(526.17) Pharmacological Evaluation of Beta-Hydroxifosphocarnitine in No-Alcoholic Esteatohepatitis Induced in Rats

Poster Board Number: D34
Introduction:

Janet Sanchez-Quevedo (Universidad Autonoma del Estado de Morelos), Jorge Luis Rosado (Universidad Autonoma de Queretaro), Lourdes Rodriguez-Fragoso (Universidad Autonoma del Estado de Morelos)

Aim: Evaluate the pharmacological effect of Β-Hydroxyphosphocarnitine (β-HFC) on non-alcoholic steatohepatitis induced in rats.

Introduction: Nonalcoholic steatotepatitis (NASH) is a serious global public health problem, it is related to other pathologies with increasing prevalence, manifested in the increased prevalence of NASH. Type 2 diabetes mellitus and obesity are the main pathologies related to NASH. There is no specific drug for NASH, the current drugs used for NASH are related to serious side effects, which is why there is an urgent need in the development of an effective therapy for NASH but with fewer side effects. L-carnitine has an effect on improving metabolic alterations related to NASH, however, its intestinal absorption is limited. B-HFC is an analog of L-carnitine that has been shown to be safe for administration, to maintain pharmacological properties of its precursor and its absorption is greater than that of L-carnitine. So it can be a good treatment for NASH.

Method: The NASH model was developed in male Wistar rats by ingesting carbonated drink as a source of fructose, coconut oil and carbon tetrachloride. 3 groups were formed with NASH (n = 8); NASH, NASH -β-HFC and NASH-pioglitazone.  Another 3 groups of healthy rats (n = 8); control, control-β-HFC and control-pioglitazone. The effect of β-HFC in rats with NASH was evaluated by staining of histological sections of liver. The stains used were Massons trichrome, hematoxylin and osin and Periodic Acid-Schiff (PAS). Biochemical analysis was performed to evaluate the effect of β-HFC on the metabolic alterations that characterize NASH.

Result: It was previously reported that β-HFC reduced the triglyceride levels of rats with NASH, as well as the levels of liver enzymes. Evidencing the effect of β-HFC in improving lipid metabolism, manifesting itself in less liver damage. For this occasion we will report the effect of β-HFC on liver glycogen levels. Glycogen is a reserve of the cell, as a source of glucose in prolonged fasting states. Our results demonstrated a higher glycogen reserve in the NASH rats. This result was expected, since the rats had a high fructose intake. It is important to mention that the rats with NASH but treated with β-HFC presented reduced glycogen levels, this effect can be attributed to a more efficient β-oxidation process, which could also justify the reduction of triglycerides and fibrosis. Therefore, we could argue that a longer treatment time, the liver alterations in NASH would improve significantly.

Conclusion: β-HFC has an effect on improving liver and metabolic alterations characteristic of the development of NASH.