Neurotrophic and metabolic consequences of virgin coconut oil and ethanol: implications for growth and antioxidant defense

Document Type

Article

Department

Biological and Biomedical Sciences

Abstract

The hypothalamus serves as a central regulator of metabolism, integrating signals pertinent to food intake and energy balance. Brain-Derived Neurotrophic Factor (BDNF) is widely distributed in brain, including expression in hypothalamic nuclei, which regulates feeding behavior. Chronic ethanol (EtOH) consumption has adverse effects on metabolic function, affecting the hypothalamus and striatum, a reward-associated region. Virgin coconut oil (VCO), a dietary lipid rich in medium-chain triglycerides, which have been shown to modulate BDNF expression. Based on these findings, we hypothesized that chronic EtOH consumption would impair metabolic regulation and causes oxidative stress, while VCO would counteract these effects. To test this, water drinking control and EtOH drinking Wistar male rats received water as vehicle or VCO by gavage (12 days). Growth, diet and fluid consumption were recorded throughout the experiment. Hypothalamic BDNF, striatal oxidative stress, and serum metabolic markers following EtOH and VCO exposure were examined. Statistical analysis utilized t-test, two-way ANOVA and Kruskal-Wallis test. Findings revealed that VCO reduced hypothalamic BDNF, decreased food and food caloric intake, and led to weight loss in EtOH exposed rats. Metabolic effects were further modulated by alterations in serum glucose, cholesterol, and triglycerides, where EtOH lowered glucose and cholesterol due to reduced caloric intake, while VCO increased all three markers. Additionally, VCO restored oxidative stress markers in the striatum, potentially mitigating EtOH- induced neurotoxicity by normalizing catalase and peroxide levels. This study highlights the complex interaction between EtOH and VCO in metabolic regulation, oxidative stress, and neuroendocrine function, warranting further research to explore its potential therapeutic implications

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Pagination is not provided by author/publisher

Publication (Name of Journal)

Molecular biology reports

DOI

10.1007/s11033-026-11846-3

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