ABSTRACT

Hyperlipidemia is viewed as a primary mediator of cardiovascular disease. The aim of the study is to

evaluate the effect of camel milk on Poloxamer 407 induced hyperlipidemic Wistar rats. Thirty adult

male Wistar rats weighing between 150-200g were randomly assigned into six groups of five animals

each; Group I: administered distilled water, Group II: Hyperlipidemic negative control, Group III:

Hyperlipidemic positive control treated with Atorvastatin (20mg/kg) and Group IV, V and

VI:Hyperlipidemic groups treated with camel milk 0.25ml/kg, 0.50ml/kg and 1ml/kg respectively.

After three weeks, blood samples drawn fordetermination of Total       cholesterol (TC),

Triglyceride(TG),High      Density     Lipoprotein     (LDL),     Low          Density     Lipoprotein(LDL),

Malondialdhyde(MDA),      Catalase(CAT)      Superoxide      Dismutase(SOD)      and      Gluthatione

Peroxidase(GPx), Total Protein, Albumin, Globulin, A/G ratio, Alkaline Phospatase (ALP), Alanine

Aminotransferase (ALT), Aspartate Aminotransferase (AST) and serum electrolytes(Na+, K+, Cl- and

HCO3-) respectively were carried out. Total cholesterol(174.68 ±46.92 mg/dL)and triglyceride

(91.38±5.52mg/dL) level in Wistar rats were significantly (p< 0.05) reduced in 1ml/kg treated groups

compared to the hyperlipidemic negative control group (727.24 ±126.59 mg/dL and 203.16 ±

27.64mg/dL) respectively. Camel milk at the dose of 1ml/kg hadhighest lipid lowering activity

especially LDL (from414.09±25.96mg/dL to 114.75±42.83mg/dL) while at 0.25ml/kgit showed an

increase in the level of HDL (from 35.97 ± 2.43mg/dL to 208.72±7.88 mg/dL).Camel milk at doses of

0.25ml/kg and 0.5ml/kg showed significant (p<0.05) increase in the level of SOD(9.25±0.51 U/ml and

11.04± 1.14 U/ml) compared to the hyperlipidemic negative control (3.25 ± 1.05U/ml). There was also

significant (p <0.05) decrease in the serum levels of total protein and globulin at

0.25ml/kg(5.55±0.56g/dL,    2.41±0.51mg/dL)    and    1ml/kg     (6.42±0.53g/dL,    3.43±0.60g/dL)and

significant increase in A/G ratio in all camel milk treated groups (1.33±0.11, 0.87±0.11 and

0.94±0.11) compared to the hyperlipidemic negative control group (11.23±1.25g/dL, 7.75±1.28g/dL

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CHAPTER ONE

1.0 Introduction

Cardiovascular diseases (CVD) are the leading cause of death for both men and women among all racial and ethnic groups (Smith, 2004). It accounts for nearly 50% of all deaths in the developed world (Thomas and Rich, 2007) and has also been predicted by the World Health Organization to remain the leading causes of deaththat will affect approximately 23.6 million people globallyby 2030(Ooi and Liong,2010).Hyperlipidemia is viewed as the primary mediator of a cascade of heart diseases such as atherosclerosis, stroke, myocardial infarction and pancreatitis (Olorunnisola et al., 2012; Harikumar et al., 2013). It may be due to heredity or acquired secondarily from underlying disease such as; type 2 diabetes mellitus, liver cholestasis, alcohol, nephrotic syndrome, chronic renal failure, hypothyroidism, cigarette smoking, drugs, hormone and obesity (Olorunnisola et al., 2012; Harikumar et al., 2013; Onwe et al., 2015). Irrespective of the etiology of hyperlipidemia, common features include elevated serum total cholesterol, triglyceride, low density lipoprotein, very low density lipoprotein, and reduced high density lipoprotein (Olorunnisola et al., 2012). The current hy