Immunologic and metabolic effects of high-refined carbohydrate-containing diet in food allergic mice

Yamada, Letícia Tamie Paiva; Oliveira, Marina C.; Batista, Nathália Vieira; Fonseca, Roberta Cristelli; Pereira, Rafaela Vaz Sousa; Perez, Denise; Teixeira, Mauro Martins; Cara, Denise Carmona; Ferreira, Adaliene Versiani Matos

doi:10.1016/j.nut.2015.08.011

Cited by 6 publications

(2 citation statements)

References 36 publications

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“…There is evidence supporting that Th1 cytokines, including IFN-γ, play a key role in the immune-inflammatory pathophysiology of obesity (Svec et al, 2007;Strissel et al, 2010;Lee and Lee, 2014). This is reinforced by preclinical findings showing that genetically or diet-induced obese mice produce more pro-inflammatory cytokines, including IFN-γ and TNFα, than control mice (Kawanishi et al, 2010;Yamada et al, 2016;Zhou et al, 2015). Furthermore, administration of TNFα or IL-6 to pregnant rats results in considerable expansion of adipose tissue in their offspring and increased vulnerability to obesity (Dahlgren et al, 2001).…”

Section: Ido Activation and Increased Try Metabolism In Obesitymentioning

confidence: 99%

IDO chronic immune activation and tryptophan metabolic pathway: A potential pathophysiological link between depression and obesity

Filho

Lima

Vasconcelos

et al. 2018

Progress in Neuro-Psychopharmacology and Biological Psychiatry

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Obesity and depression are among the most pressing health problems in the contemporary world. Obesity and depression share a bidirectional relationship, whereby each condition increases the risk of the other. By inference, shared pathways may underpin the comorbidity between obesity and depression. Activation of cell-mediated immunity (CMI) is a key factor in the pathophysiology of depression. CMI cytokines, including IFN-γ, TNFα and IL-1β, induce the catabolism of tryptophan (TRY) by stimulating indoleamine 2,3-dioxygenase (IDO) resulting in the synthesis of kynurenine (KYN) and other tryptophan catabolites (TRYCATs). In the CNS, TRYCATs have been related to oxidative damage, inflammation, mitochondrial dysfunction, cytotoxicity, excitotoxicity, neurotoxicity and lowered neuroplasticity. The pathophysiology of obesity is also associated with a state of aberrant inflammation that activates aryl hydrocarbon receptor (AHR), a pathway involved in the detection of intracellular or environmental changes as well as with increases in the production of TRYCATs, being KYN an agonists of AHR. Both AHR and TRYCATS are involved in obesity and related metabolic disorders. These changes in the TRYCAT pathway may contribute to the onset of neuropsychiatric symptoms in obesity. This paper reviews the role of immune activation, IDO stimulation and increased TRYCAT production in the pathophysiology of depression and obesity. Here we suggest that increased synthesis of detrimental TRYCATs is implicated in comorbid obesity and depression and is a new drug target to treat both diseases.

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Section: Ido Activation and Increased Try Metabolism In Obesitymentioning

confidence: 99%

IDO chronic immune activation and tryptophan metabolic pathway: A potential pathophysiological link between depression and obesity

Filho

Lima

Vasconcelos

et al. 2018

Progress in Neuro-Psychopharmacology and Biological Psychiatry

View full text Add to dashboard Cite

show abstract

“…Emerging epidemiological evidence suggests a positive association between lipid metabolism disorder and the risk of allergic diseases. , High-fat diets (HFD) alter gut microbiota composition because saturated fats and cholesterol induce intestinal epithelial cells to release inflammatory mediators, thereby increasing intestinal permeability. − Inflammation of the intestinal tract is a sign of food allergy . The development of obesity is a detrimental consequence resulting from prolonged consumption of a high-fat diet (HFD), which can be attributed to the compromised integrity of the intestinal barrier. − The pro-inflammatory status observed in obese persons and disruption of the gastrointestinal barrier caused by HFD could explain the association between obesity and food allergies.…”

Section: Discussionmentioning

confidence: 99%

Cow’s Milk Allergy May Induce Lipid Metabolism Disorder in BALB/c Mice via Exosomes

Ma,

Xia,

Gong

et al. 2024

J. Agric. Food Chem.

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Allergic diseases and lipid-metabolism-disorder-derived diseases are both significant public health issues. Recent studies have shown that exosomes are associated with the course of allergic diseases and are involved in lipid metabolism. In this study, exosomes derived from cow's milk allergic (CMA) mice medially loaded lesser proteins favoring cholesterol metabolism. The levels of total cholesterol (TC) and low-density lipoprotein cholesterol (LDL-c) in the serum were increased in the CMA mice, and hepatic lipid deposition was observed in the liver, but these phenomena were improved by inhibiting the exosome release. Specifically, the higher expression of the sterol regulatory element binding factor 2 (SREBP2) protein and HMGCR gene in the liver of CMA mice indicated an increase in cholesterol synthesis. NPC1L1 was also highly expressed in the small intestine of CMA mice, and fecal TC level was decreased, suggesting that the reabsorption of cholesterol was elevated. The biosynthesis of cholesterol, the reverse cholesterol transport (RCT) process, and the synthesis of bile acid in the liver were improved by inhibiting exosome release, as well as the reabsorption of cholesterol in the small intestine. This study has for the first time demonstrated the lipid metabolism disorder caused by CMA, especially the important role of exosomes in food allergies and lipid metabolism.

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Exploring diet-induced promoter hypomethylation and PDK4 overexpression: implications for type 2 diabetes mellitus

Putra,

Humardani,

Mulyanata

et al. 2023

Mol Biol Rep

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Immunologic and metabolic effects of high-refined carbohydrate-containing diet in food allergic mice

Cited by 6 publications

References 36 publications

IDO chronic immune activation and tryptophan metabolic pathway: A potential pathophysiological link between depression and obesity

IDO chronic immune activation and tryptophan metabolic pathway: A potential pathophysiological link between depression and obesity

Cow’s Milk Allergy May Induce Lipid Metabolism Disorder in BALB/c Mice via Exosomes

Exploring diet-induced promoter hypomethylation and PDK4 overexpression: implications for type 2 diabetes mellitus

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