Maternal high-fat diets cause insulin resistance through inflammatory changes in fetal adipose tissue

Murabayashi, Nao; Sugiyama, Takashi; Zhang, L.; Kamimoto, Yuki; Umekawa, Takashi; Ma, Ning; Sagawa, Norimasa

doi:10.1016/j.ejogrb.2013.02.003

Cited by 99 publications

(93 citation statements)

References 25 publications

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“…Indeed, a greater percentage of large adipocytes associated with increased PPAR␥ were observed in adulthood, suggesting enhanced adipogenesis (102). In agreement with these findings, fetuses from obese mice fed a cafeteria diet before mating and throughout gestation exhibited larger adipocytes (83). A sheep model of maternal overfeeding during late gestation was also associated with higher WAT mass in the fetus with enhanced PPAR␥ and leptin mRNA expression levels sensitizing to postnatal adiposity (81,82).…”

Section: Malnourished Offspring Display Altered Adipogenesis and Fat supporting

confidence: 67%

“…Indeed, fetuses of obese mice fed a cafeteria diet before mating and throughout gestation exhibited an increase in several proinflammatory markers in adipose tissue, suggesting macrophage infiltration in WAT. The level of GLUT4 that mediates insulin-stimulated glucose uptake in WAT was decreased (83). Similarly, enlarged adipocytes of rat offspring reared in small litters displayed a postnatal induction of proinflammatory cytokine (i.e., TNF␣ and IL-6) mRNA expression levels that were exacerbated under a HF diet (14).…”

Section: Offspring Of Malnourished Mothers Exhibit a Loss Of Insulin mentioning

confidence: 98%

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Nutritional manipulations in the perinatal period program adipose tissue in offspring

Lukaszewski

Eberlé

Vieau

et al. 2013

American Journal of Physiology-Endocrinology and Metabolism

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Epidemiological studies demonstrated initially that maternal undernutrition results in low birth weight with increased risk for long-lasting energy balance disorders. Maternal obesity and diabetes associated with high birth weight, excessive nutrition in neonates, and rapid catchup growth also increase the risk of adult-onset obesity. As stated by the Developmental Origin of Health and Disease concept, nutrient supply perturbations in the fetus or neonate result in long-term programming of individual body weight set point. Adipose tissue is a key fuel storage unit involved mainly in the maintenance of energy homeostasis. Studies in numerous animal models have demonstrated that the adipose tissue is the focus of developmental programming events in a sex- and depot-specific manner. In rodents, adipose tissue development is particularly active during the perinatal period, especially during the last week of gestation and during early postnatal life. In contrast to rodents, this process essentially takes place before birth in bigger mammals. Despite these different developmental time windows, altricial and precocial species share several mechanisms of adipose tissue programming. Offspring from malnourished dams present adipose tissue with a series of alterations: impaired glucose uptake, insulin and leptin resistance, low-grade inflammation, modified sympathetic activity with reduced noradrenergic innervations, and thermogenesis. These modifications reprogram adipose tissue metabolism by changing fat distribution and composition and by enhancing adipogenesis, predisposing the offspring to fat accumulation. Subtle adipose tissue circadian rhythm changes are also observed. Inappropriate hormone levels, modified tissue sensitivity (especially glucocorticoid system), and epigenetic mechanisms are key factors for adipose tissue programming during the perinatal period.

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Section: Malnourished Offspring Display Altered Adipogenesis and Fat supporting

confidence: 67%

Section: Offspring Of Malnourished Mothers Exhibit a Loss Of Insulin mentioning

confidence: 98%

Nutritional manipulations in the perinatal period program adipose tissue in offspring

Lukaszewski

Eberlé

Vieau

et al. 2013

American Journal of Physiology-Endocrinology and Metabolism

View full text Add to dashboard Cite

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“…The prenatal period can be influenced by multiple factors from both the maternal and paternal environment. Rodent studies suggest that maternal obesity enhances adipose tissue inflammation in the offspring independent of offspring adiposity (32)(33)(34). Paternal obesity leads to epigenetic alterations in the sperm in rodents and can potentiate hypothalamic inflammation in offspring (35).…”

Section: When Does Metainflammation Begin?mentioning

confidence: 99%

The initiation of metabolic inflammation in childhood obesity

Singer

Lumeng

2017

Journal of Clinical Investigation

143

124

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“…However, maternal obesity before conception and gestation is also able to program similar outcomes during the embryonic period. Indeed, despite normal fetal weight, fetus from mice fed a HF diet prior and throughout pregnancy displayed larger adipocytes (Murabayashi et al 2013, Umekawa et al 2015 and increased mRNA expression levels of Zfp423, a key transcriptional factor initiating adipogenic commitment (Yang et al 2013). Adult mouse offspring also exhibited increased mRNAs levels of several genes involved in de novo lipogenesis and lipid droplet size in visceral WAT (Dahlhoff et al 2014).…”

Section: Figurementioning

confidence: 99%

“…These studies confirmed that maternal obesity has common long-term metabolic consequences sensitizing the offspring to metabolic syndrome features. In particular, maternal obesity at conception programs enhanced adipogenesis and lipogenesis from the fetal period to adulthood resulting in higher WAT mass and larger adipocytes (Muhlhausler & Smith 2009, Borengasser et al 2013, Murabayashi et al 2013. Overfeeding during lactation and/or postweaning periods leads to accelerated growth and consistently worsens adipogenesis and lipogenesis programming (Desai & Ross 2011, Guberman et al 2013, Masuyama & Hiramatsu 2014.…”

Section: Introductionmentioning

confidence: 99%

Depot- and sex-specific effects of maternal obesity in offspring’s adipose tissue

Lecoutre

Deracinois

Laborie

et al. 2016

Journal of Endocrinology

100

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According to the Developmental Origin of Health and Disease (DOHaD) concept, alterations of nutrient supply in the fetus or neonate result in long-term programming of individual body weight (BW) setpoint. In particular, maternal obesity, excessive nutrition, and accelerated growth in neonates have been shown to sensitize offspring to obesity. The white adipose tissue may represent a prime target of metabolic programming induced by maternal obesity. In order to unravel the underlying mechanisms, we have developed a rat model of maternal obesity using a high-fat (HF) diet (containing 60% lipids) before and during gestation and lactation. At birth, newborns from obese dams (called HF) were normotrophs. However, HF neonates exhibited a rapid weight gain during lactation, a key period of adipose tissue development in rodents. In males, increased BW at weaning (+30%) persists until 3 months of age. Nine-month-old HF male offspring was normoglycemic but showed mild glucose intolerance, hyperinsulinemia, and hypercorticosteronemia. Despite no difference in BW and energy intake, HF adult male offspring was predisposed to fat accumulation showing increased visceral (gonadal and perirenal) depots weights and hyperleptinemia. However, only perirenal adipose tissue depot exhibited marked adipocyte hypertrophy and hyperplasia with elevated lipogenic (i.e. sterol-regulated element binding protein 1 (Srebp1), fatty acid synthase (Fas), and leptin) and diminished adipogenic (i.e. peroxisome proliferator-activated receptor gamma (Pparγ), 11β-hydroxysteroid dehydrogenase type 1 (11β-Hds1)) mRNA levels. By contrast, very few metabolic variations were observed in HF female offspring. Thus, maternal obesity and accelerated growth during lactation program offspring for higher adiposity via transcriptional alterations of visceral adipose tissue in a depot-and sex-specific manner.

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Maternal high-fat diets cause insulin resistance through inflammatory changes in fetal adipose tissue

Cited by 99 publications

References 25 publications

Nutritional manipulations in the perinatal period program adipose tissue in offspring

Nutritional manipulations in the perinatal period program adipose tissue in offspring

The initiation of metabolic inflammation in childhood obesity

Depot- and sex-specific effects of maternal obesity in offspring’s adipose tissue

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