Project Materials

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

CHAPTER ONE

INTRODUCTION

The Background of the Study 

Respiratory Complex Two (RCII), often referred to as succinate dehydrogenase, is a crucial part of the electron transport chain (ETC) in the mitochondria that produces cellular energy via oxidative phosphorylation. It is essential for the electron transfer from succinate to coenzyme Q, which promotes ATP synthesis and preserves cellular redox equilibrium. Numerous metabolic conditions, including as cancer, neurological diseases, and mitochondrial diseases, have been linked to RCII dysfunction.

An essential organ, the liver is engaged in many metabolic functions, such as energy metabolism, detoxification, and biomolecule production. Through oxidative phosphorylation, the liver’s mitochondria provide the energy required for these processes.

Additionally, the liver is extremely vulnerable to dietary deficits, such as insufficient protein consumption, which can result in malnutrition or protein undernutrition. Undernutrition in protein is linked to mitochondrial dysfunction, altered metabolism, and compromised liver function.

In many tropical places, coconut oil is a common dietary fat that has drawn interest due to its possible health advantages. It contains a lot of medium-chain fatty acids (MCFAs), especially lauric acid, which has been demonstrated to have antioxidant, antibacterial, and anti-inflammatory qualities.

Coconut oil has also been shown to enhance energy metabolism, insulin sensitivity, and lipid profiles. However, little is known about how coconut oil affects protein under nutrient-deficient settings and mitochondrial function, particularly RCII activity, in the liver under normal circumstances.

It is crucial to comprehend how coconut oil affects RCII activity in the liver since this information may help determine how coconut oil might be used therapeutically in the setting of protein undernutrition and mitochondrial dysfunction. Furthermore, it might provide insight into the processes behind the metabolic advantages linked to coconut oil ingestion.

The impact of dietary changes on liver mitochondrial function has been examined in earlier research. However, little research has been done on the precise effects of coconut oil on RCII function, especially when protein undernutrition is present.

By assessing the activities of RCII in the livers of rats given coconut oil who are normal and those who are protein undernourished, this study seeks to close this information gap.

Supplementing with coconut oil is thought to increase RCII activity in the liver, which could lessen the detrimental effects of protein undernutrition on mitochondrial function.

This theory is supported by earlier research showing the possible advantages of coconut oil on lipid profiles, antioxidant status, and energy metabolism.

Male Wistar rats will be used as an animal model to test this theory. The rats will be split into four groups: protein undernourished, normal control, coconut oil control, and protein undernourished.

Either coconut oil or an isocaloric quantity of maize oil will be added to the rats’ regular laboratory diet. Groups that are undernourished in protein will be fed a diet low in protein.

Following the intervention period, spectrophotometric evaluation of RCII activity will be performed on liver tissue samples.

In tropical nations with high coconut oil output, coconut oil is widely used. Hair care, skin care, stress reduction, cholesterol maintenance, weight loss, immune system stimulation, healthy digestion, and controlled metabolism are among the health advantages of coconut oil (Kabara, 1978).

Along with helping to strengthen bones and improve dental quality, it also relieves kidney issues, heart disease, high blood pressure, diabetes, HIV, and cancer. The inclusion of lauric acid, capric acid, and other compounds in oil is responsible for these advantages.