be degraded by intestinal microflora producing indoles and its derivatives [9, 10]. This process implies strong competition in using tryptophan between the serotonin and kynurenine synthesis. In inflammatory conditions such as diabetes, tryptophan catabolism for kynurenine will be greater than for serotonin synthesis [11]. The presence of tryptophan, which only comes from the diet, will determine the brain’s ability to synthesize serotonin [12]

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