ABSTRACT
Alcohol has many biological actions, and adverse effects on lipid metabolism. The main objective of this present study was designed to study the effects of alcohol administration on serum lipid profile, total protein, liver enzymes and histopathological effect in rats. A total twenty five male wistar rats (190-200g) were divided into five groups of five animals each. The animals were grouped so that the mean difference in the various groups would not vary significantly. Group one served as the control whereas groups two, three, four and five were made up of ethanol treated rats. The ethanol was administered intraperitoneally (I.P) and the treatment was carried out for three months and analysis of the parameters done on a four week basis. After .the last dose of every four weeks, blood was collected, centrifuged to form the serum. Ethanol administration on rats produced a marked and significant (p<0 .05="" a="" activities.="" activities="" administration.="" administration="" alanine="" alkaline="" aminotransferase="" an="" and="" aspartate="" by="" caused="" cholesterol="" compared="" control.="" decline.="" density="" enhanced="" enzymes="" ethanol="" first="" four="" furthermore="" high="" in="" increase="" increased="" increasing="" indicated="" initial="" it="" levels="" lipid="" lipoprotein="" liver="" low="" made="" normal.="" of="" p="" phosphatase="" profile="" protein="" serum="" significant="" significantly="" span="" the="" their="" to="" total="" treatment="" triacylglycerol.="" weeks="" when="" with="">
Alcoholism is a progressive disease. Liver disease is the most common complication from ethanol abuse. Alcoholic fatty liver may progress to alcoholic hepatitis and finally to cirrhosis and liver failure.
TABLE OF CONTENTS
Title Page
Abstract
Table of Contents
List of Figures
List of Tables
List of Abbreviations
List of Plates
CHAPTER ONE: INTRODUCTION
1.1 Alcohols
1.2 Lipids
1.2.2 Plasma Lipids
1.3 Liver’s central role in lipid transport
1.4 Effects of alcohol on the liver
1.5 Cholesterol
1.5.1 Biosynthesis of cholesterol
1.5.2 Functions of cholesterol
1.6 High density lipoprotein cholesterol (HDL-C)
1.6.1 Structure and functions of high density lipoproteins cholesterol
1.6.2 Medications that raise high density lipoproteins cholesterol
1.6.3 Diet and lifestyle
1.7 Low density lipoprotein cholesterol (LDL-C)
1.7.1 Biochemistry of low density lipoprotein
1.7.2 LDL subtype patterns
1.7.3 Transport into the cell
1.7.4 Lowering LDL
1.8 Triacylglycerol
1.8.1 Metabolism
1.8.1 Role in disease
1.9 Total protein
1.10 Liver Enzymes
1.10.1 Aspartate and alanine amino transferase
1.10.2 Alkaline phosphatase
1.11 Justification of the study
1.12 Objectives of the study
1.12.1 Specific objectives of the study
CHAPTER TWO: MATERIALS AND METHODS
2.1 Materials
2.1.1 Animals
2.1.2 Chemicals
2.1.3 Equipment/ Instrument
2.1.4 Preparation of reagents
2.2 Methods
2.2.1 Experimental design
2.2.2 Collection of samples
2.2.3 Preparation of samples
2.2.4 Assays
2.2.4.1 Determination of lipid profile
2.2.4.1.1 Determination of total cholesterol level
2.2.4.1.2 Determination of high density lipoprotein-cholesterol level
2.2.4.1.3 Determination of low density lipoprotein-cholesterol level
2.2.4.1.4 Determination of triacylglycerol (TAG) level
2.2.4.2 Determination of serum total protein level
2.2.4.3 Determination of liver enzymes
2.2.4.3.1 Determination of alanine aminotransferase activity
2.2.4.3.2 Determination of aspartate aminotransferase activity
2.2.4.3.3 Determination of alkaline phosphatase activity
2.3 Statistical analysis
CHAPTER THREE: RESULTS
3.1 Effect of varying ethanol concentration on the total cholesterol levels of albino Wistar rats
3.2 Effect of varying ethanol concentration on the high density lipoprotein cholesterol levels of albino Wistar rats
3.3 Effect of varying ethanol concentration on the low density lipoprotein cholesterol levels of albino Wistar rats
3.4 Effect of varying ethanol concentration on the triacylglycerol levels of albino Wistar rats
3.5 Effect of varying ethanol concentration on the total protein levels of albino Wistar rats
3.6 Effect of varying ethanol concentration on the alanine aminotransferase activity of albino Wistar rat
3.7 Effect of varying ethanol concentration on the aspartate aminotransferase activity of albino Wistar rats
3.8 Effect of varying ethanol concentration on the alkaline phosphatase activity of albino Wistar rats
CHAPTER FOUR: DISCUSSION
4.1 Discussion
4.2 Conclusion
4.3 Suggestions for further studies
REFERENCES
APPENDICES
CHAPTER ONE
INTRODUCTION
Alcoholism leads to fat accumulation in the liver, hyperlipidemia, and ultimately cirrhosis (Murray et al., 2006). The fatty liver is caused by a combination of impaired fatty acid oxidation and increased lipogenesis, which is thought to be due to changes in the [NADH]/ [NAD+] redox balance in the liver. Lipid homeostasis is altered by chronic ethanol consumption leading to the development of a fatty liver as well as lipid alterations in other organs (Carrasco et al., 2002). Liver disease is the most common complication from ethanol abuse (Mello et al., 2007). It is estimated that 15 to 30% of chronic heavy drinkers eventually develop severe liver diseases. Alcoholic fatty liver may progress to alcoholic hepatitis and finally to cirrhosis and liver failure (Reuben, 2008). In the USA, chronic alcohol abuse is the leading cause of liver cirrhosis and the need for liver transplantation (Masters, 2001). On the other hand, it has been shown that alcohol consumption may protect against severe coronary atherosclerosis, but the mechanism through which alcohol might exert its protective effect remains unclear (Dai and Miller, 1997). High-density lipoprotein-cholesterol (HDL-C) like other lipids shows a dose-dependent relationship to alcohol intake. Because HDL-C is thought to play an important role in preventing atherosclerosis (Seppa et al., 1992), it has been proposed that alcohol protection occurs via increasing HDL-C. Sillanaukee et al., (2000) showed that all lipid values, except low density lipoprotein cholesterol (LDL-C), positively correlated with reported alcohol consumption.
1.1. Alcohols
Alcohols are compounds that have hydroxyl groups bonded to saturated carbon atoms. Alcohols can be thought of as organic derivative of water in which one of the water hydrogen is replaced by an organic group (Fig. 1).
H-O-H versus R-O-H.
Fig. 1: Formular of alcohol.
Alcohols occur widely in nature and have a great many industrial and pharmaceutical applications. Ethanol, for instance is one of the simplest yet best known of all organic substances, usually used as a fuel additive, an industrial solvent and a beverage.
Alcohols are classified as primary (1), secondary (2) or tertiary (3) depending on the number of the organic groups bonded to the hydroxyl bearing carbon and ethanol is a primary alcohol (Garrett and Grisham, 2005).
Ethanol was one of the first organic chemicals to be prepared and purified. Its production by fermentation of grains and sugar has been carried out for millennia and its purification by distillation. Only about five percent (5%) of the ethanol produced industrially comes from fermentation.
Most ethanol is currently obtained by acid-catalyzed hydration of ethylene (Fig. 2).
H2C=CH2 + H2O --------àCH3CH2OH
Fig. 2: Equation for ethanol formation.
1.2. Lipids
Fats absorbed from the diet and lipids synthesized by the liver and adipose tissue must be transported between the various tissues and organs for utilization and storage. Since lipids are insoluble in water, the problem of how to transport them in the aqueous blood plasma is solved by associating non-polar lipids with amphipathic lipids and proteins to make water miscible lipoproteins. Lipids are transported in the plasma as lipoproteins.
1.2.1. Plasma Lipids
Plasma lipids consist of triacylglycerols, phospholipids, cholesterol and cholesteryl esters and a much smaller fraction of unesterified long chain fatty acids. These are metabolically the most active of the plasma acids. Because fat is less dense than water, the density of a lipoprotein decreases as the proportion of lipid to protein increases (Murray et al., 2006). Four major groups of lipoproteins have been identified that are physiologically important in clinical diagnosis. These are:
(a) Chylomicrons, derived from intestinal absorption of triacylglycerol and other lipids.
(b) Very low density lipoproteins (VLDL) derived from the liver for the export of triacylglycerols.
(c) Low density lipoproteins representing a final stage in the catabolism of VLDL.
(d) High density lipoproteins, involved in cholesterol transport and also in VLDL metabolism. Triacyglycerols are the predominant lipids in chylomicrons and VLDL, whereas cholesterol and phospholipids are the predominant lipids in LDL and HDL.....
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