Maternal High-fat Diet Accelerates Development of Crohnʼs Disease-like Ileitis in TNFΔARE/WT Offspring

Gruber, Lisa; Hemmerling, Jana; Schüppel, Valentina; Müller, Michael; Boekschoten, Mark V.; Haller, Dirk

doi:10.1097/mib.0000000000000465

Cited by 16 publications

(8 citation statements)

References 53 publications

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“…76 Exposure to maternal high-fat diet during gestation was similarly found to promote early ileitis onset and increase disease severity in TNFARE progeny as compared to control diet-exposed cohorts. 71 Enhanced inflammation and tissue damage in early adulthood was commensurate with increased mucosal neutrophil infiltration and proinflammatory cytokine expression, while TNF plasma levels were significantly correlated with portal vein endotoxemia and tissue pathology. Whether increased mucosal barrier permeability in this TNF-driven model results from aggravated intestinal injury or from a direct influence of maternal nutrition remains to be determined.…”

Section: Tumor Necrosis Factor (Tnf)mentioning

confidence: 96%

“…71 The impact of Westernized diet and maternal obesity on offspring metabolic and inflammatory status has been intensely investigated in mice 72 and a number of studies have now demonstrated a link between diet-induced obesity and perturbed intestinal immunity and barrier function. 73, 74 Maternal exposure to high-fat diet in the nonobese diabetic (NOD) mouse model correlates with altered offspring gut function, including enhanced intestinal permeability, increased oxidative stress and reduced goblet cell density.…”

Section: Tumor Necrosis Factor (Tnf)mentioning

confidence: 99%

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Inflammatory Bowel Disease

Glover

Fennimore

Wingfield

2016

Inflammatory Bowel Diseases

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The incidence and prevalence of inflammatory bowel disease (IBD) continues to rise with time, signifying its emergence as a global disease. Clinical onset of IBD, comprising Crohn’s disease and ulcerative colitis, typically occurs prior to or at peak reproductive age. Although active disease in female patients is associated with reduced fertility and adverse obstetric outcomes in pregnancy, the molecular mechanisms underlying this altered reproductive course, as well as its impact on IBD transmission to offspring, remain poorly understood. Clinical and experimental studies have now begun to elucidate the hormonal, environmental and microbial factors that modulate immune-reproductive crosstalk in IBD, and define their impact on maternal health, fetal development and heritability of disease risk. Evolving insight into maternal-fetal imprinting in IBD has important implications for patient counseling and disease management during pregnancy, and may help predict clinical outcomes for both mother and child.

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Section: Tumor Necrosis Factor (Tnf)mentioning

confidence: 96%

Section: Tumor Necrosis Factor (Tnf)mentioning

confidence: 99%

Inflammatory Bowel Disease

Glover

Fennimore

Wingfield

2016

Inflammatory Bowel Diseases

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“…Показано, что ожирение часто сопровождается активацией провоспалительных реакций, в связи с чем в плазме крови увеличивается концентрация специфических маркеров воспаления -С-реактивного белка, интерлейкина 6, фактора некроза опухоли альфа [50]. Потребление беременными большого количества насыщенных жиров увеличивает в их плазме концентрацию жирных кислот и способствует активации реакций хронического воспаления у потомства [51]. У таких матерей отмечены увеличение концентрации в крови триглицеридов, соединений, характерных для окислительного стресса, увеличение инсулинорезистентности, гипертензия и изменения функций эндотелия [52].…”

Section: повышенное питание матери и факторы риска развития кардиометunclassified

Maternal Nutrition and the Problem of Intrauterine Disease Programming in Children

et al. 2018

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Environmental conditions during perinatal development such as maternal undernutrition or overnutrition can program changes in the integration among physiological systems leading to cardio-metabolic diseases. This phenomenon can be understood in the context of the phenotypic plasticity and refers to the adjustment of a phenotype in response to environmental input without genetic change. Experimental studies indicate that fetal exposure to an adverse maternal environment may alter the morphology and physiology that contribute to the development of cardio-metabolic diseases. The significance and role of genetic polymorphism, markers of chronic inflammation, oxidative stress, endothelial dysfunction, leptin synthesis disruption, rennin-angiotensin system in intrauterine cardio-metabolic disease programming are discussed. The study demonstrated that both maternal protein restriction and overnutrition alter the central and peripheral control of arterial pressure and metabolism. Breastfeeding may have beneficial effect on obesity risk later in life in genetically predisposed groups. Understanding the mechanisms which affect health outcomes in the offspring influenced by the macronutrient composition of the maternal diet during pregnancy or lactation may lead to new maternal nutrition recommendations, disease prevention strategies, and therapies that reduce the increasing incidence of cardio-metabolic diseases in children and adults.

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“…Maternal HFD chronic consumption enhances the circulating free fatty acids and induce the activation of inflammatory pathways, enhancing chronic inflammation in offspring (Gruber et al, 2015). Studies of Roberts et al (2015) found that cardiometabolic dysfunction was associated with changes such as elevated serum triglycerides, elevated oxidative stress levels, insulin resistance, vascular disorders, and development of hypertension (Roberts et al, 2015).…”

Section: Maternal Overnutrition and Risk Factor For The Cardiometabolmentioning

confidence: 99%

Developmental Origins of Cardiometabolic Diseases: Role of the Maternal Diet

2016

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Developmental origins of cardiometabolic diseases have been related to maternal nutritional conditions. In this context, the rising incidence of arterial hypertension, diabetes type II, and dyslipidemia has been attributed to genetic programming. Besides, environmental conditions during perinatal development such as maternal undernutrition or overnutrition can program changes in the integration among physiological systems leading to cardiometabolic diseases. This phenomenon can be understood in the context of the phenotypic plasticity and refers to the adjustment of a phenotype in response to environmental input without genetic change, following a novel, or unusual input during development. Experimental studies indicate that fetal exposure to an adverse maternal environment may alter the morphology and physiology that contribute to the development of cardiometabolic diseases. It has been shown that both maternal protein restriction and overnutrition alter the central and peripheral control of arterial pressure and metabolism. This review will address the new concepts on the maternal diet induced-cardiometabolic diseases that include the potential role of the perinatal malnutrition.

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Maternal High-fat Diet Accelerates Development of Crohnʼs Disease-like Ileitis in TNFΔARE/WT Offspring

Abstract: Maternal HFD promotes the early onset of severe CD-like ileitis in genetically susceptible offspring independent of metabolic alterations.

Cited by 16 publications

References 53 publications

Inflammatory Bowel Disease

Inflammatory Bowel Disease

Maternal Nutrition and the Problem of Intrauterine Disease Programming in Children

Developmental Origins of Cardiometabolic Diseases: Role of the Maternal Diet

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