Tissue Lipid Profile of Rats Administered Saponin Extract From The Root of Bitter kola
Alli Smith Y. R.,
Adanlawo I. G.
Issue:
Volume 1, Issue 1, April 2013
Pages:
1-4
Received:
20 March 2013
Accepted:
Published:
2 April 2013
Abstract: The present study was undertaken to investigate the effect of saponin extract from the root of Bitter kola (Garcinia kola) on the lipid profile of albino rats tissues (Liver, Kidney and Heart). Twenty albino rats were divided into 4 groups of 5 rats each. They were given rats mash and water ad libitum for 2 weeks to acclimatize them; they were then subjected to different doses of saponin extract from the root of Garcinia kola. Group I (control) received an equivalent volume of water, group II received 100mg/Kg body weight of extract, and group III was given 200mg/Kg body weight, while group IV received 400mg/Kg body weight of saponin extract orally everyday for 21days. The serum, heart, liver and kidney were then analysed for Total cholesterol(TC), High density lipoprotein cholesterol (HDL-C), Low density lipoprotein cholesterol (LDL-C) and Triglycerides(TG). Administration of 100, 200 and 400 mg/kg doses of saponin extract from the root of Garcinia kola led to a significant reduction (P <05) in total cholesterol, LDL cholesterol and Triglyceride levels in the serum, Liver, kidney and heart when compared with the control and a significant increase (P <05) in HDL cholesterol concentration when compared with control. Hyperlipidemia, being an important risk factor for cardiovascular disease, is a serious public health problem in the world. This result suggests a dose dependent hypolipidemic potential of saponin extract from the root of Garcinia kola and could play a cardio protective role.
Abstract: The present study was undertaken to investigate the effect of saponin extract from the root of Bitter kola (Garcinia kola) on the lipid profile of albino rats tissues (Liver, Kidney and Heart). Twenty albino rats were divided into 4 groups of 5 rats each. They were given rats mash and water ad libitum for 2 weeks to acclimatize them; they were then...
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Peroxisomal Heat Generation and Possible Relationship With Peroxisomal Disorders
Issue:
Volume 1, Issue 1, April 2013
Pages:
5-6
Received:
28 March 2013
Accepted:
Published:
2 April 2013
Abstract: Peroxisomal disorders encompass a variety of pathologies with different clinical manifestations. X-linked adrenoleukodystrophy, an inherited neurodegenerative pathology, is characterized by mutation of a peroxisomal transport protein involved in the catabolism of very long-chain fatty acids (VLCFAs). These particular fatty acids abnormally accu-mulate in plasma and in all tissues due to the enhancement of fatty acid elongation and the impairment of fatty acid catabolism which takes place initially in the peroxisomes and afterward in the mitochondria. VLCFA accumulation cannot explain the molecular mechanisms underlying clinical manifestations in patients. Peroxisomal pathways include a product that is considered lost, but that could have a role in peroxisomal disorders: the heat produced during VLCFA catabolism. VLCFA accumulation is due to peroxisomal beta-oxidation impairment and to the enhancement of fatty acid elongation. The heat produced during peroxisomal metabolism could be a crucial factor related to the molecular mechanisms altered in X-linked adrenoleukodystrophy. VLCFA accumulation could be strongly related to the impairment of heat production, which is lost in X-linked adrenoleukodystrophy, a sort of energy necessary for the cell metabolism, which could contribute to the secondary clinical manifestations of peroxisomal disorders. Heat is not only produced during peroxisomal catabolism but also in countless metabolic pathways. It is a form of energy that could influence several parameters and could be involved in peroxisomal and metabolic disorders in general.
Abstract: Peroxisomal disorders encompass a variety of pathologies with different clinical manifestations. X-linked adrenoleukodystrophy, an inherited neurodegenerative pathology, is characterized by mutation of a peroxisomal transport protein involved in the catabolism of very long-chain fatty acids (VLCFAs). These particular fatty acids abnormally accu-mul...
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