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Obesity is closely associated with non-alcoholic fatty liver disease (NAFLD), characterized by hepatic fat accumulation and hepatocyte injury. Preclinical studies have shown exacerbated weight gain associated with an obesogenic gluten-containing diet. However, whether gluten affects obesity-induced hepatic lipid accumulation still remains unclear. We hypothesized that gluten intake could affect fatty liver development in high-fat diet (HFD)-induced obese mice. Thus, we aimed to investigate the impact of gluten intake on NAFLD in HFD-induced obese mice. Male apolipoprotein E-deficient (Apoe-/-) mice were fed with a HFD containing (GD) or not (GFD) vital wheat gluten (4.5%) for 10 weeks. Blood and liver were collected for further analysis. We found that gluten exacerbated weight gain, hepatic fat deposition, and hyperglycemia without affecting the serum lipid profile. Livers of the GD group showed a larger area of fibrosis, associated with the expression of collagen and MMP9, and higher expression of apoptosis-related factors, p53, p21, and caspase-3. The expression of lipogenic factors, such as PPARγ and Acc1, was more elevated and factors related to beta-oxidation, such as PPARα and Cpt1, were lower in the GD group compared to the GFD. Further, gluten intake induced a more significant expression of Cd36, suggesting higher uptake of free fatty acids. Finally, we found lower protein expression of PGC1α followed by lower activation of AMPK. Our data show that gluten-containing high-fat diet exacerbated NAFLD by affecting lipogenesis and fatty acid oxidation in obese Apoe-/- mice through a mechanism involving lower activation of AMPK., (© 2023. The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature.)

The damaging effects of obesity extend to multiple pre-existing tissue/organs. However, the influence of this condition on key components (inflammation and angiogenesis) of fibrovascular connective proliferating tissue, essential in repair processes, has been neglected. Our objective in this study was to investigate whether obesity would influence inflammatory-angiogenesis induced by synthetic matrix of polyether-polyurethane implanted subcutaneously in high-fat-fed obese C57/BL6 mice. Fourteen days after implantation, the inflammatory and angiogenic components of the newly formed tissue intra-implant were evaluated. The pro-inflammatory enzyme activities, myeloperoxidase (MPO) and N-acetyl-β-D-glucosaminidase (NAG), the levels of TNF-α, CXCL1/KC and CCL2 and NF-κB transcription factor were examined. Angiogenesis was determined by morphometric analysis of implant blood vessels, intra-implant levels of hemoglobin content, VEGF levels, and western blot for VEGFR2. All inflammatory and angiogenic markers were increased in the implants of obese mice compared with their non-obese counterparts. Similarly, activation of the NF-κB pathway and phosphorylation of VEGFR2 were higher in implants of obese mice (1.60 ± 0.28 Np65/Cp65; 0.96 ± 0.08 p-VEGFR2/VEGFR2-T) compared with implants of non-obese animals (1.40 ± 0.14; 0.49 ± 0.08). These observations suggest that obesity exerts critical role in sponge-induced inflammatory-angiogenesis, possibly by activating fibrovascular components in the inflamed microenvironment. Thus, this pathological condition causes damage not only to pre-existing tissues/organs but also to newly formed proliferating fibrovascular tissue. This is relevant to the development of therapeutic approaches to improve healing processes in patients with obesity., Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2020 Elsevier Inc. All rights reserved.)

Associations between obesity, diabetes type II, and steatosis have long been recognized. However, a pharmacotherapy that acts in a multifactorial manner controlling the interactions between these conditions is not available. A variety of natural plants, functional fatty acids, and other natural dietary compounds have been used in various anti-obesity products. We investigated the effects of oral administration of an antioxidant carotenoid pigment Bixin and Bixin: β-Cyclodextrin in an obese murine model. C57BL/6 male mice (4-5 weeks) received standard diet (2.18 kcal per 1 g) (CT) and high-fat diet (4.38 kcal per 1 g) (CT/OB, BIX and BIX/βCD) (n = 10 per group). After 16 weeks, the BIX and BIX/βCD were treated by gavage (100 μL day-1) for six weeks, with water (CT and CT/OB groups) and (50 mg kg-1 day-1), Bixin (BIX group) or Bix: β-CD (BIX/βCD). Body weight, Lee's Index, adiposity, CHT, TG, CHT/HDL-c, glucose levels (metabolic markers) and, liver markers (AST and ALT) were determined. All metabolic and liver parameters exhibited down-regulation after oral administration of BIX and BIX/βCD. Particularly relevant was Lee's Index and adiposity in BIX- and BIX/βCD-treated groups (339.18 g/cm -BIX and 327.58 g/cm -BIX/βCD vs. 360.68 g/cm -CT/OB animals), this finds associated with the insulin sensitivity test, showed a clear association between reduction of adipose tissue and decrease of peripherical insulin resistant. In conclusion, our study suggested that the oral administration of the Bixin and Bix: β-CD inclusion compound improved the metabolic parameters evaluate in obese mice, being more palatable and hepatoprotective., (Copyright © 2018. Published by Elsevier Masson SAS.)

Objective: Obesity is a highly prevalent multifactorial metabolic condition in which the need for functional bioengineered substitutes (e.g., scaffolds for tissue engineering) is likely to occur. However, the adverse foreign body response (FBR) that invariably takes place adjacent to implant devices impairing their function is poorly characterized in this condition. This study investigated the influence of obesity on the host response to a synthetic matrix implanted subcutaneously in high-fat-fed obese mice.Methods: Histological analysis of 14-day-old implants was performed to identify collagen deposition, capsule thickness, fibroblast-like cells, foreign body giant cells, and mast cells. In addition, transforming growth factor β1 (TGF-β1) levels in the implants and serum were determined.Results: All fibrogenic markers (and TGF-β1 levels) increased in the implants of obese mice compared with their nonobese counterparts. Particularly relevant was the fibrous capsule thickness in implants of obese mice (234.2 ± 22.1 µm vs. 109.2 ± 13.4 µm in implants of nonobese animals).Conclusions: The study results showing that obesity upregulates the main features of the FBR induced by subcutaneous implants in mice may be relevant in understanding biomaterial integration and performance in this condition. This is crucial to the development of strategies to maintain the integrity and function of implantable devices. [ABSTRACT FROM AUTHOR]