Chronic high-fat diet-induced obesity in gerbils increases pro-inflammatory cytokines and mTOR activation, and elicits neuronal death in the striatum following brief transient ischemia

2018 ◽  
Vol 121 ◽  
pp. 75-85 ◽  
Author(s):  
Minah Song ◽  
Ji Hyeon Ahn ◽  
Hyunjung Kim ◽  
Dae Won Kim ◽  
Tae-Kyeong Lee ◽  
...  
Keyword(s):  
Inflammatory Cytokines ◽  
Neuronal Death ◽  
High Fat Diet ◽  
High Fat ◽  
Transient Ischemia ◽  
Diet Induced Obesity ◽  
Pro Inflammatory Cytokines

scholarly journals Effect of Omega-3 Fatty Acid Rich Oils; Fish Oil and Perilla Oil on High-Fat Diet Fed DSS-Induced Colitis Mice

2020 ◽  
Vol 4 (Supplement_2) ◽  
pp. 1525-1525
Author(s):  
Kyung-Ah Kim ◽  
Shalom Sara Thomas ◽  
Youn-Soo Cha
Keyword(s):  
Fish Oil ◽  
Inflammatory Cytokines ◽  
High Fat Diet ◽  
Experimental Colitis ◽  
Normal Diet ◽  
Protective Effects ◽  
Omega 3 ◽  
High Fat ◽  
Perilla Oil ◽  
Pro Inflammatory Cytokines

Abstract Objectives The incidence of inflammatory bowel disease is increasing in newly developing countries, mainly awing to the westernization of the society. Consumption of high-fat diet has known to aggravate colitis. Omega-3 fatty acids are known to have several health benefits including anti-inflammatory effects and some studies have reported the effect of fish oil in experimental colitis. Perilla oil is obtained from the seeds of Perilla frutescens and is known to exert protective effects against obesity, inflammation and hepatic steatosis. We have previously shown that perilla oil has a similar effect like fish oil in high-fat diet induced colon inflammation. In this study, we wanted to investigate the effect fish oil and perilla oil on high-fat-fed, dextran sodium sulfate (DSS)-induced colitis in mice. Methods Six weeks old mice were divided into 4 groups; normal diet without DSS administration (ND), and three high-fat diet with DSS groups; control (HD + DSS), with fish oil supplementation (HDFO+DSS), with perilla oil supplementation (HDPO+DSS). The mice were fed with high-fat diet for 5 weeks prior to DSS administration by water for one week. The mice were sacrificed on the 7th day of DSS administration. Colon length and macroscopic score were measured. The levels of pro-inflammatory cytokines in serum were measured. The stools of the mice were collected for microbial analysis. Results The levels of pro-inflammatory cytokines such as TNF-α, IL-6 and IL-1β were significantly reduced in FO and PO supplemented groups compared to HD + DSS. The colon length was reduced due to DSS administration compared to ND, and supplementation with FO and PO improved colon length and macroscopic score. Number of Enterobacteriaceae was higher in all DSS administered groups. However, FO and PO treated groups had significantly reduced Enterobacteriaceae. Conclusions The results of this study showed that fish oil and perilla oil exert protective effect against high-fat diet fed DSS-induced colitis. Both fish oil and perilla oil action on colon protection is similar. The experiments to confirm the mechanism of action which includes mRNA and protein analysis are ongoing. Funding Sources This work was supported by the National Research Foundation of Korea (NRF) grant funded by the Korea government (Ministry of Education).

scholarly journals Effects of Distinct n-6 to n-3 Polyunsaturated Fatty Acid Rations on Insulin Resistant and AD-like Phenotypes in High-Fat Diets-Fed APP/PS1 Transgenic Mice

2021 ◽  
Author(s):  
Xiaojun Ma ◽  
Yujie Guo ◽  
Pengfei Li ◽  
Jingjing Xu ◽  
Shengqi Dong ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Fatty Acid ◽  
Protein Expression ◽  
Signaling Pathway ◽  
Inflammatory Cytokines ◽  
Insulin Signaling ◽  
High Fat Diet ◽  
High Fat ◽  
Pufa Ratio ◽  
Pro Inflammatory Cytokines

Abstract Background: Type 2 diabetes mellitus (T2DM) and Alzheimer’s disease (AD) are two prevalent diseases with comparable pathophysiological features and genetic predisposition. Polyunsaturated fatty acids (PUFAs) are essential in maintaining normal brain function. However, little is known about the impact of dietary n-6/n-3 PUFA ratio on AD-like pathology, especially in high-fat diet (HFD)-fed AD model mice. Methods: In the present study, the APP/PS1 mice were treated with 60% HFD for 3.5 months to induced insulin resistance. After that, 45% HFD with different n-6/n-3 PUFA ratios (n-6/n-3=1:1, 5:1 or 16:1) was applied for additional 3.5 months treatment. Following the dietary intervention, the behavior of mice was observed using the Water maze. Following behavioral testing, the animals were euthanized, and serum and tissue samples were collected for biochemical, histological and pathological analyses and evaluation. Cortical fatty acid profile was measured by gas chromatography. Western Blot and immunohistochemistry methods were used to detect protein expression of molecules related to AD pathology and insulin signaling pathway(s) in the brain sample tissues. Immunofluorescence assay was used to uncover the expression and migration of NF-κB in the cortex. qPCR method was applied to determine the gene expression of cortical pro-inflammatory cytokines.Results: HFD caused insulin resistance, increased serum IL-6 and TNF-α level, elevated cortical soluble Aβ1-40, Aβ1-42 content, and increased brain n-6/n-3 PUFAs ratio in APP/PS1 mice. Increased APP and BACE1 protein expression and p-IR/IR ratio, but decreased pro-inflammatory cytokines mRNA expression was observed in the cortex from 60% HFD-fed APP/PS1 mice. N-3 PUFAs rich diet (n-6/n-3=1:1) relieved insulin resistance and hyperlipidemia induced by 60% HFD. Cortical soluble Aβ1-40 and Aβ1-42 contents, the expression of cortical APP, GLUT3, insulin metabolism related molecules, and NF-κB pathway downstream pro-inflammatory cytokines showed a dietary n-6/n-3 PUFAs ratio-dependent way, indicating that dietary n-6/n-3 PUFA ratio plays a critical role in modifying the responses of serum inflammatory cytokine, AD pathology, cortical n-6/n-3 PUFAs ratio, insulin signaling and neuroinflammation to HFD treatment.Conclusion: Dietary n-6/n-3 PUFA ratio play an important role in modifying AD pathophysiology, insulin signaling pathway, and neuro-inflammation response to high fat diet treatment in brain.

scholarly journals MEK6 Overexpression Exacerbates Fat Accumulation and Inflammatory Cytokines in High-Fat Diet-Induced Obesity

2021 ◽  
Vol 22 (24) ◽  
pp. 13559
Author(s):  
Suyeon Lee ◽  
Myoungsook Lee
Keyword(s):  
Adipose Tissue ◽  
Inflammatory Cytokines ◽  
High Fat Diet ◽  
Liver Lipid ◽  
Mapk Signaling ◽  
Chow Diet ◽  
High Fat ◽  
Fat Accumulation ◽  
Diet Induced Obesity ◽  
Lipid Formation

Obesity is a state of abnormal fat accumulation caused by an energy imbalance potentially caused by changes in multiple factors. MEK6 engages in cell growth, such as inflammation and apoptosis, as one of the MAPK signaling pathways. The MEK6 gene was found to be related to RMR, a gene associated with obesity. Because only a few studies have investigated the correlation between MEK6 and obesity or the relevant mechanisms, we conducted an experiment using a TgMEK6 model with MEK6 overexpression with non-Tg and chow diet as the control to determine changes in lipid metabolism in plasma, liver, and adipose tissue after a 15-week high-fat diet (HFD). MEK6 overexpression in the TgMEK6 model significantly increased body weight and plasma triglyceride and total cholesterol levels. p38 activity declined in the liver and adipose tissues and lowered lipolysis, oxidation, and thermogenesis levels, contributing to decreased energy consumption. In the liver, lipid formation and accumulation increased, and in adipose, adipogenesis and hypertrophy increased. The adiponectin/leptin ratio significantly declined in plasma and adipose tissue of the TgMEK6 group following MEK6 expression and the HFD, indicating the role of MEK6 expression in adipokine regulation. Plasma and bone-marrow-derived macrophages (BMDM) of the TgMEK6 group increased MEK6 expression-dependent secretion of pro-inflammatory cytokines but decreased levels of anti-inflammatory cytokines, further exacerbating the results exhibited by the diet-induced obesity group. In conclusion, this study demonstrated the synergistic effect of MEK6 with HFD in fat accumulation by significantly inhibiting the mechanisms of lipolysis in the adipose and M2 associated cytokines secretion in the BMDM.

Abstract 61: Adipose Tissue Specific HO-1 Induction Regulates the Crosstalk between Wnt and β-catenin Pathways and Leads to Restoration of Vascular Endothelial Function in Mice Fed a High Fat Diet

Hypertension ◽  
2012 ◽  
Vol 60 (suppl_1) ◽  
Author(s):  
Jian Cao ◽  
Stephen J Peterson ◽  
Michal L Schwartzman ◽  
Komal Sodhi ◽  
Rita Rezzani ◽  
...  
Keyword(s):  
Insulin Sensitivity ◽  
Inflammatory Cytokines ◽  
High Fat Diet ◽  
Vascular Function ◽  
Vascular Dysfunction ◽  
Subcutaneous Fat ◽  
Heme Oxygenase 1 ◽  
High Fat ◽  
Diet Induced Obesity ◽  
Intracardiac Injection

The principal goal of the present study is to examine the contributions of adipocyte specific over expression of the cytoprotective gene heme oxygenase-1 (HO-1) in modulating vascular function in an animal model of diet induced obesity. A lentiviral construct of the human HO-1 was synthesized under the control of an aP2-activated promoter so as to ensure HO-1 targeting to murine adipocytes. Lentiviruses (50 μl, 2x109 TU/ml in saline) were injected into the C57BL/6 mice by a single intracardiac injection. Mice (6-7 wks old) were divided into 4 groups: Control, high fat diet (HF) mice receiving the control Lenti-aP2-GFP (HF-GFP) and high fat diet mice receiving the lenti-aP2-HO-1 (HF-HO-1) with and without treatment with SnMP. Transduction of lenti-aP2-HO-1 increased human HO-1 expression in adipose tissues without affecting endogenous mice HO-1 (p<0.01). In mice fed a HF diet, lenti-aP2-HO-1 transduction attenuated the increases in body weight (from 52.0±1.0 g to 35.6±2.1g; p<0.01), blood glucose (from 255±3.5 g to 140±2.9mg/dl), blood pressure (from 135±2.8mmHg to 101±2.2mmHg; p<0.01) and inflammatory cytokines as well as the content of both visceral (from 5.5±0.15g to 2.9±0.22g; p<0.05) and subcutaneous fat (p<0.05). Transduction of lenti-aP2-HO-1 increased the numbers of adipocytes of small cell size (p<0.05), insulin sensitivity (p<0.05), adiponectin levels (from 32.4±1.9μg/ml to 19.9±2.1μg/ml; p<0.05) as well as vascular relaxation to acetylcholine ( p<0.05) compared to HF mice administered the lenti-aP2- GFP. Adipocytes of mice fed a HF diet expressed high levels of PPARγ, aP2, C/EBP and Wnt5b proteins and displayed marked increases in Peg1/Mest (p<0.03). Lenti-aP2-HO-1 transduction lowered the elevated levels of these proteins and increased Shh, Wnt10b and β-catenin (p<0.05). Inhibition of HO activity by administration of tin mesoporphyrin (SnMP) to HF-fed mice transduced with the lenti-aP2-HO-1 reversed the decrease in Peg 1/Mest, TNFα and MCP-1 levels. This novel study demonstrate that adipocyte-specific overexpression of HO-1 attenuates HF-mediated adiposity and vascular dysfunction, increases insulin sensitivity and improves adipocyte function by increasing adiponectin, Shh and WNT10b and decreasing inflammatory cytokines.

scholarly journals Dietary choline supplementation attenuated high-fat diet-induced inflammation through regulation of lipid metabolism and suppression of NFκB activation in juvenile black seabream (Acanthopagrus schlegelii)

2019 ◽  
Vol 8 ◽  
Author(s):  
Min Jin ◽  
Tingting Pan ◽  
Douglas R. Tocher ◽  
Mónica B. Betancor ◽  
Óscar Monroig ◽  
...  
Keyword(s):  
Lipid Metabolism ◽  
Inflammatory Cytokines ◽  
High Fat Diet ◽  
Sea Bream ◽  
Lipid Lowering ◽  
Whole Body ◽  
High Fat ◽  
Acanthopagrus Schlegelii ◽  
Dietary Choline ◽  
Pro Inflammatory Cytokines

Abstract The present study aimed to investigate whether dietary choline can regulate lipid metabolism and suppress NFκB activation and, consequently, attenuate inflammation induced by a high-fat diet in black sea bream (Acanthopagrus schlegelii). An 8-week feeding trial was conducted on fish with an initial weight of 8·16 ± 0·01 g. Five diets were formulated: control, low-fat diet (11 %); HFD, high-fat diet (17 %); and HFD supplemented with graded levels of choline (3, 6 or 12 g/kg) termed HFD + C1, HFD + C2 and HFD + C3, respectively. Dietary choline decreased lipid content in whole body and tissues. Highest TAG and cholesterol concentrations in serum and liver were recorded in fish fed the HFD. Similarly, compared with fish fed the HFD, dietary choline reduced vacuolar fat drops and ameliorated HFD-induced pathological changes in liver. Expression of genes of lipolysis pathways were up-regulated, and genes of lipogenesis down-regulated, by dietary choline compared with fish fed the HFD. Expression of nfκb and pro-inflammatory cytokines in liver and intestine was suppressed by choline supplementation, whereas expression of anti-inflammatory cytokines was promoted in fish fed choline-supplemented diets. In fish that received lipopolysaccharide to stimulate inflammatory responses, the expression of nfκb and pro-inflammatory cytokines in liver, intestine and kidney were all down-regulated by dietary choline compared with the HFD. Overall, the present study indicated that dietary choline had a lipid-lowering effect, which could protect the liver by regulating intrahepatic lipid metabolism, reducing lipid droplet accumulation and suppressing NFκB activation, consequently attenuating HFD-induced inflammation in A. schlegelii.

scholarly journals Green Tea Polyphenol (−)-Epigallocatechin Gallate (EGCG) Attenuates Neuroinflammation in Palmitic Acid-Stimulated BV-2 Microglia and High-Fat Diet-Induced Obese Mice

2019 ◽  
Vol 20 (20) ◽  
pp. 5081 ◽  
Author(s):  
Limin Mao ◽  
Danielle Hochstetter ◽  
Liyun Yao ◽  
Yueling Zhao ◽  
Jihong Zhou ◽  
...  
Keyword(s):  
Palmitic Acid ◽  
Inflammatory Cytokines ◽  
High Fat Diet ◽  
Epigallocatechin Gallate ◽  
Janus Kinase ◽  
Obese Mice ◽  
High Fat ◽  
Stat3 Signaling ◽  
Green Tea Polyphenol ◽  
Pro Inflammatory Cytokines

Obesity is closely associated with neuroinflammation in the hypothalamus, which is characterized by over-activated microglia and excessive production of pro-inflammatory cytokines. The present study was aimed at elucidating the effects of (−)-epigallocatechin gallate (EGCG) on palmitic acid-stimulated BV-2 microglia and high-fat-diet-induced obese mice. The results indicated the suppressive effect of EGCG on lipid accumulation, pro-inflammatory cytokines (TNF-α, IL-6, and IL-1β) release, and microglial activation in both cellular and high-fat-diet rodent models. These results were associated with lower phosphorylated levels of the janus kinase 2/signal transducers and activators of transcription 3 (JAK2/STAT3) signaling pathway. In conclusion, EGCG can attenuate high-fat-induced hypothalamic inflammation via inhibiting the JAK2/STAT3 signaling pathways in microglia.

Sign in / Sign up

Export Citation Format

Share Document