The combination of maternal and offspring high-fat diets causes marked oxidative stress and development of metabolic syndrome in mouse offspring

Polyphenols extracted from Shanxi-aged vinegar (SAVEP) can alleviate oxidative stress and inflammatory stress caused by high-fat diets, improving intestinal microbial disorders. SAVEP may be a novel treatment of the metabolic syndrome.

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Resveratrol toxicity: Effects on risk factors for atherosclerosis and hepatic oxidative stress in standard and high-fat diets

Food and Chemical Toxicology ◽

10.1016/j.fct.2009.03.010 ◽

2009 ◽

Vol 47 (6) ◽

pp. 1362-1367 ◽

Cited By ~ 71

Author(s):

K.K.R. Rocha ◽

G.A. Souza ◽

G.X. Ebaid ◽

F.R.F. Seiva ◽

A.C. Cataneo ◽

...

Keyword(s):

Oxidative Stress ◽

Risk Factors ◽

High Fat ◽

Hepatic Oxidative Stress ◽

High Fat Diets ◽

Fat Diets ◽

Toxicity Effects

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Changing the paradigm for myoglobin: a novel link between lipids and myoglobin

Journal of Applied Physiology ◽

10.1152/japplphysiol.00973.2013 ◽

2014 ◽

Vol 117 (3) ◽

pp. 307-315 ◽

Cited By ~ 9

Author(s):

Amber E. Schlater ◽

Michael A. De Miranda ◽

Melinda A. Frye ◽

Stephen J. Trumble ◽

Shane B. Kanatous

Keyword(s):

Oxidative Stress ◽

Nitric Oxide ◽

Tissue Sample ◽

Oxidative Stress Marker ◽

Oxygen Binding ◽

High Fat ◽

Western Blots ◽

High Fat Diets ◽

Lipid Supplementation ◽

Fat Diets

Myoglobin (Mb) is an oxygen-binding muscular hemeprotein regulated via Ca2+-signaling pathways involving calcineurin (CN), with Mb increases attributed to hypoxia, exercise, and nitric oxide. Here, we show a link between lipid supplementation and increased Mb in skeletal muscle. C2C12 cells were cultured in normoxia or hypoxia with glucose or 5% lipid. Mb assays revealed that lipid cohorts had higher Mb than control cohorts in both normoxia and hypoxia, whereas Mb Western blots showed lipid cohorts having higher Mb than control cohorts exclusively under hypoxia. Normoxic cells were compared with soleus tissue from normoxic rats fed high-fat diets; whereas tissue sample cohorts showed no difference in CO-binding Mb, fat-fed rats showed increases in total Mb protein (similar to hypoxic cells), suggesting increases in modified Mb. Moreover, Mb increases did not parallel CN increases but did, however, parallel oxidative stress marker augmentation. Addition of antioxidant prevented Mb increases in lipid-supplemented normoxic cells and mitigated Mb increases in lipid-supplemented hypoxic cells, suggesting a pathway for Mb regulation through redox signaling independent of CN.

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The interconnection of high-fat diets, oxidative stress, the heart, and carcinogenesis

Cancer ◽

10.1016/b978-0-12-819547-5.00011-0 ◽

2021 ◽

pp. 111-120

Author(s):

Bianka Bojková ◽

Natalia Kurhaluk ◽

Pawel J. Winklewski

Keyword(s):

Oxidative Stress ◽

High Fat ◽

High Fat Diets ◽

Fat Diets

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The Combination of Mulberry Extracts and Silk Amino Acids Alleviated High Fat Diet-Induced Nonalcoholic Hepatic Steatosis by Improving Hepatic Insulin Signaling and Normalizing Gut Microbiome Dysbiosis in Rats

Evidence-based Complementary and Alternative Medicine ◽

10.1155/2019/8063121 ◽

2019 ◽

Vol 2019 ◽

pp. 1-17 ◽

Cited By ~ 1

Author(s):

Sunmin Park ◽

Ting Zhang ◽

Jing Yi Qiu ◽

Xuangao Wu

Keyword(s):

Oxidative Stress ◽

Amino Acids ◽

Disease Control ◽

Normal Control ◽

Insulin Signaling ◽

High Fat ◽

Hepatic Insulin Signaling ◽

High Fat Diets ◽

Fat Diets ◽

Better Than

Mulberry water extracts (MB) and silk amino acids (SA) are reported to improve oxidative stress and inflammation, respectively. We hypothesized whether the mixture of mulberry water extracts and silk amino acids can alleviate nonalcoholic fatty liver disease (NAFLD) induced by high fat diets. Male Sprague Dawley rats were orally provided with high fat diets containing different ratios of MB and SA (1:3, MS1:3, or 1:5, MS1:5) or cellulose (the disease-control) for 12 weeks. Rats had 200 or 600 mg/kg bw of MS1:3 and MS1:5 (MS1:3-L, MS1:3-H; MS1:5-L, and MS1:5-H). Rats in the normal-control group were fed the 20% fat diet with cellulose. Disease-control rats exhibited much greater triglyceride (TG) deposition in the liver than the normal-control rats along with increased body weight gain, visceral fat mass, serum concentrations of cholesterol, triglyceride and nonesterified fatty acid (NEFA), and insulin resistance. Disease-control rats also had liver damage with increased oxidative stress and inflammation compared to the normal-control rats. MS1:3-H and MS1:5-H were found to have greater hepatic glycogen accumulation and decreased hepatic TG, insulin resistance, and dyslipidemia, with MS1:5-H being similar to the normal-control. MS1:3-H alleviated oxidative stress with lower hepatic lipid peroxide compared to MS1:5-H whereas MS1:5-H ameliorated inflammation and hepatocyte damage better than MS1:3-H. Both MS1:3-H and MS1:5-H potentiated hepatic insulin signaling (pAkt⟶pACC) and reduced the mRNA expression of TG synthesis genes mRNA (FAS and SREBP-1c). In the gut microbiome MS1:3-H elevated the ratio of Bacteroidales to Clostridiales in the cecum better than MS1:5-H but MS1:5-H reduced the proinflammatory Turicibacterales. In conclusion, both MS1:3-H and MS1:5-H prevented liver damage induced by high fat diets, mainly by suppressing oxidative stress and inflammation, respectively. MS1:3 and MS1:5 might be used as therapeutic agent for NAFLD.

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Metabolic imprinting: critical impact of the perinatal environment on the regulation of energy homeostasis

Philosophical Transactions of the Royal Society B Biological Sciences ◽

10.1098/rstb.2006.1851 ◽

2006 ◽

Vol 361 (1471) ◽

pp. 1107-1121 ◽

Cited By ~ 145

Author(s):

Barry E Levin

Keyword(s):

Metabolic Syndrome ◽

Energy Homeostasis ◽

Perinatal Period ◽

Neural Pathways ◽

High Fat ◽

Maternal Undernutrition ◽

The Metabolic Syndrome ◽

Obesity And Diabetes ◽

High Fat Diets ◽

Fat Diets

Epidemiological studies in humans suggest that maternal undernutrition, obesity and diabetes during gestation and lactation can all produce obesity in offspring. Animal models have allowed us to investigate the independent consequences of altering the pre- versus post-natal environments on a variety of metabolic, physiological and neuroendocrine functions as they effect the development in the offspring of obesity, diabetes, hypertension and hyperlipidemia (the ‘metabolic syndrome’). During gestation, maternal malnutrition, obesity, type 1 and type 2 diabetes and psychological, immunological and pharmacological stressors can all promote offspring obesity. Normal post-natal nutrition can reduce the adverse impact of some of these pre-natal factors but maternal high-fat diets, diabetes and increased neonatal access to food all enhance the development of obesity and the metabolic syndrome in offspring. The outcome of these perturbations of the perinatal environmental is also highly dependent upon the genetic background of the individual. Those with an obesity-prone genotype are more likely to be affected by factors such as maternal obesity and high-fat diets than are obesity-resistant individuals. Many perinatal manipulations appear to promote offspring obesity by permanently altering the development of central neural pathways, which regulate food intake, energy expenditure and storage. Given their strong neurotrophic properties, either excess or an absence of insulin and leptin during the perinatal period are likely to be effectors of these developmental changes. Because obesity is associated with an increased morbidity and mortality and because of its resistance to treatment, prevention is likely to be the best strategy for stemming the tide of the obesity epidemic. Such prevention should begin in the perinatal period with the identification and avoidance of factors which produce permanent, adverse alterations in neural pathways which control energy homeostasis.

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