Shifting to a control diet after a high-fat, high-sucrose diet intake induces epigenetic changes in retroperitoneal adipocytes of Wistar rats

Astaxanthin n-octanoic acid diester (AOD) is a type of astaxanthin connecting medium-chain fatty acids with a more stable structure. In this study, we examined the role of AOD in ameliorating insulin resistance (IR) induced by a high-fat and high-sucrose diet (HFD) as well as its effect on modulating gut microbiota in mice, with free astaxanthin (AST) as a comparison. Four groups of male C57BL/6J mice (6 weeks old; n = 10 per group) were fed with a normal control diet (NC), HFD orally administered with AOD, AST (50 mg/kg body weight), or vehicle for 8 weeks. AOD improved glucose tolerance, IR, systematic and intestinal inflammation, and intestinal integrity better than AST. Further, both AOD and AST modulated gut microbiota. A significantly higher abundance of Bacteroides and Coprococcus was found in AOD than in AST, and the predicted pathway of carbohydrate metabolism was significantly impacted by AOD. Overall, AOD may play a role in alleviating IR and inflammation with the modulating effect on microbiota in HFD-fed mice. Our findings could facilitate the development of AOD as a bioactive nutraceutical and more stable alternative to AST.

Download Full-text

Modulation of methotrexate-induced intestinal mucosal injury by dietary factors

Human & Experimental Toxicology ◽

10.1177/0960327119896605 ◽

2019 ◽

Vol 39 (4) ◽

pp. 500-513

Author(s):

T Higuchi ◽

M Yoshimura ◽

S Oka ◽

K Tanaka ◽

T Naito ◽

...

Keyword(s):

Control Diet ◽

Survival Rates ◽

Mucosal Injury ◽

Dietary Factors ◽

Gastrointestinal Disorders ◽

High Fat ◽

Sucrose Diet ◽

Intestinal Mucosal Injury ◽

High Sucrose Diet ◽

High Sucrose

Methotrexate (MTX)-induced intestinal mucosal injury in animals has been studied to understand how MTX can cause gastrointestinal disorders, but the pathogenesis of gastrointestinal disorders is still uncertain. We have attempted to reveal how dietary factors influence intestinal toxicity due to MTX. Mice were fed normal chow (NC) or a high-fat high-sucrose diet (HFHSD) before oral administration of MTX. While MTX significantly decreased the survival rates of mice fed HFHSD, the intestinal epithelial injury was detected. MTX excretion in the feces of mice fed HFHSD was reduced. Change of diets between NC and HFHSD influences the survival. The survival rates of the mice fed a high-sucrose diet or control diet were higher than those fed HFHSD. Higher survival rates were observed in mice fed a high-fat high-sucrose diet modified (HFHSD-M) in which casein was replaced by soybean-derived proteins. The survival rates of mice treated with vancomycin were lower than those administered neomycin. Microbiome and metabolome analyses on feces suggest a similarity of the intestinal environments of mice fed NC and HFHSD-M. HFHSD may modify MTX-induced toxicity in intestinal epithelia on account of an altered MTX distribution as a result of change in the intestinal environment.

Download Full-text

Effect of Beilschmedia obscura on the prevention of high fat/high sucrose diet induced metabolic syndrome on male Albino Wistar rats

Metabolism Open ◽

10.1016/j.metop.2021.100156 ◽

2021 ◽

pp. 100156

Author(s):

Florine Essouman Mbappe ◽

Ferdinand Lanvin Edoun Ebouel ◽

Fils Armand Ella ◽

Bruno Dupon Ambamba Akamba ◽

Jules Kamga Nanhah ◽

...

Keyword(s):

Metabolic Syndrome ◽

Wistar Rats ◽

High Fat ◽

Sucrose Diet ◽

High Sucrose Diet ◽

High Sucrose

Download Full-text

Replacing SNAP-25b with SNAP-25a expression results in metabolic disease

Proceedings of the National Academy of Sciences ◽

10.1073/pnas.1511951112 ◽

2015 ◽

Vol 112 (31) ◽

pp. E4326-E4335 ◽

Cited By ~ 20

Author(s):

Ismael Valladolid-Acebes ◽

Teresa Daraio ◽

Kerstin Brismar ◽

Tibor Harkany ◽

Sven Ove Ögren ◽

...

Keyword(s):

Metabolic Disease ◽

Splice Variants ◽

Control Diet ◽

Liver Steatosis ◽

Snare Complex ◽

High Fat ◽

Sucrose Diet ◽

High Sucrose Diet ◽

High Sucrose ◽

Deficient Mice

Synaptosomal-associated protein of 25 kDa (SNAP-25) is a key molecule in the soluble N-ethylmaleimide–sensitive factor attachment protein (SNARE) complex mediating fast Ca2+-triggered release of hormones and neurotransmitters, and both splice variants, SNAP-25a and SNAP-25b, can participate in this process. Here we explore the hypothesis that minor alterations in the machinery mediating regulated membrane fusion can increase the susceptibility for metabolic disease and precede obesity and type 2 diabetes. Thus, we used a mouse mutant engineered to express normal levels of SNAP-25 but only SNAP-25a. These SNAP-25b–deficient mice were exposed to either a control or a high-fat/high-sucrose diet. Monitoring of food intake, body weight, hypothalamic function, and lipid and glucose homeostases showed that SNAP-25b–deficient mice fed with control diet developed hyperglycemia, liver steatosis, and adipocyte hypertrophy, conditions dramatically exacerbated when combined with the high-fat/high-sucrose diet. Thus, modified SNARE function regulating stimulus-dependent exocytosis can increase the vulnerability to and even provoke metabolic disease. When combined with a high-fat/high-sucrose diet, this vulnerability resulted in diabesity. Our SNAP-25b–deficient mouse may represent a diabesity model.

Download Full-text