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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
vi
and 0.49±0.08)respectively. Serum ALT, ASTand HCO3- were significantly decreased in all camel
milk treated groups (6.40±1.03u/L, 10.20± 2.26U/L and 11.20± 1.39U/L), (20.00±3.17U/L, 28.40±
4.51U/L and 33.20± 5.51U/L)and (24.40±1.80 mmol/L, 26.8±1.68 mmol/L and 26.00±0.70 mmol/L)
compared to the hyperlipidemic negative control group (42.50± 4.54U/L, 122.75±22.45U/L and
40.50±0.50 mmol/L)respectively. In conclusion, camel milk demonstrated a potenthypolipidemic,
anti-oxidantand hepatoprotective effect onPoloxamer 407 induced hyperlipidemicWistar rats.
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
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