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ACTIVITIES OF RESPIRATORY COMPLEX TWO ON THE LIVER OF NORMAL AND PROTEIN UNDERNOURISHED RAT FED WITH COCONUT OIL

CHAPTER ONE

INTRODUCTION

BACKGROUND OF THE STUDY

Respiratory Complex Two (RCII), also known as succinate dehydrogenase, is an essential component of the mitochondrial electron transport chain (ETC) responsible for cellular energy production through oxidative phosphorylation. It plays a critical role in the transfer of electrons from succinate to coenzyme Q, facilitating the generation of ATP and maintaining cellular redox balance. RCII dysfunction has been implicated in various metabolic disorders, including mitochondrial diseases, neurodegenerative diseases, and cancer.

The liver is a vital organ involved in numerous metabolic processes, including energy metabolism, detoxification, and synthesis of biomolecules. Mitochondria in the liver play a crucial role in these functions by providing the necessary energy through oxidative phosphorylation. The liver is also highly sensitive to nutritional deficiencies, including inadequate protein intake, which can lead to protein undernutrition or malnutrition. Protein undernutrition is associated with impaired liver function, altered metabolism, and mitochondrial dysfunction.

Coconut oil is a widely consumed dietary fat in many tropical regions and has gained attention for its potential health benefits. It is rich in medium-chain fatty acids (MCFAs), primarily lauric acid, which has been shown to possess antimicrobial, anti-inflammatory, and antioxidant properties. Additionally, coconut oil has been reported to improve lipid profiles, insulin sensitivity, and energy metabolism. However, the effects of coconut oil on mitochondrial function, specifically the activity of RCII, in the liver under normal and protein undernutrition conditions remain largely unexplored.

Understanding the impact of coconut oil on RCII activity in the liver is essential, as it may provide insights into the potential therapeutic applications of coconut oil in the context of mitochondrial dysfunction and protein undernutrition. Moreover, it could shed light on the mechanisms underlying the observed metabolic benefits associated with coconut oil consumption.

Previous studies have investigated the effects of dietary interventions on mitochondrial function in the liver. However, the specific effects of coconut oil on RCII activity, particularly in the context of protein undernutrition, have not been extensively explored. This study aims to bridge this knowledge gap by evaluating the activities of RCII in the liver of normal and protein undernourished rats fed with coconut oil.

The hypothesis is that coconut oil supplementation may enhance RCII activity in the liver, potentially mitigating the negative effects of protein undernutrition on mitochondrial function. This hypothesis is based on previous studies demonstrating the potential benefits of coconut oil on energy metabolism, lipid profiles, and antioxidant status.

To test this hypothesis, male Wistar rats will be utilized as an animal model. The rats will be divided into four groups: normal control, coconut oil control, protein undernourished, and protein undernourished with coconut oil. The rats will be fed standard laboratory chow supplemented with either coconut oil or an isocaloric amount of corn oil. Protein undernourished groups will receive a low-protein diet. After the intervention period, liver tissue samples will be collected, and RCII activity will be assessed spectrophotometrically.

Coconut oil is used extensively in tropical countries which have a good production of coconut oil. The health benefits of coconut oil include haircare, skin care, stress relief, cholesterol levelmaintenance, weight loss, boosted immunesystem, proper digestion and regulatedmetabolism (Kabara, 1978). It also provides relief from kidneyproblems, heart diseases, high blood pressure,diabetes, HIV, and cancer, while helping toimprove dental quality and bone strength. Thesebenefits of oil can be attributed to the presenceof lauric acid, capric acid and