High-fat diet during pregnancy and lactation impairs the cholinergic anti-inflammatory pathway in the liver and white adipose tissue of mouse offspring

Payolla, Tanyara Baliani; Lemes, Simone Ferreira; Fante, Thaís de; Reginato, Andressa; Silva, Cristiano Mendes da; Micheletti, Thayana de Oliveira; Rodrigues, Hosana Gomes; Torsoni, Adriana Souza; Milanski, Marciane; Torsoni, Márcio Alberto

doi:10.1016/j.mce.2015.12.004

Cited by 28 publications

(24 citation statements)

References 55 publications

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“…In dams fed a HFD, infiltrating macrophages are elevated in the mammary gland [38]. Serum and mammary gland mRNA expression levels of Tnfa are increased during pregnancy and lactation in HFD compared to standard chow dams [38,39,40]. In this study, mammary gland expression of Tnfa was shown to be elevated in the WT HFD dams, and this expression was attenuated in the Tph1 deficient dams.…”

Section: Discussionmentioning

confidence: 58%

Serotonin Deficiency Rescues Lactation on Day 1 in Mice Fed a High Fat Diet

Weaver¹,

Bohrer²,

Prichard³

et al. 2016

PLoS ONE

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Obesity is an inflammatory state associated with delayed lactogenesis stage II and altered mammary gland morphology. Serotonin mediates inflammation and mammary gland involution. The objective of this study was to determine if a genetic deficiency of tryptophan hydroxylase 1, the rate-limiting enzyme in peripheral serotonin synthesis, would result in an improved ability to lactate in dams fed a high fat diet. Twenty-six female mice were fed a high (HFD) or low fat (LFD) diet throughout pregnancy and lactation. Fourteen mice were genetically deficient for Tph1 (Tph1-/-), and twelve were wild type. Milk yield, pup mortality, and dam weights were recorded and milk samples were collected. On day 10 of lactation, dams were sacrificed and mammary glands were harvested for RT-PCR and histological evaluation. HFD dams weighed more than LFD dams at the onset of lactation. WT HFD dams were unable to lactate on day 1 of lactation and exhibited increased pup mortality relative to all other treatments, including Tph1-/- HFD dams. mRNA expression of immune markers C-X-C motif chemokine 5 and tumor necrosis factor alpha were elevated in WT HFD mammary glands. Mammary gland histology showed a reduced number of alveoli in WT compared to Tph1-/- dams, regardless of diet, and the alveoli of HFD dams were smaller than those of LFD dams. Finally, fatty acid profile in milk was dynamic in both early and peak lactation, with reduced de novo synthesis of fatty acids on day 10 of lactation in the HFD groups. Administration of a HFD to C57BL/6 dams produced an obese phenotype in the mammary gland, which was alleviated by a genetic deficiency of Tph1. Serotonin may modulate the effects of obesity on the mammary gland, potentially contributing to the delayed onset of lactogenesis seen in obese women.

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Section: Discussionmentioning

confidence: 58%

Serotonin Deficiency Rescues Lactation on Day 1 in Mice Fed a High Fat Diet

Weaver¹,

Bohrer²,

Prichard³

et al. 2016

PLoS ONE

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“…JNK and IKK activation are also observed in diet-induce obesity (DIO) and genetic models 17,18 . In metabolic programming, maternal obesity also contributes to the activation of inflammatory pathways, hypothalamic endoplasmic reticulum stress and damage to glucose homeostasis [9][10][11][12] .…”

Section: Discussionmentioning

confidence: 99%

“…Statistical significance was analysed by ANOVA and Bonferroni post-hoc tests (*p < 0.05, **p < 0.01, ***p < 0.001). 11 , we have not investigated the relationship with the development of insulin resistance. Here, HFD-O mice did not show difference in the basal glycaemia (data not shown), but AKT phosphorylation stimulated by insulin was reduced in HFD-O compared to SC-O mice.…”

Section: Discussionmentioning

confidence: 99%

“…Characteristics of obesity-induced inflammation include elevated production of proinflammatory molecules by adipose tissue and activation of a network of inflammatory signalling pathways. These are important factors for the development of insulin resistance 7,8 . In previous studies, we showed that diet-induced maternal obesity leads to increased susceptibility to obesity and impairment of insulin signalling in offspring in early and late life 9 , inflammatory pathway activation [10][11][12] and hypothalamic endoplasmic reticulum stress 12 . Recently, we also showed that high-fat diet (HFD) during pregnancy and lactation impairs the cholinergic anti-inflammatory pathway in liver and white adipose tissue and exacerbates cytokine production in response to LPS 11 .…”

Section: The Activation Of Nicotinic Acetylcholine Receptor α7 Subunimentioning

confidence: 99%

“…Previously we showed that hepatic cyclic adenosine monophosphate (cAMP) response element binding protein (CREB) phosphorylation was reduced in HFD-O mice compared to SC-O mice 11 . CREB phosphorylation is induced by cAMP and it plays an important role in the recruitment of coactivators and activation of gluconeogenesis [21][22][23][24] .…”

Section: Sc-o Micementioning

confidence: 99%

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Maternal high fat diet consumption reduces liver alpha7 nicotinic cholinergic receptor expression and impairs insulin signalling in the offspring

Costa

Souza

Lanza

et al. 2020

Sci Rep

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LpS treatment. To induce inflammatory response, mice were treated with LPS diluted in sterile saline and administered intraperitoneally (IP) once a day for three days (1 mg kg −1 bw-IP). Mice were euthanized 2 hours after LPS treatment, and fragments of liver were collected, froze in liquid nitrogen and stored at −80 °C until processing. In vitro experiments. Hepatoma cell line, Hepa-1c1c7 (ATCC ® CRL-2026 ™), derived from mice was used to evaluate the ability of the cholinergic pathway to modulate AKT phosphorylation induced by insulin. Cells were cultivated in alpha modified Eagle's medium (αMEM; Invitrogen, USA) supplemented with 10% foetal bovine serum (Invitrogen, USA) and 1% penicillin (100 U/mL)/streptomycin (100 µg/mL) (Invitrogen, USA) at 37 °C and 5% CO 2. Cells were treated with 500 µM palmitate (palmitic acid from Sigma-Aldrich at 500 μM was first diluted in NaOH conjugated to BSA (3:1) for 45 minutes at 37 °C) for 3 hours in 6-well culture plate. The protein content was extracted and analysed by Western blotting. When necessary, 1 µM PNU-282987 (P6499-10MG; Sigma-Aldrich, Brazil) or 1 µM nicotine (N0267-100MG; Sigma-Aldrich, Brazil) was added to the medium for 15 minutes after palmitate treatment. To evaluate the insulin signalling, cells were treated with 100 nM insulin (Humulin, Eli Lilly and Company, USA) for 10 minutes after the 3 hours of palmitate treatment.

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Obesogenic Programming of Foetal Hepatic Metabolism by microRNAs

Simino

Torsoni

2017

Diet, Nutrition, and Fetal Programming

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High-fat diet during pregnancy and lactation impairs the cholinergic anti-inflammatory pathway in the liver and white adipose tissue of mouse offspring

Cited by 28 publications

References 55 publications

Serotonin Deficiency Rescues Lactation on Day 1 in Mice Fed a High Fat Diet

Serotonin Deficiency Rescues Lactation on Day 1 in Mice Fed a High Fat Diet

Maternal high fat diet consumption reduces liver alpha7 nicotinic cholinergic receptor expression and impairs insulin signalling in the offspring

Obesogenic Programming of Foetal Hepatic Metabolism by microRNAs

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