Abstract
AimsThis study aimed to examine the effect of high fat diet (HFD) to modulate brain dysfunction, and understand the linkages between obesity, metabolic disturbances and the brain oxidative stress (BOS) dysfunction and modulation with hydroxyl citric acid of G. Cambogia.MethodsRats were divided into 3 groups; 1st control, maintained on standard normal rat chow diet, 2nd HFD, maintained on high fat diet along 12 week and 3rd HFD+G, administered G. Cambogia for 4 weeks and each group include 8 rats. Blood, brain and abdominal fat were collected for biochemical measurements.ResultsHFD group showed significant increase in energy intake, final BW and BW gain. Also significant increase in weight of abdominal fat in HFD group. HFD induce metabolic disturbance through increasing the lipid profile (LDL, TG, TC), γGT and α-amylase activity, uric acid level and hyperglycemia, while decreasing creatine kinase (CK) activity.These changes associated with lowering in brain nitric oxide (NO) level and rising in serum butyrylcholinesterase (BChE), brain catalase activity and MDA levels as oxidative stress markers. These alterations improved by G. Cambogia that decrease BOS and increased NO level.ConclusionsRats fed HFD showed, metabolic disturbances produce hyperglycemia, hypertriglyceridemia, hypercholesterolemia and increased LDL associated with increased BOS. Involvement of BuChE, NO and oxidative stress associated with metabolic disturbances in the pathophysiological progression in brain, suggesting association between obesity, metabolic disorders and brain alteration while, using G. Cambogia, ameliorate the damaging effects of the HFD via lowering feed intake and BOS.
Highlights
The brain is exceptionally susceptible to oxidative stress that may be caused by high fat diet and xenobiotics such as ethanol
high fat diet (HFD) induce metabolic disturbance through increasing the lipid profile (LDL, TG, TC), gGT and a-amylase activity, uric acid level and hyperglycemia, while decreasing creatine kinase (CK) activity. These changes associated with lowering in brain nitric oxide (NO) level and rising in serum butyrylcholinesterase (BChE), brain catalase activity and MDA levels as oxidative stress markers
Rats fed HFD showed, metabolic disturbances produce hyperglycemia, hypertriglyceridemia, hypercholesterolemia and increased LDL associated with increased brain oxidative stress (BOS)
Summary
The brain is exceptionally susceptible to oxidative stress that may be caused by high fat diet and xenobiotics such as ethanol. Prolonged HFD promotes a variety of morbidity factors experimental evidence for short-term western diet (WD) mediating brain dysfunction remains to be elucidated. It has been shown that the disturbances originated by high-fat feeding closely resemble the metabolic disturbances observed in humans [2]. Regardless of the remarkable progress which has been made in our understanding of dietary fat and obesity/type 2 diabetes (T2DM) with using HFD [3], it is important to point out that relatively little is currently available in regards to the study of HFDs and brain function and homeostasis, they have an obvious limitation in the study of brain dysfunction. HFD-induced models of metabolic dysfunction should be considered the best option for studying the effects of metabolic dysfunction on brain function
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