The role of oxidative stress and inflammatory response in high-fat diet induced peripheral neuropathy

Objective. For patients with severe acute pancreatitis (SAP), a high body mass index (BMI) increases the possibility of infection derived from the intestine. In this study, we evaluate whether TAK242 can alleviate severe acute pancreatitis-associated injury of intestinal barrier in high-fat diet-fed rats. Methods. A SAP model was established by retrograde injection of 5% sodium taurocholate into the biliary-pancreatic duct. Thirty Sprague-Dawley (SD) adult rats were randomly divided into five groups: standard rat chow (SRC) normal (SN), SRC SAP (SAP), high-fat diet normal (HN), HFD SAP (HSAP), and TLR4 inhibitor pretreatment HFD SAP (HAPT) groups. Intraperitoneal injection of 3 mg/kg TAK242 was administered 30 minutes before SAP model establishment in the HAPT group. Rats were sacrificed 12 hours after SAP modeling, followed by blood and pancreatic and distal ileum tissue collection for further analyses. Changes in the pathology responses of the rats in each group were assessed. Result. Analyses of serum amylase, lipase, cholesterol, triglyceride, IL-1β, IL-6, DAO, and serum endotoxin as well as tight junction protein expression including zonula occluden-1 and occludin indicated that high-fat diet aggravated SAP-induced intestinal barrier injury via increasing inflammatory response. In addition, the level of necroptosis was significantly higher in the SAP group compared with the SN group while the HSAP group exhibited more necroptosis compared with the SAP group, indicating the important role of necroptosis in pancreatitis-associated gut injury and illustrating that high-fat diet aggravated necroptosis of the ileum. Pretreatment with TLR4 inhibitor significantly alleviated inflammatory response and reduced necroptosis and level of oxidative stress while improving intestinal barrier function. Conclusion. High-fat diet aggravated SAP-induced intestinal barrier injury via inflammatory reactions, necroptosis, and oxidative stress. Inhibition of TLR4 by TAK242 reduced inflammation, alleviated necroptosis, and lowered the level of oxidative stress and then protected the intestinal barrier dysfunction from SAP in high-fat diet-fed rats.

Download Full-text

Every-other day fasting prevents memory impairment induced by high fat-diet: Role of oxidative stress

Physiology & Behavior ◽

10.1016/j.physbeh.2020.113263 ◽

2021 ◽

Vol 229 ◽

pp. 113263

Author(s):

Karem H. Alzoubi ◽

Omar F. Khabour ◽

Rafat M Al-Awad ◽

Zainah O. Aburashed

Keyword(s):

Oxidative Stress ◽

High Fat Diet ◽

Memory Impairment ◽

High Fat

Download Full-text

Long term effects of high fat diet given early in life in prenatally stressed rats: role of the inflammatory response

European Neuropsychopharmacology ◽

10.1016/j.euroneuro.2018.11.366 ◽

2019 ◽

Vol 29 ◽

pp. S225-S226

Author(s):

M. Mazzelli ◽

N. Cattane ◽

C. Mora ◽

V. Begni ◽

A. Berry ◽

...

Keyword(s):

Inflammatory Response ◽

High Fat Diet ◽

Long Term Effects ◽

High Fat ◽

Prenatally Stressed

Download Full-text

Role of Supplementary Selenium on the Induction of Insulin Resistance and Oxidative Stress in NSY Mice Fed a High Fat Diet

Biological and Pharmaceutical Bulletin ◽

10.1248/bpb.b17-00622 ◽

2018 ◽

Vol 41 (1) ◽

pp. 92-98 ◽

Cited By ~ 4

Author(s):

Koichi Murano ◽

Hirofumi Ogino ◽

Tomofumi Okuno ◽

Tomohiro Arakawa ◽

Hitoshi Ueno

Keyword(s):

Oxidative Stress ◽

Insulin Resistance ◽

High Fat Diet ◽

High Fat ◽

And Oxidative Stress

Download Full-text

The high-fat diet induces myocardial fibrosis in the metabolically healthy obese minipigs—The role of ER stress and oxidative stress

Clinical Nutrition ◽

10.1016/j.clnu.2016.06.002 ◽

2017 ◽

Vol 36 (3) ◽

pp. 760-767 ◽

Cited By ~ 14

Author(s):

Sin-Jin Li ◽

Chia-Hsin Liu ◽

Hsien-Pin Chu ◽

Harry J. Mersmann ◽

Shih-Torng Ding ◽

...

Keyword(s):

Oxidative Stress ◽

Er Stress ◽

Myocardial Fibrosis ◽

High Fat Diet ◽

High Fat ◽

Metabolically Healthy Obese ◽

Healthy Obese ◽

Metabolically Healthy ◽

And Oxidative Stress

Download Full-text

Pretreatment with n-6 PUFA protects against subsequent high fat diet induced atherosclerosis—Potential role of oxidative stress-induced antioxidant defense

Atherosclerosis ◽

10.1016/j.atherosclerosis.2011.10.001 ◽

2012 ◽

Vol 220 (1) ◽

pp. 53-58 ◽

Cited By ~ 18

Author(s):

M. Penumetcha ◽

M. Song ◽

N. Merchant ◽

S. Parthasarathy

Keyword(s):

Oxidative Stress ◽

High Fat Diet ◽

Antioxidant Defense ◽

Potential Role ◽

High Fat

Download Full-text

Effect of Acute Ingestion of Green Tea Extract and Lemon Juice on Oxidative Stress and Lipid Profile in Pigs Fed a High-Fat Diet

Antioxidants ◽

10.3390/antiox8060195 ◽

2019 ◽

Vol 8 (6) ◽

pp. 195 ◽

Cited By ~ 4

Author(s):

Xi Fang ◽

Michael Azain ◽

Kristi Crowe-White ◽

Jennifer Mumaw ◽

Janet A. Grimes ◽

...

Keyword(s):

Oxidative Stress ◽

Single Dose ◽

Lipid Profile ◽

Green Tea ◽

High Fat Diet ◽

Lemon Juice ◽

Green Tea Extract ◽

High Fat ◽

Tea Extract

Green tea and its catechins have been shown to ameliorate high fat diet-induced oxidative stress and hyperlipidemia. However, low bioavailability of catechins limits their therapeutic potential. Lemon juice (LJ) has been suggested to enhance the bioavailability of catechins in vitro. This study investigated the antioxidative and hypolipidemic efficacy of a single dose of green tea extract (GTE) or GTE plus LJ (GTE + LJ) in high-fat diet fed pigs. Sixteen pigs ingested a single dose of GTE (190 mg/kg/day) or GTE + LJ (0.75 mL/kg/day) mixed with low-fat (LF; 5% fat) or high-fat (HF; 22% fat) diets and blood samples were collected for 24 h. Plasma catechin level peaked at two hours, and gradually returned to baseline after six hours following the intake. The addition of LJ significantly increased plasma catechin level. The diet containing GTE did not lower plasma cholesterol and triacylglycerol (TG) concentrations, superoxide dismutase (SOD) and catalase activity, or malondialdehyde concentration in 24 h in HF-fed pigs. Addition of a single dose of LJ, however, significantly decreased plasma TG level in LF groups but did not cause further changes on any other markers compared to the GTE alone. Our findings indicate limited effect of a single meal containing GTE on plasma antioxidant enzymes, lipid profile, and lipid peroxidation in pigs and no significant synergistic/additive action of adding LJ to GTE within 24 h in pigs. A study with a longer treatment period is warranted to further understand the potential role of GTE in reducing HF diet-induced oxidative stress and the possible synergistic role of LJ.

Download Full-text

Role of sigma 1 receptor in high fat diet-induced peripheral neuropathy

Biological Chemistry ◽

10.1515/hsz-2017-0117 ◽

2017 ◽

Vol 398 (10) ◽

pp. 1141-1149 ◽

Cited By ~ 2

Author(s):

Tieying Song ◽

Jianhui Zhao ◽

Xiaojing Ma ◽

Zaiwang Zhang ◽

Bo Jiang ◽

...

Keyword(s):

Spinal Cord ◽

Peripheral Neuropathy ◽

High Fat Diet ◽

Tactile Allodynia ◽

Wild Type ◽

High Fat ◽

Sigma 1 Receptor ◽

Sigma 1 ◽

Nmdar Subunits

Abstract The neurobiological mechanisms of obesity-induced peripheral neuropathy are poorly understood. We evaluated the role of Sigma-1 receptor (Sig-1R) and NMDA receptor (NMDARs) in the spinal cord in peripheral neuropathy using an animal model of high fat diet-induced diabetes. We examined the expression of Sig-1R and NMDAR subunits GluN2A and GluN2B along with postsynaptic density protein 95 (PSD-95) in the spinal cord after 24-week HFD treatment in both wild-type and Sig-1R−/− mice. Finally, we examined the effects of repeated intrathecal administrations of selective Sig-1R antagonists BD1047 in HFD-fed wild-type mice on peripheral neuropathy. Wild-type mice developed tactile allodynia and thermal hypoalgesia after 24-week HFD treatment. HFD-induced peripheral neuropathy correlated with increased expression of GluN2A and GluN2B subunits of NMDARs, PDS-95, and Sig-1R, as well as increased Sig-1R-NMDAR interaction in the spinal cord. In contrast, Sig-1R−/− mice did not develop thermal hypoalgesia or tactile allodynia after 24-week HFD treatment, and the levels of GluN2A, GluN2B, and PSD-95 were not altered in the spinal cord of HFD-fed Sig-1R−/− mice. Finally, repeated intrathecal administrations of selective Sig-1R antagonists BD1047 in HFD-fed wild-type mice attenuated peripheral neuropathy. Our results suggest that obesity-associated peripheral neuropathy may involve Sig-1R-mediated enhancement of NMDAR expression in the spinal cord.

Download Full-text