Diet induced obesity has an influence on intrahepatic T cell responses

Gaur, Pratibha; Cebula, Marcin; Riehn, Mathias; Hillebrand, Upneet; Hauser, Hansjörg; Wirth, Dagmar

doi:10.1016/j.metabol.2017.01.022

Cited by 5 publications

(6 citation statements)

References 17 publications

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“…Pathway analysis showed an inflammation mediated response through chemokine and cytokine signalling as well as T cell activation. Indeed, T cells play an important role in liver diseases [41,42]. However, this module was not significantly (p = 0.5) correlated with maternal diet, meaning that this cluster of genes would be showing the same expression pattern, regardless of maternal diet.…”

Section: Discussionmentioning

confidence: 95%

Maternal dietary resistant starch does not improve piglet’s gut and liver metabolism when challenged with a high fat diet

et al. 2020

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Background: In the past several years, the use of resistant starch (RS) as prebiotic has extensively been studied in pigs, and this mostly in the critical period around weaning. RS is believed to exert beneficial effects on the gastrointestinal tract mainly due to higher levels of short chain fatty acids (SCFAs) and an improved microbiota profile. In this study, sows were fed digestible starch (DS) or RS during late gestation and lactation and the possible maternal effect of RS on the overall health of the progeny was assessed. Since RS is also described to have a positive effect on metabolism, and to investigate a metabolic programming of the progeny, half of the piglets per maternal diet were assigned to a high fat diet from weaning on to 10 weeks after. Results: No bodyweight differences were found between the four experimental piglet groups. The high fat diet did however impact back fat thickness and meat percentage whereas maternal diet did not influence these parameters. The impact of the high fat diet was also reflected in higher levels of serum cholesterol. No major differences in microbiota could be distinguished, although higher levels of SCFA were seen in the colon of piglets born from RS fed sows, and some differences in SCFA production were observed in the caecum, mainly due to piglet diet. RNAsequencing on liver and colon scrapings revealed minor differences between the maternal diet groups. Merely a handful of genes was differentially expressed between piglets from DS and RS sows, and network analysis showed only one significant cluster of genes in the liver due to the maternal diet that did not point to meaningful biological pathways. However, the high fat diet resulted in liver gene clusters that were significantly correlated with piglet diet, of which one is annotated for lipid metabolic processes. These clusters were not correlated with maternal diet. Conclusions: There is only a minor impact of maternal dietary RS on the progeny, reflected in SCFA changes. A high fat diet given to the progeny directly evokes metabolic changes in the liver, without any maternal programming by a RS diet.

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Section: Discussionmentioning

confidence: 95%

Maternal dietary resistant starch does not improve piglet’s gut and liver metabolism when challenged with a high fat diet

et al. 2020

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“…A study by Gaur et al using a mouse model to investigate the impact of obesity on T cells in the liver demonstrated a reduction in antigen clearance capacity in obese mice in the setting of autoimmunity. [ 3 ] It also showed that obesity affects T cell function and increases the severity of AIH. [ 3 ] With the above-mentioned link between obesity and inflammation in the setting of inflammatory liver damage in AIH, we hypothesized that the liver-related complications would be mitigated upon significant weight loss by BS in a reduced inflammatory state.…”

Section: Discussionmentioning

confidence: 99%

“…[ 3 ] It also showed that obesity affects T cell function and increases the severity of AIH. [ 3 ] With the above-mentioned link between obesity and inflammation in the setting of inflammatory liver damage in AIH, we hypothesized that the liver-related complications would be mitigated upon significant weight loss by BS in a reduced inflammatory state. Although there was reduced in-patient mortality associated with BS, potentially due to improvement of fibrosis by BS-induced weight loss, the prevalence of ascites and hepatic encephalopathy was higher in the BS group compared to the control group.…”

Section: Discussionmentioning

confidence: 99%

“…Obesity leads to a low-grade systemic inflammatory state with impaired immune cell functions, altered lymphocyte numbers, and dysregulated cytokine profiles. [ 3 ] In previous studies, such as a study by Kral et al [ 4 ] , weight loss induced by bariatric surgery (BS) in severely obese patients reduced the inflammatory state, and liver fibrosis. In addition to its contribution to systemic inflammatory states, obesity has also been shown to affect T cell function and increase the severity of AIH without significantly reducing the acute T cell response.…”

Section: Introductionmentioning

confidence: 99%

“…In addition to its contribution to systemic inflammatory states, obesity has also been shown to affect T cell function and increase the severity of AIH without significantly reducing the acute T cell response. [ 3 ]…”

Section: Introductionmentioning

confidence: 99%

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The impact of bariatric surgery on in-patient clinical outcomes among patients with autoimmune hepatitis

et al. 2020

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Autoimmune hepatitis (AIH) is a form of liver inflammation in which immune cells target hepatocytes, inducing chronic inflammatory states. Bariatric surgery (BS) was shown to reduce inflammation in severely obese patients. We hypothesize that obese patients with AIH and BS have lower prevalence of liver-related complications and in-patient mortality compared to those without BS. The National Inpatient Sample from 2007 to 2013 was queried for hospitalizations of adults over 18 years of age with a diagnosis of AIH. Of those, hospitalizations with BS were selected as cases and those with morbid obesity as controls. Case-control 1:2 matching was done based on sex, age, race, and comorbidities. Primary outcomes were prevalence of liver-related complications and in-patient mortality. Independent risk factors of in-patient clinical outcomes were identified using multivariate regression analysis. From 137,834 hospitalizations with a diagnosis of AIH, 688 with BS were selected as cases, and 1295 were matched as controls. The prevalence of ascites was higher in the BS group compared to the control (odds ratio 1.73, 95% confidence interval (CI) 1.27–2.36). The prevalence of cirrhosis (36.8% vs 33.2%), portal hypertension (7.4% vs 10.0%), hepatic encephalopathy (10.6% vs 8.7%), and varices and variceal bleeding (3.9% vs 5.5%) was not statistically different from case controls, ( P > .05). BS was an independent risk factor for ascites (adjusted odds ratio (aOR) 1.87; 95% CI 1.36–2.56) and hepatic encephalopathy (aOR 1.42; 95% CI 1.03–1.97) but was an independent protective factor against in-patient mortality (aOR 0.21, 95% CI 0.08–0.55) once adjusted for age, sex, race, and comorbidities.

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Defective interferon amplification and impaired host responses against influenza virus in obese mice

Gaur

Riehn

Zha

et al. 2021

Obesity

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Objective Obesity is a major risk factor that increases morbidity and mortality upon infection. Although type I and type III interferon (IFN)‐induced innate immune responses represent the first line of defense against viral infections, their functionality in the context of metabolic disorders remains largely obscure. This study aimed to investigate IFN responses upon respiratory viral infection in obese mice. Methods The activation of IFNs as well as IFN regulatory factors (IRFs) upon H3N2 influenza infection in mice upon high‐fat‐diet feeding was investigated. Results Influenza infection of obese mice was characterized by higher mortalities. In‐depth analysis revealed impaired induction of both type I and type III IFNs as well as markedly reduced IFN responses. Notably, it was found that IRF7 gene expression in obese animals was reduced in homeostasis, and its induction by the virus was strongly attenuated. Conclusions The results suggest that the attenuated IRF7 expression and induction are responsible for the reduced expression levels of type I and III IFNs and, thus, for the higher susceptibility and severity of respiratory infections in obese mice.

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Diet induced obesity has an influence on intrahepatic T cell responses

Cited by 5 publications

References 17 publications

Maternal dietary resistant starch does not improve piglet’s gut and liver metabolism when challenged with a high fat diet

Maternal dietary resistant starch does not improve piglet’s gut and liver metabolism when challenged with a high fat diet

The impact of bariatric surgery on in-patient clinical outcomes among patients with autoimmune hepatitis

Defective interferon amplification and impaired host responses against influenza virus in obese mice

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