Diet-Induced Maternal Obesity Alters Insulin Signalling in Male Mice Offspring Rechallenged with a High-Fat Diet in Adulthood

Fante, Thaís de; Simino, Laís Angélica de Paula; Reginato, Andressa; Payolla, Tanyara Baliani; Vitoréli, Débora Cristina Gustavo; Souza, Monique de; Torsoni, Márcio Alberto; Milanski, Marciane; Torsoni, Adriana Souza

doi:10.1371/journal.pone.0160184

Cited by 40 publications

(46 citation statements)

References 55 publications

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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, or Student's t-test for analysis of two groups (*p < 0.05, **p < 0.01, ***p < 0.001). www.nature.com/scientificreports www.nature.com/scientificreports/ tissue and soleus muscle also presented insulin resistance 9 . These effects were stable considering that insulin resistance in offspring from obese dams was detected until 82-days-old mice 9 .…”

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%

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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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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: The Activation Of Nicotinic Acetylcholine Receptor α7 Subunimentioning

confidence: 99%

See 1 more Smart Citation

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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“…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

241

202

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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 HF feeding has been demonstrated to result in long-term metabolic dysregulation in the rodent offspring, such as steatosis, even when offspring are fed a normal low-fat diet after weaning [6]. Exposing offspring to a postnatal HF diet in addition to maternal HF feeding further exacerbates metabolic abnormalities, resulting in obesity [7,8], increased food intake [7], steatohepatitis [9], inflammation [8,10], hyperglycemia [11], and impaired insulin signaling in central and peripheral tissues [7]. Underlying the phenotypic alterations in HF offspring are gene expression changes, such as the upregulation of phosphoenolpyruvate carboxykinase (PEPCK) that mediates gluconeogenesis [12] and stearoyl-Coenzyme A desaturase 1 (SCD1) [13] that mediates lipogenesis in the liver, and downregulation of the peroxisome proliferator-activated receptor gamma (PPAR-γ) [7], a critical regulator of peripheral insulin resistance that promotes triglyceride storage and reduces free fatty acid (FFA) release in the white adipose tissue.…”

Section: Introductionmentioning

confidence: 99%

Prenatal Choline Supplementation during High-Fat Feeding Improves Long-Term Blood Glucose Control in Male Mouse Offspring

et al. 2020

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Maternal obesity increases the risk of metabolic dysregulation in rodent offspring, especially when offspring are exposed to a high-fat (HF), obesogenic diet later in life. We previously demonstrated that maternal choline supplementation (MCS) in HF-fed mouse dams during gestation prevents fetal overgrowth and excess adiposity. In this study, we examined the long-term metabolic influence of MCS. C57BL/6J mice were fed a HF diet with or without choline supplementation prior to and during gestation. After weaning, their pups were exposed to either a HF or control diet for 6 weeks before measurements. Prenatal and post-weaning dietary treatments led to sexually dimorphic responses. In male offspring, while post-weaning HF led to impaired fasting glucose and worse glucose tolerance (p < 0.05), MCS in HF dams (HFCS) attenuated these changes. HFCS (versus maternal normal fat control) appeared to improve metabolic functioning of visceral adipose tissue during post-weaning HF feeding, preventing the elevation in leptin and increasing (p < 0.05) mRNA expression of insulin receptor substrate 1 (Irs1) that promotes peripheral insulin signaling in male offspring. In contrast, MCS had minimal effects on metabolic outcomes of female offspring. In conclusion, MCS during HF feeding in mice improves long-term blood glucose homeostasis in male offspring when they are faced with a postnatal obesogenic environment.

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Diet-Induced Maternal Obesity Alters Insulin Signalling in Male Mice Offspring Rechallenged with a High-Fat Diet in Adulthood

Cited by 40 publications

References 55 publications

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

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

The nutrition‐gut microbiome‐physiology axis and allergic diseases

Prenatal Choline Supplementation during High-Fat Feeding Improves Long-Term Blood Glucose Control in Male Mouse Offspring

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