scholarly journals Regular Intake of Pistachio Mitigates the Deleterious Effects of a High Fat-Diet in the Brain of Obese Mice

Antioxidants ◽  
2020 ◽  
Vol 9 (4) ◽  
pp. 317 ◽  
Author(s):  
Domenico Nuzzo ◽  
Giacoma Galizzi ◽  
Antonella Amato ◽  
Simona Terzo ◽  
Pasquale Picone ◽  
...  
Keyword(s):  
High Fat Diet ◽  
Serum Levels ◽  
Standard Diet ◽  
High Fat ◽  
Neuroprotective Effects ◽  
Extracellular Signal Regulated Kinase ◽  
Extracellular Signal ◽  
The Brain ◽  
Superoxide Dismutase 2 ◽  
Regular Intake

Obesity has been associated with neurodegeneration and cognitive dysfunctions. Recent data showed that pistachio consumption is able to prevent and ameliorate dyslipidemia, hepatic steatosis, systemic and adipose tissue inflammation in mice fed a high-fat diet (HFD). The present study investigated the neuroprotective effects of pistachio intake in HFD mice. Three groups of mice were fed a standard diet (STD), HFD, or HFD supplemented with pistachio (HFD-P) for 16 weeks. Metabolic parameters (oxidative stress, apoptosis, and mitochondrial dysfunction) were analyzed by using specific assays and biomarkers. The pistachio diet significantly reduced the serum levels of triglycerides and cholesterol in the HFD model. No difference was observed in the index of insulin resistance between HFD and HFD-P. A higher number of fragmented nuclei were found in HFD cerebral cortex compared to STD and HFD-P. A decrease in reactive oxygen species, singlet oxygen and phosphorylated extracellular signal-regulated kinase, and an increase of superoxide dismutase 2 and heme oxygenase expression were found in the brains of the HFD-P samples compared to HFD. Furthermore, the impaired mitochondrial function found in HFD brain was partially recovered in HFD-P mice. These results suggest that the regular intake of pistachio may be useful in preventing obesity-related neurodegeneration, being able to reduce both metabolic and cellular dysfunctions.

scholarly journals Palmitoleic Acid (N-7) Attenuates the Immunometabolic Disturbances Caused by a High-Fat Diet Independently of PPARα

2014 ◽  
Vol 2014 ◽  
pp. 1-12 ◽  
Author(s):  
Camila O. Souza ◽  
Alexandre A. S. Teixeira ◽  
Edson A. Lima ◽  
Helena A. P. Batatinha ◽  
Lara M. Gomes ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Oleic Acid ◽  
High Fat Diet ◽  
Palmitoleic Acid ◽  
Serum Levels ◽  
Standard Diet ◽  
Liver Inflammation ◽  
Wild Type ◽  
High Fat

Palmitoleic acid (PMA) has anti-inflammatory and antidiabetic activities. Here we tested whether these effects of PMA on glucose homeostasis and liver inflammation, in mice fed with high-fat diet (HFD), are PPAR-αdependent. C57BL6 wild-type (WT) and PPAR-α-knockout (KO) mice fed with a standard diet (SD) or HFD for 12 weeks were treated after the 10th week with oleic acid (OLA, 300 mg/kg of b.w.) or PMA 300 mg/kg of b.w. Steatosis induced by HFD was associated with liver inflammation only in the KO mice, as shown by the increased hepatic levels of IL1-beta, IL-12, and TNF-α; however, the HFD increased the expression of TLR4 and decreased the expression of IL1-Ra in both genotypes. Treatment with palmitoleate markedly attenuated the insulin resistance induced by the HFD, increased glucose uptake and incorporation into muscle in vitro, reduced the serum levels of AST in WT mice, decreased the hepatic levels of IL1-beta and IL-12 in KO mice, reduced the expression of TLR-4 and increased the expression of IL-1Ra in WT mice, and reduced the phosphorylation of NF𝜅B (p65) in the livers of KO mice. We conclude that palmitoleate attenuates diet-induced insulin resistance, liver inflammation, and damage through mechanisms that do not depend on PPAR-α.

scholarly journals Assessment of DNA Methylation and Oxidative Changes in the Heart and Brain of Rats Receiving a High-Fat Diet Supplemented with Various Forms of Chromium

Animals ◽  
2020 ◽  
Vol 10 (9) ◽  
pp. 1470
Author(s):  
Wojciech Dworzański ◽  
Ewelina Cholewińska ◽  
Bartosz Fotschki ◽  
Jerzy Juśkiewicz ◽  
Piotr Listos ◽  
...  
Keyword(s):  
Dna Methylation ◽  
High Fat Diet ◽  
Protein Carbonyl ◽  
Global Dna Methylation ◽  
Standard Diet ◽  
Epigenetic Changes ◽  
Oxidation Reactions ◽  
High Fat ◽  
Repair Enzymes ◽  
The Brain

The aim of the study was to determine how feeding rats a high-fat diet supplemented with various forms of chromium affects DNA methylation and oxidation reactions as well as the histology of heart and brain tissue. The rats received standard diet or high-fat diet and chromium at 0.3 mg/kg body weight (BW) in form of chromium (III) picolinate, chromium (III)-methionine, or nano-sized chromium. The content of malondialdehyde (MDA), protein carbonyl (PC), and 8-hydroxydeoxyguanosine (8-OHDG), the level of global DNA methylation and the activity of selected DNA repair enzymes were determined in the blood. In the brain and heart, the content of MDA, PC, 8-OHDG, and levels of global DNA methylation were determined. The brain was subjected to histological examination. The use of a high-fat diet was found to intensify epigenetic changes and oxidation reactions in the heart and brain. It was concluded that epigenetic changes and oxidation of lipids, proteins, and DNA in the heart and brain of rats resulting from the use of a high-fat diet cannot be limited by supplementing the diet with chromium. It was established that the use of chromium to supplement a high-fat diet intensifies the negative epigenetic and oxidative changes in the heart and brain, especially in the case of chromium nanoparticles.

scholarly journals Oenothein B, a Bioactive Ellagitannin, Activates the Extracellular Signal-Regulated Kinase 2 Signaling Pathway in the Mouse Brain

Plants ◽  
2021 ◽  
Vol 10 (5) ◽  
pp. 1030
Author(s):  
Satoshi Okuyama ◽  
Yoshiko Furukawa ◽  
Morio Yoshimura ◽  
Yoshiaki Amakura ◽  
Mitsunari Nakajima ◽  
...  
Keyword(s):  
Inflammatory Responses ◽  
Camp Response Element Binding ◽  
Abnormal Behavior ◽  
Neuroprotective Effects ◽  
Extracellular Signal Regulated Kinase ◽  
Treatment And Prevention ◽  
Extracellular Signal ◽  
Oenothein B ◽  
The Brain

(1) Background: Oenothein B, a cyclic dimeric ellagitannin present in various medicinal plants, has been reported to exert diverse effects that are beneficial for the treatment and prevention of diseases, including cancer and infections. We recently showed that oenothein B also functions in the brain because its oral administration to systemic inflammatory model mice reduced inflammatory responses in the brain and suppressed abnormal behavior. (2) Results: The present in vivo results demonstrated that oenothein B activated extracellular signal-regulated kinase 2 and cAMP response element-binding protein in the brain, both of which play important roles in synaptic transmission and learning/memory in the central nervous system (CNS). (3) Conclusions: These results suggest that oenothein B exerts neuroprotective effects on the CNS by not only its anti-inflammatory activity but also by enhancing neuronal signaling pathways.

scholarly journals Supplementation of concentrated Kurozu, a Japanese black vinegar, reduces the onset of hepatic steatosis in mice fed with a high-fat diet

2019 ◽  
Vol 9 (4) ◽  
pp. 276
Author(s):  
Yoshihiko Shibayama ◽  
Masanobu Nagano ◽  
Kazunori Hashiguchi ◽  
Akira Fujii ◽  
Ken Iseki
Keyword(s):  
Hepatic Steatosis ◽  
High Fat Diet ◽  
Serum Levels ◽  
Standard Diet ◽  
Chronic Liver Diseases ◽  
High Fat ◽  
Body Weights ◽  
Common Causes ◽  
All Cause Mortality ◽  
Lipid Metabolism Genes

Background: Hepatic steatosis is among the most common causes of chronic liver diseases, although established effective treatments are not evident.  Previous studies reported that Kurozu improved hypercholesterolemia and carbohydrate metabolism. However, the effect of Kurozu on the incidence of hepatic steatosis is not clear.Objective: The effect of Kurozu on the onset of hepatic steatosis by administering a high-fat diet (HFD) for 110 weeks was evaluated in C57BL/6J mice. Methods: HFD treatment for 110 weeks accelerated the onset of hepatic steatosis more than a standard diet, whereas concentrated Kurozu (CK) supplementation ameliorated the effect of an HFD feeding. The effect of supplementation with resveratrol in an HFD on the onset of hepatic steatosis was also evaluated. To elucidate the mechanism of the effect of Kurozu on the expression of lipid metabolism genes, acute treatment for 10 days with Kurozu was also examined.Results: Supplementation with resveratrol in HFD-fed mice did not ameliorate hepatic steatosis. Body weights were significantly lower in the CK + HFD and Resveratrol + HFD groups than in the control HFD group in middle age. No significant differences in all-cause mortality were observed following supplementation with CK or resveratrol. CK and resveratrol supplements significantly inhibited decreases in dehydroepiandrosterone sulphate serum levels at postnatal week 120. CK and resveratrol supplements did not affect the survival of mice. The ingestion of Kurozu for 10 days significantly elevated the expression levels of Sirt1, Pgc-1α, Lpin1, and Igfbp1 in the liver. Conclusion: These results suggest that ingesting CK may delay the onset of hepatic steatosis HFD feeding causes.Keywords: Kurozu, steatosis, Sirt1, Igfbp1, Lpin1, Pgc-1α, resveratrol

Abstract 122: Hyperinsulinmia Promotes Cardiac Dysfunction via Upregulation of Phosphodiesterase in Heart

2015 ◽  
Vol 117 (suppl_1) ◽  
Author(s):  
Yang K Xiang
Keyword(s):  
Insulin Signaling ◽  
Cardiac Dysfunction ◽  
High Fat Diet ◽  
Erk Pathway ◽  
High Fat ◽  
Heart Dysfunction ◽  
Extracellular Signal Regulated Kinase ◽  
Extracellular Signal ◽  
Attractive Therapeutic Target ◽  
Phosphodiesterase 4D

Accumulating evidence suggests that hyperinsulinemia contributes to heart dysfunction. Here we show that insulin signaling is responsible for high fat diet (HFD) feeding-induced expression of phosphodiesterase 4D (PDE4D) in the myocardium of mice. The increased expression of PDE4D, in concert with reduced phosphorylation of phospholamban (PLB), promotes systolic and diastolic heart dysfunction. We revealed that insulin-mediated induction of PDE4D was dependent on β2AR-mediaed β-arrestin2-ERK pathway, which is transactivated in a GRK2-dependent fashion. Deletion of β2AR gene significantly attenuated insulin-induced phosphorylation of extracellular signal-regulated kinase (ERK) and Akt, as well as the upregulation of PDE4D expression, which prevented the heart dysfunction. β-arrestin2 KO mice did not display increased PDE4D expression and did not develop systolic or diastolic dysfunction following HFD. In brief, these data indicate that chronic hyperinsulinimia leads to heart dysfunction by increasing PDE4D expression via β2AR-GRK2-β-arrestin2 -ERK pathway, which suggests that β2AR signaling could be an attractive therapeutic target for preserving or improving cardiac function in subjects with insulin resistance.

scholarly journals High-intensity interval training ameliorates high-fat diet-induced elevation of aminotransferases in male Wistar rats

2021 ◽  
Vol 23 (3) ◽  
pp. 111-115
Author(s):  
Qazaleh Asqari ◽  
Farhad Gholami ◽  
Jabbar Bashiri ◽  
Adel Donyaei
Keyword(s):  
High Fat Diet ◽  
Wistar Rats ◽  
Interval Training ◽  
Serum Levels ◽  
Diet Group ◽  
Standard Diet ◽  
High Intensity Interval Training ◽  
High Fat ◽  
Male Wistar Rats ◽  
High Intensity Interval

Background and aims: A high-fat diet increases triglyceride (TG) accumulations in hepatocytes and results in non-alcoholic fatty liver diseases (NAFLDs). In this regard, this study investigated the effect of high-intensity interval training (HIIT), along with a high-fat diet on the serum levels of aminotransferases in male Wistar rats. Methods: Forty male Wistar rats were randomly assigned to the standard diet, high-fat diet, exercise + standard diet, and exercise + high-fat diet groups (each containing 10 animals). HIIT program consisted of 6-12 repetitions of 2-minute highs-intensity exercise (85-90% of the maximum speed) interspersed with 1-minute low-intensity exercise (45-50% peak speed) with the frequency of 5 sessions a week over 12 weeks. High-fat diet groups received a diet regimen including 58% fat, 25% protein, and 17% carbohydrate, ad libitum. The blood samples were taken from the left ventricle 48 hours following the last intervention to assess TG, alanine aminotransferase (ALT), and aspartate amino-transferase (AST) concentrations. Data were analyzed using one-way ANOVA and Tukey’s post-hoc tests. Results: The findings showed the mean of ALT, AST, and TG in the high-fat diet group was significantly greater compared to the standard diet group (P=0.001). Furthermore, the mean of ALT, AST, and TG in the exercise + high-fat diet group was significantly lower in comparison with the high-fat diet group (P=0.01, P=0.017, and P=0.012, respectively). Conclusion: Although HIIT ameliorated high-fat diet-induced elevations in the serum levels of TG, ALT, and AST, they did not reach the baseline levels. Thus, it may indicate that a diet as the underlying cause of NAFLDs is more important than any other interventions such as exercise.

Pengaruh Pemberian Ekstrak Anggur Laut terhadap Penurunan Kadar Kolesterol LDL Rattus norvegicus Jantan yang Mendapat Diet Tinggi Lemak

2020 ◽  
Vol 17 (2) ◽  
pp. 192
Author(s):  
RONALDO LAU ◽  
SULISTIANA PRABOWO ◽  
RIAMI RIAMI
Keyword(s):  
Cholesterol Level ◽  
Rattus Norvegicus ◽  
High Fat Diet ◽  
Ldl Cholesterol ◽  
White Male ◽  
Standard Diet ◽  
High Fat ◽  
Caulerpa Racemosa ◽  
Significant Difference ◽  
Male Wistar Rats

<p align="justify"><strong>ABSTRACT</strong><strong></strong></p><p align="justify"><strong>Background</strong>: High fat diet increase the absorption of lipid in the intestinum, that can lead to increase LDL cholesterol level in the blood. Sea grapes extract (<em>Caulerpa racemosa</em>) contains antioxidant polyphenolic group that can reduce MTP and ACAT-2 in the body that can decrease LDL cholesterol level in the blood.The purpose of this study is to know the effect of sea grapes extract  on decreasing LDL cholesterol of white male Wistar rats (<em>Rattus norvegicus</em>) fed with high fat diet.</p><p align="justify"><strong>Method</strong>:  24 white male Wistar rats, that divided into 3 groups: 1) group of rats fed with standard diet for 28 days; 2) group of rats fed with high fat diet for 28 days; 3) group of rats fed with high fat diet for 28 days and given 10 gram/kg body weight/day of sea grapes extract on 15<sup>th</sup>-28<sup>th</sup> days. Then the blood LDL cholesterol level measured on the 29<sup>th</sup> day.</p><p align="justify"><strong>Result :</strong> One-Way ANOVA Test showed there was significant difference (p=0.004) of LDL level between the group of rats fed with standard diet (12.37 mg/dl) compared to group of rats fed with high fat diet (17.87 mg/dl). There was significant difference (p=0.001) of LDL level between the group of rats fed with high fat diet (17.87 mg/dl) compared to group of rats fed with high fat diet and sea grapes extract (10.12 mg/dl).</p><p align="justify"><strong>Conclusion: </strong>high fat diet significantly increase blood LDL cholesterol level and sea grapes extract (<em>Caulerpa racemosa</em>) significantly decrease blood LDL cholesterol level.</p><p align="justify"> </p><p align="justify"><strong>Keywords :</strong>Sea grapes extract, LDL cholesterol, high fat diet</p>

Formononetin Ameliorates Cognitive Disorder via PGC-1α Pathway in Neuroinflammation Conditions in High-Fat Diet-Induced Mice

2019 ◽  
Vol 18 (7) ◽  
pp. 566-577 ◽  
Author(s):  
Xinxin Fu ◽  
Tingting Qin ◽  
Jiayu Yu ◽  
Jie Jiao ◽  
Zhanqiang Ma ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
High Fat Diet ◽  
Trifolium Pratense ◽  
Amyloid Β ◽  
Cognitive Disorder ◽  
Mechanism Study ◽  
High Fat ◽  
Neuroprotective Effects ◽  
Underlying Mechanisms

Background: Alzheimer’s disease is one of the most common neurodegenerative diseases in many modern societies. The core pathogenesis of Alzheimer’s disease includes the aggregation of hyperphosphorylated Tau and abnormal Amyloid-β generation. In addition, previous studies have shown that neuroinflammation is one of the pathogenesis of Alzheimer’s disease. Formononetin, an isoflavone compound extracted from Trifolium pratense L., has been found to have various properties including anti-obesity, anti-inflammation, and neuroprotective effects. But there are very few studies on the treatment of Alzheimer’s disease with Formononetin. Objective: The present study focused on the protective activities of Formononetin on a high-fat dietinduced cognitive decline and explored the underlying mechanisms. Methods: Mice were fed with HFD for 10 weeks and intragastric administrated daily with metformin (300 mg/kg) and Formononetin (20 and 40 mg/kg). Results: We found that Formononetin (20, 40 mg/kg) significantly attenuated the learning and memory deficits companied by weight improvement and decreased the levels of blood glucose, total cholesterol and triglyceride in high-fat diet-induced mice. Meanwhile, we observed high-fat diet significantly caused the Tau hyperphosphorylation in the hippocampus of mice, whereas Formononetin reversed this effect. Additionally, Formononetin markedly reduced the levels of inflammation cytokines IL-1β and TNF-α in high-fat diet-induced mice. The mechanism study showed that Formononetin suppressed the pro-inflammatory NF-κB signaling and enhanced the anti-inflammatory Nrf-2/HO-1 signaling, which might be related to the regulation of PGC-1α in the hippocampus of high-fat diet -induced mice. Conclusion: Taken together, our results showed that Formononetin could improve the cognitive function by inhibiting neuroinflammation, which is attributed to the regulation of PGC-1α pathway in HFD-induced mice.

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