Gut-liver axis modulation in fructose-fed mice: a role for PPAR-alpha and linagliptin

2020 ◽  
Vol 247 (1) ◽  
pp. 11-24
Author(s):  
Flávia Maria Silva-Veiga ◽  
Carolline Santos Miranda ◽  
Fabiane Ferreira Martins ◽  
Julio Beltrame Daleprane ◽  
Carlos Alberto Mandarim-de-Lacerda ◽  
...  
Keyword(s):  
Hepatic Steatosis ◽  
Glucose Intolerance ◽  
Control Diet ◽  
Intestinal Barrier ◽  
Mice Model ◽  
Ppar Alpha ◽  
Beneficial Effects ◽  
Hepatic Energy Metabolism ◽  
High Fructose ◽  
Alpha Agonist

Fructose dietary intake affects the composition of the intestinal microbiota and influences the development of hepatic steatosis. Endotoxins produced by gram-negative bacteria alter intestinal permeability and cause bacterial translocation. This study evaluated the effects of gut microbiota modulation by a purified PPAR-alpha agonist (WY14643), a DPP-4 inhibitor (linagliptin), or their association on intestinal barrier integrity, endotoxemia, and hepatic energy metabolism in high-fructose-fed C57BL/6 mice. Fifty mice were divided to receive the control diet (C group) or the high-fructose diet (HFRU) for 12 weeks. Subsequently, the HFRU group was divided to initiate the treatment with PPAR-alpha agonist (3.5 mg/kg/BM) and DPP-4 inhibitor (15 mg/kg/BM). The HFRU group had glucose intolerance, endotoxemia, and dysbiosis (with increased Proteobacteria) without changes in body mass in comparison with the C group. HFRU group showed damaged intestinal ultrastructure, which led to liver inflammation and marked hepatic steatosis in the HFRU group when compared to the C group. PPAR-alpha activation and DPP-4 inhibition countered glucose intolerance, endotoxemia, and dysbiosis, ameliorating the ultrastructure of the intestinal barrier and reducing Tlr4 expression in the liver of treated animals. These beneficial effects suppressed lipogenesis and mitigated hepatic steatosis. In conclusion, the results herein propose a role for PPAR-alpha activation, DPP-4 inhibition, and their association in attenuating hepatic steatosis by gut-liver axis modulation in high-fructose mice model. These observations suggest these treatments as potential targets to treat hepatic steatosis and avoid its progression.

scholarly journals Dietary Purple Potato Supplementation Ameliorates Gut Inflammation and Associated Colitis

2021 ◽  
Vol 5 (Supplement_2) ◽  
pp. 535-535
Author(s):  
Shima Bibi ◽  
Yansong Xue ◽  
Yang He ◽  
Min Du ◽  
Boon Chew ◽  
...  
Keyword(s):  
Control Diet ◽  
Goblet Cells ◽  
Protective Effects ◽  
Mice Model ◽  
Differentiation Markers ◽  
Beneficial Effects ◽  
Funding Sources ◽  
Epithelial Structure ◽  
Biochemical Analyses ◽  
Deficient Mice

Abstract Objectives The incidence of inflammatory bowel disease (IBD) is rapidly increasing worldwide. Patients with IBD experience increased susceptibility to colorectal cancer and are associated with morbidity and mortality. Diets are known factors associated with IBD. This study examined the beneficial effects of dietary purple potato against spontaneous colitis and improving gut microbiota in interleukin (IL)-10-deficient mice, a commonly used IBD mice model. Methods IL-10-deficient mice at 7-week-old were assigned to a standard rodent diet (CON) or a control diet supplemented with 10% purple potato (dry feed weight) for 11 weeks, when colonic tissues were collected for histological and biochemical analyses. Results Purple potato supplementation had no effect on feed intake and body weight in IL-10-deficient mice during the 11-week feeding trial. Purple potato supplementation improved the colitis symptom and the integrity of the colonic epithelial structure with reduced inflammation and pathological scores. Furthermore, the density of goblet cells and differentiation markers for goblet cells was enhanced due to PP supplementation. Conclusions Data collectively showed that dietary purple potato supplementation had protective effects against colitis onset in IL-10-deficient mice and improved gut epithelial structure, providing a promising dietary approach for the management and prevention of colitis. Funding Sources USDA-NIFA and Northwest Potato Research Consortium.

Beneficial effects of maternal swimming during pregnancy on offspring metabolism when the father is obese

2018 ◽  
Vol 10 (4) ◽  
pp. 502-506 ◽  
Author(s):  
R. Tarevnic ◽  
F. Ornellas ◽  
C. A. Mandarim-de-Lacerda ◽  
M. B. Aguila
Keyword(s):  
Body Size ◽  
Exercise Training ◽  
Glucose Intolerance ◽  
High Fat Diet ◽  
Control Diet ◽  
High Fat ◽  
Beneficial Effects ◽  
Maternal Exercise ◽  
The Impact ◽  
Old Mice

AbstractWe aimed to evaluate the impact of maternal exercise training on the offspring metabolism and body size caused by father obesity. C57BL/6 male 4-week-old mice were fed a high-fat diet (HF father) or control diet (C father), while equal age female mice were fed only a C diet and were separated into two groups: trained (T mother) and non-trained (NT mother), and at 12 weeks of age mice were mated. A continuous swimming protocol was applied for 10 weeks (before and during gestation), and offspring were followed since weaning until sacrifice (at 12 weeks of age). HF father, compared to C father, showed obesity, elevated total cholesterol (TC) and triglycerides (TG), and glucose intolerance. Both sexes HF/NT offspring showed hyperglycemia, glucose intolerance and high levels of TC and TG, without obesity. However, HF/T offspring showed data close to C/NT, demonstrating the beneficial effect of maternal exercise in the offspring of obese fathers.

scholarly journals Fortifying Butterfat with Soybean Oil Attenuates the Onset of Diet-Induced Non-Alcoholic Steatohepatitis and Glucose Intolerance

Nutrients ◽  
2021 ◽  
Vol 13 (3) ◽  
pp. 959
Author(s):  
Victor Sánchez ◽  
Annette Brandt ◽  
Cheng Jun Jin ◽  
Dragana Rajcic ◽  
Anna Janina Engstler ◽  
...  
Keyword(s):  
Soybean Oil ◽  
Mrna Expression ◽  
Glucose Intolerance ◽  
Barrier Function ◽  
Control Diet ◽  
Saturated Fatty Acids ◽  
Interleukin 1 ◽  
Intestinal Barrier ◽  
Intestinal Barrier Function ◽  
Alcoholic Steatohepatitis

The addition of plant oils such as soybean oil (S) to a diet rich in saturated fatty acids is discussed as a possible route to prevent or diminish the development of metabolic disease. Here, we assessed whether a butterfat-rich diet fortified with S affects the development of early non-alcoholic steatohepatitis (NASH) and glucose intolerance. Female C57BL/6J mice were fed a standard-control diet (C); a fat-, fructose-, and cholesterol-rich diet (FFC, 25E% butterfat, 50% (wt./wt.) fructose, 0.16% (wt./wt.) cholesterol); or FFC supplemented with S (FFC + S, 21E% butterfat + 4E% S) for 13 weeks. Indicators of liver damage, inflammation, intestinal barrier function, and glucose metabolism were measured. Lipopolysaccharide (LPS)-challenged J774A.1 cells were incubated with linolenic and linoleic acids (ratio 1:7.1, equivalent to S). The development of early NASH and glucose intolerance was significantly attenuated in FFC + S–fed mice compared to FFC-fed mice associated with lower hepatic toll-like receptor-4 mRNA expression, while markers of intestinal barrier function were significantly higher than in C-fed mice. Linolenic and linoleic acid significantly attenuated LPS-induced formation of reactive nitrogen species and interleukin-1 beta mRNA expression in J774A.1 cells. Our results indicate that fortifying butterfat with S may attenuate the development of NASH and glucose intolerance in mice.

Beneficial effects of the ketogenic diet on glucose intolerance and hepatic lipid accumulation in obese mice model

2021 ◽  
Vol 46 ◽  
pp. S583-S584
Author(s):  
A. Charlot ◽  
A.-L. Charles ◽  
I. Georg ◽  
F. Goupilleau ◽  
L. Debrut ◽  
...  
Keyword(s):  
Ketogenic Diet ◽  
Glucose Intolerance ◽  
Lipid Accumulation ◽  
Obese Mice ◽  
Mice Model ◽  
Hepatic Lipid ◽  
Hepatic Lipid Accumulation ◽  
Beneficial Effects

scholarly journals Dietary Interventions to Prevent High Fructose Diet-associated Worsening of Colitis and Colitis-associated Tumorigenesis in Mice

2021 ◽  
Author(s):  
Ryohei Nishiguchi ◽  
Srijani Basu ◽  
Hannah A Staab ◽  
Naotake Ito ◽  
Xi Kathy Zhou ◽  
...  
Keyword(s):  
Gut Microbiota ◽  
Control Diet ◽  
Experimental Colitis ◽  
Protective Effects ◽  
Diet Change ◽  
Chronic Colitis ◽  
Acute Colitis ◽  
High Fructose Diet ◽  
High Consumption ◽  
High Fructose

Abstract Diet is believed to be an important factor in the pathogenesis of Inflammatory Bowel Disease. High consumption of dietary fructose has been shown to exacerbate experimental colitis, an effect mediated through the gut microbiota. This study evaluated whether dietary alterations could attenuate the detrimental effects of a high fructose diet (HFrD) in experimental colitis. First, we determined whether the pro-colitic effects of a HFrD could be reversed by switching mice from a HFrD to a control diet. This diet change completely prevented HFrD-induced worsening of acute colitis, in association with a rapid normalization of the microbiota. Second, we tested the effects of dietary fiber, which demonstrated that psyllium was the most effective type of fiber for protecting against HFrD-induced worsening of acute colitis, compared to pectin, inulin or cellulose. In fact, supplemental psyllium nearly completely prevented the detrimental effects of the HFrD, an effect associated with a shift in the gut microbiota. We next determined whether the protective effects of these interventions could be extended to chronic colitis and colitis-associated tumorigenesis. Using the azoxymethane/dextran sodium sulfate model, we first demonstrated that HFrD feeding exacerbated chronic colitis and increased colitis-associated tumorigenesis. Using the same dietary changes tested in the acute colitis setting, we also showed that mice were protected from HFrD-mediated enhanced chronic colitis and tumorigenesis, upon either diet switching or psyllium supplementation. Taken together, these findings suggest that high consumption of fructose may enhance colon tumorigenesis associated with long-standing colitis, an effect that could be reduced by dietary alterations.

scholarly journals Protective Role of Natural and Semi-Synthetic Tocopherols on TNFα-Induced ROS Production and ICAM-1 and Cl-2 Expression in HT29 Intestinal Epithelial Cells

Antioxidants ◽  
2021 ◽  
Vol 10 (2) ◽  
pp. 160
Author(s):  
Vladana Domazetovic ◽  
Irene Falsetti ◽  
Caterina Viglianisi ◽  
Kristian Vasa ◽  
Cinzia Aurilia ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Antioxidant Properties ◽  
Intestinal Barrier ◽  
Protective Role ◽  
Intercellular Adhesion Molecule ◽  
Intestinal Epithelial ◽  
Intercellular Adhesion Molecule 1 ◽  
Beneficial Effects ◽  
Bowel Diseases

Vitamin E, a fat-soluble compound, possesses both antioxidant and non-antioxidant properties. In this study we evaluated, in intestinal HT29 cells, the role of natural tocopherols, α-Toc and δ-Toc, and two semi-synthetic derivatives, namely bis-δ-Toc sulfide (δ-Toc)2S and bis-δ-Toc disulfide (δ-Toc)2S2, on TNFα-induced oxidative stress, and intercellular adhesion molecule-1 (ICAM-1) and claudin-2 (Cl-2) expression. The role of tocopherols was compared to that of N-acetylcysteine (NAC), an antioxidant precursor of glutathione synthesis. The results show that all tocopherol containing derivatives used, prevented TNFα-induced oxidative stress and the increase of ICAM-1 and Cl-2 expression, and that (δ-Toc)2S and (δ-Toc)2S2 are more effective than δ-Toc and α-Toc. The beneficial effects demonstrated were due to tocopherol antioxidant properties, but suppression of TNFα-induced Cl-2 expression seems not only to be related with antioxidant ability. Indeed, while ICAM-1 expression is strongly related to the intracellular redox state, Cl-2 expression is TNFα-up-regulated by both redox and non-redox dependent mechanisms. Since ICAM-1 and Cl-2 increase intestinal bowel diseases, and cause excessive recruitment of immune cells and alteration of the intestinal barrier, natural and, above all, semi-synthetic tocopherols may have a potential role as a therapeutic support against intestinal chronic inflammation, in which TNFα represents an important proinflammatory mediator.

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