A maternal high-fat diet may accelerate adipo-immunologic aging in offspring

Imai, Atsushi; Fujimoto, Eka; Tamura, Kaho; Utsuyama, Masanori; Sato, Kazuto

doi:10.1016/j.lfs.2019.01.008

Cited by 6 publications

(3 citation statements)

References 27 publications

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“…30 Accelerated ageing was also evident in female mouse offspring of dams fed a HFD from one week pre-mating: offspring were heavier as adults (12 weeks) but reached their maximum weight sooner and lost relatively more fat mass with further ageing when compared to offspring of control-fed dams. 31 They also showed increased prevalence of senescence-associated T cells as well as hepatic inflammation and fibrosis at 70 weeks of age, 31 indicative of immunological ageing. In another study of maternal overfeeding, increased fur thinning and markers of osteoporosis were indicative of accelerated ageing in female offspring of HFD-fed mice.…”

Section: Cardiovascular Diseasementioning

confidence: 99%

Developmental programming by maternal obesity: Lessons from animal models

Schoonejans

Ozanne

2021

Diabet Med

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Section: Cardiovascular Diseasementioning

confidence: 99%

Developmental programming by maternal obesity: Lessons from animal models

Schoonejans

Ozanne

2021

Diabet Med

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“…In addition, animal model studies have also shed light on the mechanisms that drove this linkage [9]. Studies in rodent models have suggested that offspring of obese mothers respond worse to bacterial infection and experimentally induced autoimmunity [10][11][12][13].…”

Section: Introductionmentioning

confidence: 99%

Maternal Obesity and Kawasaki Disease-like Vasculitis: A New Perspective on Cardiovascular Injury and Inflammatory Response in Offspring Male Mice

Zheng,

Wang,

Huo

et al. 2023

Nutrients

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Maternal obesity affects the risk of cardiovascular disease and inflammatory response in offspring. However, the impact of maternal obesity on offspring with Kawasaki disease (KD), the leading cause of childhood acquired heart disease, is still an understudied area. This study aimed to elucidate the impact of maternal obesity on offspring in KD-like vasculitis and the underlying mechanisms. Offspring of obese female mice and normal diet dams were randomly divided into two subgroups. The pups were injected intraperitoneally with either Candida albicans water-soluble fraction (CAWS) or phosphate buffered saline (PBS) to establish the obesity (OB)-CAWS group, OB group, wild type (WT)-CAWS group, and WT group. Their weight was monitored during the study. After four weeks, echocardiography was applied to obtain the alternation of cardiac structures. Mouse cytokine panel, Hematoxylin-Eosin (HE) staining, western blot, and real-time qPCR were used to study the pathological changes and protein and RNA expression alternations. Based on the study of pathology, serology and molecular biology, maternal obesity lead to more severe vasculitis and induced altered cardiac structure in the offspring mice and promoted the expression of pro-inflammatory cytokines through activating the NF-κB signaling pathway. Maternal obesity aggravated the inflammatory response of offspring mice in KD-like vasculitis.

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“…While epidemiological studies in humans are limited in their ability to separate the effects of maternal obesity from those of the maternal diet on fetal development, some evidence suggests that a maternal high-fat diet (HFD) increases the likelihood of obesity in the offspring irrespective of maternal weight (3) . Animal models using maternal HFD have shown a range of effects on the offspring such as altered lung development and function (4) , metabolic disorders (5) and adipoimmunological ageing (6) . We have previously shown that maternal obesity leads to long-term changes in vascular function in mice (7) but whether maternal exposure to a HFD alters immune regulation in the offspring through fatty acid dysregulation remains unknown.…”

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confidence: 99%

Maternal high-fat diet in mice alters immune regulation and lung function in the offspring

et al. 2020

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Polyunsaturated fatty acids (PUFA) modulate immune function and have been associated with risk of childhood atopy and asthma. We investigated the effect of maternal fat intake in mice on PUFA status, elongase and desaturase gene expression, inflammatory markers and lung function in the offspring. C57BL/6J mice (n=32) were fed either standard chow (C, 21% kcal fat) or a high fat diet (HFD, 45% kcal fat) for 4 weeks prior to conception and during gestation and lactation. At 21 days of age, offspring were weaned onto either the HFD or C, generating four experimental groups: C/C, C/HF, HF/C and HF/HF. Plasma and liver fatty acid composition were measured by gas chromatography and gene expression by qPCR. Lung resistance to methacholine was assessed. Arachidonic acid concentrations in offspring plasma and liver phospholipids were increased by HFD; this effect was greater in the post-natal HFD group. Docosahexaenoic acid concentration in offspring liver phospholipids was increased in response to HFD and was higher in the post-natal HFD group. Post-natal HFD increased hepatic FADS2 and ELOVL5 expression in male offspring, whereas maternal HFD elevated expression of FADS1 and FADS2 in female offspring comparing to males. Post-natal HFD increased expression of IL-6 and CCL2 in perivascular adipose tissue. The HFD lowered lung resistance to methacholine. Excessive maternal fat intake during development modifies hepatic PUFA status in offspring through regulation of gene expression of enzymes that are involved in PUFA biosynthesis and modifies the development of the offspring lungs leading to respiratory dysfunction.

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A maternal high-fat diet may accelerate adipo-immunologic aging in offspring

Cited by 6 publications

References 27 publications

Developmental programming by maternal obesity: Lessons from animal models

Developmental programming by maternal obesity: Lessons from animal models

Maternal Obesity and Kawasaki Disease-like Vasculitis: A New Perspective on Cardiovascular Injury and Inflammatory Response in Offspring Male Mice

Maternal high-fat diet in mice alters immune regulation and lung function in the offspring

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