Maternal high-fat diet during lactation impairs thermogenic function of brown adipose tissue in offspring mice

Liang, Xingwei; Yang, Qiyuan; Zhang, Lupei; Maricelli, Joseph; Rodgers, Buel D.; Zhu, Mei‐Jun; Du, Min

doi:10.1038/srep34345

Cited by 74 publications

(76 citation statements)

References 47 publications

(75 reference statements)

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“…Recently, it has been suggested that diet‐induced obesity might cause functional hypoxia in BAT ultimately leading to a functional shift from thermogenesis toward lipid storage . Our data exploring BAT content and gene expression resonate with previous studies showing that exposure to hypercaloric diets enlarges the interscapular BAT depot and does not alter Ucp‐1 or Cidea expression but reduces the expression of Pgc‐1α , suggesting an impaired mitochondrial function upon caloric overload. As previously stated, there is consensus about the potential of Foxc2 in counteracting diet‐induced insulin resistance .…”

Section: Discussionsupporting

confidence: 89%

Impact of Free‐Choice Diets High in Fat and Different Sugars on Metabolic Outcome and Anxiety‐Like Behavior in Rats

Peris-Sampedro

Mounib

Schéle

et al. 2019

Obesity

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Objective Rats were exposed to free‐choice diets (fat plus one of two different sugar solutions, glucose or sucrose), and the metabolic consequences and impact on locomotor activity and anxiety‐like behavior were explored. Methods For 3 weeks, 7‐week‐old male rats were offered either chow only or free‐choice high‐fat diets differing in their added sugar: no sugar, sucrose, or glucose. In a second experiment, after 2 weeks on the diets, rats were switched from high sucrose to high glucose for two additional weeks. Metabolic end points included body weight, food intake, food choice, glycemic control, metabolic hormones, fat pad weight, brown adipose tissue weight, and gene expression. Behavioral analysis included locomotor and anxiety‐like activity in the open field and elevated plus maze. Results Both sugar diets enhanced adiposity and induced hyperphagia, favoring unhealthier dietary selection above that of the control diets (chow or free‐choice high‐fat with no sugar). Despite isocaloric intake in the sugar‐containing diets, offering glucose instead of sucrose was associated with improved insulin sensitivity. The sugar‐containing diets reduced activity (but with movements of increased velocity) and induced an anxiety‐like phenotype. Conclusions Although free‐choice diets negatively impacted on metabolism and anxiety‐like behavior, replacing sucrose with glucose improved insulin sensitivity and may therefore be better for health.

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Section: Discussionsupporting

confidence: 89%

Impact of Free‐Choice Diets High in Fat and Different Sugars on Metabolic Outcome and Anxiety‐Like Behavior in Rats

Peris-Sampedro

Mounib

Schéle

et al. 2019

Obesity

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“…Our data confirm previous findings showing that maternal HFD feeding during lactation in rodents results in metabolic alterations in the offspring (5, 6, 8, 43). From postnatal d 1 to 21, offspring from HFD‐fed mothers gained 23% more body weight than those from CD‐fed dams (Fig.…”

Section: Resultssupporting

confidence: 92%

“…Bars without lines are rat PRL (endogenous) levels quantified by radioimmunoassay; lined bars are ovine PRL levels delivered by pumps and measured by using the Nb2 assay. C) Milk yield on d 8 and 19 of lactation of dams fed with CD or HFD in the absence or presence of osmotic minipumps delivering PRL (HFD + PRL) during lactation (n =[40][41][42][43][44][45][46][47][48]. Data are means 6 SEM.…”

mentioning

confidence: 99%

Impaired prolactin actions mediate altered offspring metabolism induced by maternal high‐fat feeding during lactation

et al. 2018

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Maternal diet during lactation affects offspring metabolic health throughout life. Prolactin (PRL) is present in high quantities in maternal milk; however, the effects of milk PRL on the offspring remain poorly characterized. In this study, we evaluated whether feeding a high-fat diet (HFD) to rats during lactation alters PRL, both in the mother's serum and in milk, and whether this factor contributes to HFD-induced metabolic dysfunction in the offspring. Maternal HFD resulted in decreased PRL levels in milk (but not in serum), reduced mammary gland (MG) PRL receptor expression, and altered MG structure and function. Offspring from HFD-fed dams had increased body weight and adiposity, and developed fatty liver, hyperinsulinemia, and insulin resistance at weaning. Increasing PRL levels in the HFD-fed mothers by subcutaneous osmotic minipumps releasing PRL normalized MG function and PRL levels in milk. Moreover, PRL treatment in HFD-fed mothers, or directly in their pups via oral PRL administration, increased liver STAT5 phosphorylation, reduced visceral adiposity, ameliorated fatty liver, and improved insulin sensitivity in offspring. Our results show that HFD impairs PRL actions during lactation to negatively affect MG physiology and directly impair offspring metabolism.-De los Ríos, E. A., Ruiz-Herrera, X., Tinoco-Pantoja, V., López-Barrera, F., Martínez de la Escalera, G., Clapp, C., Macotela, Y. Impaired prolactin actions mediate altered offspring metabolism induced by maternal high-fat feeding during lactation.

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“…Women with altered metabolic homeostasis during pregnancy give birth to children that are prone to develop obesity, type 1 diabetes, or cardiovascular diseases later in life . In mice, maternal high‐fat diet feeding during lactation predisposes offspring to obesity and impaired glucose homeostasis . Thus, diet and metabolites of the mother affect metabolic syndrome disorders.…”

Section: Diet As An Alternative or Additional Contributor Over Hygienementioning

confidence: 99%

The nutrition‐gut microbiome‐physiology axis and allergic diseases

McKenzie

Tan

Macia

et al. 2017

Immunological Reviews

225

193

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Dietary and bacterial metabolites influence immune responses. This raises the question whether the increased incidence of allergies, asthma, some autoimmune diseases, cardiovascular disease, and others might relate to intake of unhealthy foods, and the decreased intake of dietary fiber. In recent years, new knowledge on the molecular mechanisms underpinning a 'diet-gut microbiota-physiology axis' has emerged to substantiate this idea. Fiber is fermented to short chain fatty acids (SCFAs), particularly acetate, butyrate, and propionate. These metabolites bind 'metabolite-sensing' G-protein-coupled receptors such as GPR43, GPR41, and GPR109A. These receptors play fundamental roles in the promotion of gut homeostasis and the regulation of inflammatory responses. For instance, these receptors and their metabolites influence Treg biology, epithelial integrity, gut homeostasis, DC biology, and IgA antibody responses. The SCFAs also influence gene transcription in many cells and tissues, through their inhibition of histone deacetylase expression or function. Contained in this mix is the gut microbiome, as commensal bacteria in the gut have the necessary enzymes to digest dietary fiber to SCFAs, and dysbiosis in the gut may affect the production of SCFAs and their distribution to tissues throughout the body. SCFAs can epigenetically modify DNA, and so may be one mechanism to account for diseases with a 'developmental origin', whereby in utero or post-natal exposure to environmental factors (such as nutrition of the mother) may account for disease later in life. If the nutrition-gut microbiome-physiology axis does underpin at least some of the Western lifestyle influence on asthma and allergies, then there is tremendous scope to correct this with healthy foodstuffs, probiotics, and prebiotics.

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Maternal high-fat diet during lactation impairs thermogenic function of brown adipose tissue in offspring mice

Cited by 74 publications

References 47 publications

Impact of Free‐Choice Diets High in Fat and Different Sugars on Metabolic Outcome and Anxiety‐Like Behavior in Rats

Impact of Free‐Choice Diets High in Fat and Different Sugars on Metabolic Outcome and Anxiety‐Like Behavior in Rats

Impaired prolactin actions mediate altered offspring metabolism induced by maternal high‐fat feeding during lactation

The nutrition‐gut microbiome‐physiology axis and allergic diseases

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