Neural Protective Effects of Millet and Millet Polyphenols on High-Fat Diet-Induced Oxidative Stress in the Brain

AbstractObesity and the brain are linked since the brain can control the weight of the body through its neurotransmitters. The aim of the present study was to investigate the effect of high-fat diet (HFD)-induced obesity on brain functioning through the measurement of brain glutamate, dopamine, and serotonin metabolic pools. In the present study, two groups of rats served as subjects. Group 1 was fed a normal diet and named as the lean group. Group 2 was fed an HFD for 4 weeks and named as the obese group. Markers of oxidative stress (malondialdehyde, glutathione, glutathione-s-transferase, and vitamin C), inflammatory cytokines (interleukin [IL]-6 and IL-12), and leptin along with a lipid profile (cholesterol, triglycerides, high-density lipoprotein, and low-density lipoprotein levels) were measured in the serum. Neurotransmitters dopamine, serotonin, and glutamate were measured in brain tissue. Fecal samples were collected for observing changes in gut flora. In brain tissue, significantly high levels of dopamine and glutamate as well as significantly low levels of serotonin were found in the obese group compared to those in the lean group (P > 0.001) and were discussed in relation to the biochemical profile in the serum. It was also noted that the HFD affected bacterial gut composition in comparison to the control group with gram-positive cocci dominance in the control group compared to obese. The results of the present study confirm that obesity is linked to inflammation, oxidative stress, dyslipidemic processes, and altered brain neurotransmitter levels that can cause obesity-related neuropsychiatric complications.

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The Protective Effects of Acer okamotoanum and Isoquercitrin on Obesity and Amyloidosis in a Mouse Model

Nutrients ◽

10.3390/nu12051353 ◽

2020 ◽

Vol 12 (5) ◽

pp. 1353

Author(s):

Ji Hyun Kim ◽

Sanghyun Lee ◽

Eun Ju Cho

Keyword(s):

Body Weight ◽

Mouse Model ◽

High Fat Diet ◽

Ethyl Acetate Fraction ◽

Control Group ◽

Protective Effects ◽

High Fat ◽

Acer Okamotoanum ◽

Related Proteins ◽

The Brain

Obesity increases risk of Alzheimer’s Disease (AD). A high fat diet (HFD) can lead to amyloidosis and amyloid beta (Aβ) accumulation, which are hallmarks of AD. In this study, protective effects of the ethyl acetate fraction of Acer okamotoanum (EAO) and isoquercitrin were evaluated on obesity and amyloidosis in the HFD- and Aβ-induced mouse model. To induce obesity and AD by HFD and Aβ, mice were provided with HFD for 10 weeks and were intracerebroventricularly injected with Aβ25–35. For four weeks, 100 and 10 mg/kg/day of EAO and isoquercitrin, respectively, were administered orally. Administration of EAO and isoquercitrin significantly decreased body weight in HFD and Aβ-injected mice. Additionally, EAO- and isoquercitrin-administered groups attenuated abnormal adipokines release via a decrease in leptin and an increase in adiponectin levels compared with the control group. Furthermore, HFD and Aβ-injected mice had damaged liver tissues, but EAO- and isoquercitrin-administered groups attenuated liver damage. Moreover, administration of EAO and isoquercitrin groups down-regulated amyloidosis-related proteins in the brain such as β-secretase, presenilin (PS)-1 and PS-2 compared with HFD and Aβ-injected mice. This study indicated that EAO and isoquercitrin attenuated HFD and Aβ-induced obesity and amyloidosis, suggesting that they could be effective in preventing and treating both obesity and AD.

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Melatonin protects against cardiac damage induced by a combination of high fat diet and isoproterenol exacerbated oxidative stress in male Wistar rats

Melatonin Research ◽

10.32794/mr11250009 ◽

2019 ◽

Vol 2 (1) ◽

pp. 9-31 ◽

Cited By ~ 1

Author(s):

Auroma Ghosh ◽

Gargi Bose ◽

Tiyasa Dey ◽

Palash Kumar Pal ◽

Sanatan Mishra ◽

...

Keyword(s):

Oxidative Stress ◽

Antioxidant Enzymes ◽

High Fat Diet ◽

Myocardial Damage ◽

Neutrophil Infiltration ◽

Protective Effects ◽

High Fat ◽

Cardiac Damage ◽

Male Wistar Rats ◽

Abnormal Mitochondria

In the current study, it was found that high fat diet (60% of total kCal) (H) or/and isoproterenol (I) exacerbated oxidative stress and caused myocardial damage. This was indicated by increased levels of LPO, PCO, abnormal mitochondria and altered activities of metabolic as well as antioxidant enzymes in myocardium of rats. Melatonin at different doses (10, 20 and 40 mg/kg) effectively protected against myocardial damage induced by H or/and I and preserved all of these altered parameters. Morphological analyses showed that combination of H and I treatment led to the extensive myofibril disintegration and neutrophil infiltration. Melatonin at the dose of 40 mg/kg almost completely prevented these pathological alterations. The mechanistical studies have uncovered that the protective effects of melatonin on the myocardial damage induced by H and I are attributed to its direct and indirect antioxidative capacity, i.e., it directly scavenges free radicals and also regulates the gene expression of antioxidant enzymes. Collectively, based on the evidences gathered from the current study, it will not be unwise to suggest that melatonin can serve as an ideal therapeutic agent for those cardiovascular diseases caused by oxidative stress.

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Effects of high fat diet on multiple indices of oxidative stress in the brain

The FASEB Journal ◽

10.1096/fasebj.23.1_supplement.507.1 ◽

2009 ◽

Vol 23 (S1) ◽

Author(s):

Ying Liu ◽

Le Zhang ◽

Sun OK Fernandez‐Kim ◽

Christopher Morrison ◽

Annadora Bruce‐Keller ◽

...

Keyword(s):

Oxidative Stress ◽

High Fat Diet ◽

High Fat ◽

The Brain

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Alleviation of liver dysfunction, oxidative stress and inflammation underlines the protective effects of polysaccharides from Cordyceps cicadae on high sugar/high fat diet‐induced metabolic syndrome in rats

Chemistry & Biodiversity ◽

10.1002/cbdv.202100065 ◽

2021 ◽

Author(s):

Xiao Zhang ◽

Jinpeng Li ◽

Bo Yang ◽

Qina Leng ◽

Ji Li ◽

...

Keyword(s):

Oxidative Stress ◽

Metabolic Syndrome ◽

Liver Dysfunction ◽

High Fat Diet ◽

Protective Effects ◽

High Fat ◽

High Sugar ◽

Cordyceps Cicadae

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Lentinan Protects against Nonalcoholic Fatty Liver Disease by Reducing Oxidative Stress and Apoptosis via the PPARα Pathway

Metabolites ◽

10.3390/metabo12010055 ◽

2022 ◽

Vol 12 (1) ◽

pp. 55

Author(s):

Tingyi Du ◽

Qin Fang ◽

Zhihao Zhang ◽

Chuanmeng Zhu ◽

Renfan Xu ◽

...

Keyword(s):

Oxidative Stress ◽

Liver Disease ◽

Fatty Liver ◽

Nonalcoholic Fatty Liver Disease ◽

High Fat Diet ◽

Fatty Liver Disease ◽

Chow Diet ◽

Protective Effects ◽

High Fat ◽

Nonalcoholic Fatty Liver

Aim: Lentinan (LNT), a type of polysaccharide derived from Lentinus edodes, has manifested protective effects during liver injury and hepatocellular carcinoma, but little is known about its effects on nonalcoholic fatty liver disease (NAFLD). This study aimed to investigate whether LNT can affect the progression of NAFLD and the associated mechanisms. Methods: C57BL/6J mice were fed a normal chow diet or a high-fat diet (HFD) with or without LNT (6 mg/kg/d). AML12 cells were exposed to 200 μM palmitate acid (PA) with or without LNT (5 μg/mL). Results: After 21 wk of the high-fat diet, LNT significantly decreased plasma triglyceride levels and liver lipid accumulation, reduced excessive reactive oxygen species production, and subsequently attenuated hepatic apoptosis in NAFLD mice. These effects were associated with increased PPARα levels, a decreased Bax/Bcl-2 ratio, and enhancement of the antioxidant defense system in vivo. Similar effects were also observed in cultured cells. More importantly, these protective effects of LNT on palmitate acid-treated AML12 cells were almost abolished by PPARα knockdown. Conclusion: In conclusion, this study demonstrates that LNT may ameliorate hepatic steatosis and decrease oxidative stress and apoptosis by activating the PPARα pathway and is a potential drug target for NAFLD.

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