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Obesity has become a leading global health problem owing to its strong association with a high incidence of diseases. Most of
the experimental studies have been carried out on fatty liver and its overall metabolic effect. In the present study the effect
of high fat diet in an acute stage has been studied with a view to evaluate the effect of fat over load on the oxidative stress markers.
The histological picture in the experimental rats did show lipid deposition but not fatty liver.
Aim:
To induce rat obesity using high fat diet (HFD) and to study the role of oxidant and antioxidant status in mice along with
adiponectin level to bring out a possible role in energy homeostasis.
Materials and Methods:
Sixty white albino rats weighing 150-200 g were randomly divided into three equal groups; group I:
received normal diet Group 2 received High fat diet for 2 weeks and Group 3 received high fat diet for 4 weeks. Blood samples
were taken for measurement of lipid profile and adiponectin, tissue samples from liver were taken for determination of alanine
and aspartate transaminases, glucose-6-phosphate dehydrogenase, total protein and Glutathione status
Results:
Data showed that feeding HFD diet for 2 weeks and 4 weeks to mice did bring about significant changes in oxidant
profile with a fall in G.SH level accompanied by a fall in glucose-6-phosphate dehydrogenase activities. The hepatic transaminases
levels were significantly increased in mice fed with high fat diet in both groups, the increase being more in alanine transaminase
compared to aspartate transaminase. The level of lipid peroxide potential reflected by hepatic MDA level reflected an increase
oxidant street induced by high fat diet. The levels of adiponectin was increased in both groups compared to the control mice.
The present study did show marked changes in liver architecture brought about by metabolic stress induced by high fat diet.
The fall in hepatic G.SH level explains the utilization of G.SH as an anti-oxidant accompanied by a fall in glucose 6 phosphate
dehydrogenase activity which keeps G.SH in the reduced state by generating NADPH. The observed increase in adiponectin
levels in high fat diet fed mice clearly indicates a role for adiponectin in energy homeostasis.Adiponectin may play a role energy
homeostasis probably throougha intracellular cross-talk between adiponectin, leptin and insulin which requires further studies.
Conclusion:
High fat diet-induces metabolic stress reflected by the elevation in reactive oxygen species. The metabolic stress is
reflected by marked increases in hepatic transaminases marker of hepatic dysfunction. The oxidant state of fat fed hepatocytes
is reflected by marked reduction in the levels of antioxidant like Glutathione (G.SH) followed by a fall in G^PDH activity due to
its over utilization to generate more NADPH to keep the available G.SH in the reduced state. The increase in serum adiponectin
levels fed high fat diet indicates a definite role for adipocytikes in the energy homeostasis.Further studies are being carried out to
elucidate the role of adiponectin in energy metabolism using different forms physical stress and its expression at the molecular
level.
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