scholarly journals Maternal high-fat diet alters lung development and function in the offspring

2019 ◽  
Vol 317 (2) ◽  
pp. L167-L174 ◽  
Author(s):  
Kathryn M. Heyob ◽  
Saya Mieth ◽  
Sophia S. Sugar ◽  
Amanda E. Graf ◽  
Scott W. Lallier ◽  
...  
Keyword(s):  
Signaling Pathways ◽  
High Fat Diet ◽  
Lung Development ◽  
Maternal Obesity ◽  
Control Diet ◽  
Tyrosine Phosphatase ◽  
Vegf Receptor ◽  
High Fat ◽  
Lung Weight ◽  
Protein Levels

The effects of maternal obesity on lung development have been recognized, and speculation is that these diseases are not simply because of accelerated pulmonary decline with aging but with a failure to achieve optimal lung development during early life. These studies tested the hypothesis that maternal obesity alters signaling pathways during the course of lung development that may affect life-long pulmonary health. Adult female mice were fed 60% fat [high-fat diet (HFD)] or 10% fat [control diet (CD)] for 8 wk before mating and through weaning. Pup lung tissues were collected at postnatal days ( PN) 7, 21, and 90 (after receiving HFD or CD as adults). At PN7, body weights from HFD were greater than CD but lung weight-to-body weight ratios were lower. In lung tissues, NFκB-mediated inflammation was greater in HFD pups at PN21 and phospho-/total STAT3, phospho-/total VEGF receptor 2, and total AKT protein levels were lower with maternal HFD and protein tyrosine phosphatase B1 levels were increased. Decreased platelet endothelial cell adhesion molecule levels were observed at PN21 and at PN90 in the pups exposed to maternal HFD. Morphometry indicated that the pups exposed to maternal or adult HFD had fewer alveoli, and the effect was additive. Decreases in pulmonary resistance, elastance, and compliance were observed because of adult HFD diet and decreases in airway resistance and increases in inspiratory capacity because of maternal HFD. In conclusion, maternal HFD disrupts signaling pathways in the early developing lung and may contribute to deficiencies in lung function and increased susceptibility in adults.

scholarly journals Maternal high-fat diet induces metabolic stress response disorders in offspring hypothalamus

2017 ◽  
Vol 59 (1) ◽  
pp. 81-92 ◽  
Author(s):  
Long The Nguyen ◽  
Sonia Saad ◽  
Yi Tan ◽  
Carol Pollock ◽  
Hui Chen
Keyword(s):  
Endoplasmic Reticulum ◽  
Body Weight ◽  
Er Stress ◽  
High Fat Diet ◽  
Maternal Obesity ◽  
Mrna Level ◽  
Metabolic Stress ◽  
High Fat ◽  
Chemical Chaperone ◽  
Protein Levels

Maternal obesity has been shown to increase the risk of obesity and related disorders in the offspring, which has been partially attributed to changes of appetite regulators in the offspring hypothalamus. On the other hand, endoplasmic reticulum (ER) stress and autophagy have been implicated in hypothalamic neuropeptide dysregulation, thus may also play important roles in such transgenerational effect. In this study, we show that offspring born to high-fat diet-fed dams showed significantly increased body weight and glucose intolerance, adiposity and plasma triglyceride level at weaning. Hypothalamic mRNA level of the orexigenic neuropeptide Y (NPY) was increased, while the levels of the anorexigenic pro-opiomelanocortin (POMC), NPY1 receptor (NPY1R) and melanocortin-4 receptor (MC4R) were significantly downregulated. In association, the expression of unfolded protein response (UPR) markers including glucose-regulated protein (GRP)94 and endoplasmic reticulum DNA J domain-containing protein (Erdj)4 was reduced. By contrast, protein levels of autophagy-related genes Atg5 and Atg7, as well as mitophagy marker Parkin, were slightly increased. The administration of 4-phenyl butyrate (PBA), a chemical chaperone of protein folding and UPR activator, in the offspring from postnatal day 4 significantly reduced their body weight, fat deposition, which were in association with increased activating transcription factor (ATF)4, immunoglobulin-binding protein (BiP) and Erdj4 mRNA as well as reduced Parkin, PTEN-induced putative kinase (PINK)1 and dynamin-related protein (Drp)1 protein expression levels. These results suggest that hypothalamic ER stress and mitophagy are among the regulatory factors of offspring metabolic changes due to maternal obesity.

scholarly journals Epigenomic Regulation of SATB2 Links Maternal Obesity to Impaired Osteoblast Differentiation (P11-034-19)

2019 ◽  
Vol 3 (Supplement_1) ◽  
Author(s):  
Jin-Ran Chen ◽  
Haijun Zhao ◽  
Oxana P Lazarenko ◽  
Kartik Shankar
Keyword(s):  
Stem Cells ◽  
Mesenchymal Stem Cells ◽  
Umbilical Cord ◽  
Epigenetic Regulation ◽  
High Fat Diet ◽  
Osteoblast Differentiation ◽  
Maternal Obesity ◽  
Control Diet ◽  
High Fat ◽  
Pregnant Mothers

Abstract Objectives Nutritional status during intrauterine and/or early postnatal life has substantial influences on adult offspring health. However, evidence on the impact of high fat diet (HFD)-induced maternal obesity on regulation of fetal bone development is sparse. Thus, we investigated the effects of maternal obesity in rodent and human cells on epigenetic regulation of osteoblast differentiation. Methods First, female Sprague-Dawley rats were fed either a low-fat AIN-93G control diet or a high fat diet (HFD) (45% fat calories) for 10 wk starting at 6 wk of age. Lean (from control diet) and obese (from HFD) female rats were then time-impregnated (n = 6 per group) by control diet fed male rats. At gestational day 18.5 (E18.5), all fetuses were taken and embryonic osteogenic calvarial cells (EOCCs) were isolated. Second, human osteo-progenitors of mesenchymal stem cells were isolated from umbilical cord following delivery from pregnant mothers. Results We found epigenetic regulation of polycomb-regulated gene Ezh2 (Enhancer of zeste homolog 2) in embryonic rats from HFD obese rat dams. Increased enrichment of repressive histone mark H3K27me3 on the gene body of SATB2 (ChIP Seq analysis) was associated with aberrant differentiation of EOCCs to mature osteoblasts. Knocking down Ezh2 in EOCCs and ST2 cells increased SATB2 expression; on the other hand, Ezh2 overexpression in EOCCs and ST2 cells decreased SATB2 expression. These data were consistent with ChIP experimental results showing strong association between H3K27me3, Ezh2 and SATB2. Second, human mesenchymal stem cells (MSCs) from umbilical cord (UC) were isolated following delivery from obese/overweight (pre-pregnancy BMI ≥ 25 kg/m2) and control (pre-pregnancy BMI between 19–25 kg/m2) pregnant mothers. We found: 1) UC-MSCs from pregnant obese/overweight mothers showed increased Ezh2 expression and decreased SATB2 mRNA expression, which was concurrent lower osteoblastogenesis potential in EOCCs; 2) ChIP experiments using H3K27me3 IP (immune-precipitation) showed significant association between H3K27me3, Ezh2 and SATB2. Conclusions These findings indicate maternal HFD-induced obesity-associated decrease of fetal pre-osteoblastic cell differentiation is under epigenetic control through SATB2 expression. Funding Sources Supported by USDA-ARS Project.

The treatment with an extract from Calafate (Berberis microphylla) induces transcript and protein expression of molecules involved in thermogenesis and adipocyte browning in adipose tissue from obese mice

2021 ◽  
pp. 1-11
Author(s):  
Lissette Duarte ◽  
Javier Quezada ◽  
Luisa A. Ramirez ◽  
Karla Vasquez ◽  
Juan F. Orellana ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
High Fat Diet ◽  
Control Diet ◽  
Obese Mice ◽  
High Fat ◽  
Total Polyphenols ◽  
Adipose Tissues ◽  
Protein Levels ◽  
Brown Adipose ◽  
Diet Control

BACKGROUND: Polyphenols intake increases the function of brown adipose tissue (BAT), stimulating energy expenditure (EE). Calafate (Berberis microphylla) is a polyphenol-rich Chilean native fruit. OBJECTIVE: To analyse the effect of a treatment with a Calafate extract in the thermogenic activity of mice adipose tissues. METHODS: Forty adult C57BL/6J male mice were subdivided into four groups (n=10 each): control diet, control+Calafate (extract: 50mg total polyphenols/kg weight), high-fat diet (HF) and HF+Calafate. RESULTS: Calafate prevented the increase in body weight and the decrease EE induced by HF. In BAT, Ucp-1 transcript was influenced by the interaction between diet and Calafate (p<0.01), Pparα showed the same expression pattern as Ucp-1 and both, diet (p<0.01) and Calafate (p<0.05), induced significant effects in Sirt1. In inguinal adipose tissue, Pgc1α, Pparα, Prdm16, Sirt1, and Dio2 transcripts presented a decreased expression caused by HF, that was reversed by Calafate. In BAT, an effect of diet (p<0.05) and an interaction between diet and Calafate (p<0.01) was observed in UCP-1 protein levels. CONCLUSIONS: A treatment with Calafate drives less weight gain in mice fed with HF, and reverses the effects generated by it on the expression of thermogenic and browning markers.

High-fat-diet induced obesity increases the proportion of linoleic acyl residues in dam serum and milk and in suckling neonate circulation

2020 ◽  
Vol 103 (4) ◽  
pp. 736-749
Author(s):  
Aridany Suarez-Trujillo ◽  
Katelyn Huff ◽  
Christina Ramires Ferreira ◽  
Tiago Jose Paschoal Sobreira ◽  
Kimberly K Buhman ◽  
...  
Keyword(s):  
High Fat Diet ◽  
Maternal Obesity ◽  
Multiple Reaction Monitoring ◽  
Control Diet ◽  
Fatty Acyl ◽  
Lipid Classes ◽  
High Fat ◽  
Diet Induced Obesity ◽  
Prepregnancy Obesity

Abstract Maternal obesity increases the risk of offspring to become obese and develop related pathologies. Exposure to maternal high-fat diet (HFD) only during lactation increases the risk of obesity-related diseases, suggesting that factors in milk affect long-term health. We hypothesized that prepregnancy obesity induced by HFD alters milk lipidome, and in turn, alterations may affect neonate serum lipidome. The objective of this study was to determine the effect of prepregnancy obesity induced by HFD on circulating lipids in dams and neonates and in milk. Female mice were fed an HFD (60% kcal fat) or control diet (CON, 10% kcal fat) beginning 4 weeks before breeding. On postnatal day 2 (PND2), pups were cross-fostered to create pup groups exposed to HFD during pregnancy, lactation, or both or exposed to CON. On PND12, dams were milked and then euthanized along with pups to collect blood. Serum and milk were processed for multiple reaction monitoring (MRM) lipidomics profiling to quantify the relative expression of lipid classes. Lipidome of HFD dam serum and milk had increased proportion of C18:2 free fatty acid and fatty acyl residues in all lipid classes. Lipidome of serum from pups exposed to maternal HFD during lactation was similarly affected. Thus, maternal HFD induced redistribution of fatty acyl residues in the dam’s circulation, which was associated with modification in milk and suckling neonate’s lipidome. Further studies are needed to determine if increased circulating levels of C18:2 in neonate affects development and predisposes offspring to obesity and metabolic syndrome.

scholarly journals A high-fat diet fed during different periods of life impairs steroidogenesis of rat Leydig cells

Reproduction ◽  
2016 ◽  
Vol 152 (6) ◽  
pp. 795-808 ◽  
Author(s):  
Maria Etelvina Pinto-Fochi ◽  
Eloísa Zanin Pytlowanciv ◽  
Vanessa Reame ◽  
Alex Rafacho ◽  
Daniele Lisboa Ribeiro ◽  
...  
Keyword(s):  
Sexual Maturation ◽  
High Fat Diet ◽  
Structural Damage ◽  
Leydig Cells ◽  
Maternal Obesity ◽  
Control Diet ◽  
High Fat ◽  
Unsaturated Fat ◽  
Conventional Diet ◽  
The Impact

This study evaluated the impact of a high-fat diet (HFD) during different stages of rat life, associated or not with maternal obesity, on the content of sex steroid hormones and morphophysiology of Leydig cells. The following periods of development were examined: gestation (O1), gestation and lactation (O2), from weaning to adulthood (O3), from lactation to adulthood (O4), gestation to adulthood (O5), and after sexual maturation (O6). The HFD contained 20% unsaturated fat, whereas the control diet had 4% fat. Maternal obesity was induced by feeding HFD 15 weeks before mating. All HFD groups presented increased body weight, hyperinsulinemia and reduced insulin sensitivity. Except for O1, all HFD groups exhibited a higher adiposity index, hyperleptinemia, reduced testosterone and estradiol testicular levels, and decreased testicular 17β-HSD enzyme . Morphometrical analyses indicated atrophy of Leydig cells in the O2 group. Myelin vesicles were observed in the mitochondrial matrix of Leydig cells in O3, O4, O5 and O6, and autophagosomes containing mitochondria were found in O5 and O6. In conclusion, HFD feeding, before or after sexual maturation, reduces the functional capacity of rat Leydig cells. Maternal obesity associated with HFD during pregnancy/lactation prejudices Leydig cell steroidogenesis and induces its atrophy in adulthood, even if it is replaced by a conventional diet at later stages of life. Regardless of the life period of exposure to HFD, deregulation of leptin is the main factor related to steroidogenic impairment of Leydig cells, and, in groups exposed for longer periods (O3, O4, O5 and O6), this is worsened by structural damage and mitochondrial degeneration of these cells.

scholarly journals Paternal Resistance Exercise Modulates Skeletal Muscle Remodeling Pathways in Fathers and Male Offspring Submitted to a High-Fat Diet

2021 ◽  
Vol 12 ◽  
Author(s):  
Rebecca Salomão ◽  
Ivo Vieira de Sousa Neto ◽  
Gracielle Vieira Ramos ◽  
Ramires Alsamir Tibana ◽  
João Quaglioti Durigan ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
High Fat Diet ◽  
Control Diet ◽  
Matrix Remodeling ◽  
Mrna Levels ◽  
High Fat ◽  
Protein Levels ◽  
Gene And Protein Expression ◽  
Muscle Homeostasis ◽  
Muscle Remodeling

Although some studies have shown that a high-fat diet (HFD) adversely affects muscle extracellular matrix remodeling, the mechanisms involved in muscle trophism, inflammation, and adipogenesis have not been fully investigated. Thus, we investigated the effects of 8 weeks of paternal resistance training (RT) on gene and protein expression/activity of critical factors involved in muscle inflammation and remodeling of fathers and offspring (offspring exposed to standard chow or HFD). Animals were randomly distributed to constitute sedentary fathers (SF; n = 7; did not perform RT) or trained fathers (TF n = 7; performed RT), with offspring from mating with sedentary females. After birth, 28 male pups were divided into four groups (n = 7 per group): offspring from sedentary father submitted either to control diet (SFO-C) or high-fat diet (SFO-HF) and offspring from trained father submitted to control diet (TFO-C) or high-fat diet (TFO-HF). Our results show that an HFD downregulated collagen mRNA levels and upregulated inflammatory and atrophy pathways and adipogenic transcription factor mRNA levels in offspring gastrocnemius muscle. In contrast, paternal RT increased MMP-2 activity and decreased IL-6 levels in offspring exposed to a control diet. Paternal RT upregulated P70s6k and Ppara mRNA levels and downregulated Atrogin1 mRNA levels, while decreasing NFκ-B, IL-1β, and IL-8 protein levels in offspring exposed to an HFD. Paternal physical training influences key skeletal muscle remodeling pathways and inflammatory profiles relevant for muscle homeostasis maintenance in offspring submitted to different diets.

scholarly journals Methionine restriction plus overload improves skeletal muscle and metabolic health in old mice on a high fat diet

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Anandini Swaminathan ◽  
Andrej Fokin ◽  
Tomas Venckūnas ◽  
Hans Degens
Keyword(s):  
Skeletal Muscle ◽  
Glucose Tolerance ◽  
Muscle Mass ◽  
Body Mass ◽  
High Fat Diet ◽  
Control Diet ◽  
Metabolic Health ◽  
High Fat ◽  
Methionine Restriction ◽  
Old Mice

AbstractMethionine restriction (MR) has been shown to reduce the age-induced inflammation. We examined the effect of MR (0.17% methionine, 10% kCal fat) and MR + high fat diet (HFD) (0.17% methionine, 45% kCal fat) on body mass, food intake, glucose tolerance, resting energy expenditure, hind limb muscle mass, denervation-induced atrophy and overload-induced hypertrophy in young and old mice. In old mice, MR and MR + HFD induced a decrease in body mass. Muscle mass per body mass was lower in old compared to young mice. MR restored some of the HFD-induced reduction in muscle oxidative capacity. The denervation-induced atrophy of the m. gastrocnemius was larger in animals on MR than on a control diet, irrespective of age. Old mice on MR had larger hypertrophy of m. plantaris. Irrespective of age, MR and MR + HFD had better glucose tolerance compared to the other groups. Young and old mice on MR + HFD had a higher resting VO2 per body mass than HFD group. Mice on MR and MR + HFD had a resting respiratory quotient closer to 0.70, irrespective of age, indicating an increased utilization of lipids. In conclusion, MR in combination with resistance training may improve skeletal muscle and metabolic health in old age even in the face of obesity.

scholarly journals Perinatal High-Fat Diet Influences Ozone-Induced Responses on Pulmonary Oxidant Status and the Molecular Control of Mito-Phagy in Female Rat Offspring

2021 ◽  
Vol 22 (14) ◽  
pp. 7551
Author(s):  
Sven H. Rouschop ◽  
Samantha J. Snow ◽  
Urmila P. Kodavanti ◽  
Marie-José Drittij ◽  
Lou M. Maas ◽  
...  
Keyword(s):  
Oxidative Phosphorylation ◽  
High Fat Diet ◽  
Control Diet ◽  
Ozone Exposure ◽  
Female Rat ◽  
Induced Responses ◽  
High Fat ◽  
Molecular Control ◽  
Rat Offspring ◽  
Oxidant Status

Previous research has shown that a perinatal obesogenic, high-fat diet (HFD) is able to exacerbate ozone-induced adverse effects on lung function, injury, and inflammation in offspring, and it has been suggested that mitochondrial dysfunction is implicated herein. The aim of this study was to investigate whether a perinatal obesogenic HFD affects ozone-induced changes in offspring pulmonary oxidant status and the molecular control of mitochondrial function. For this purpose, female Long-Evans rats were fed a control diet or HFD before and during gestation, and during lactation, after which the offspring were acutely exposed to filtered air or ozone at a young-adult age (forty days). Directly following this exposure, the offspring lungs were examined for markers related to oxidative stress; oxidative phosphorylation; and mitochondrial fusion, fission, biogenesis, and mitophagy. Acute ozone exposure significantly increased pulmonary oxidant status and upregulated the molecular machinery that controls receptor-mediated mitophagy. In female offspring, a perinatal HFD exacerbated these responses, whereas in male offspring, responses were similar for both diet groups. The expression of the genes and proteins involved in oxidative phosphorylation and mitochondrial biogenesis, fusion, and fission was not affected by ozone exposure or perinatal HFD. These findings suggest that a perinatal HFD influences ozone-induced responses on pulmonary oxidant status and the molecular control of mitophagy in female rat offspring.

scholarly journals Flavonoids from Mulberry Leaves Alleviate Lipid Dysmetabolism in High Fat Diet-Fed Mice: Involvement of Gut Microbiota

2020 ◽  
Vol 8 (6) ◽  
pp. 860 ◽  
Author(s):  
Yinzhao Zhong ◽  
Bo Song ◽  
Changbing Zheng ◽  
Shiyu Zhang ◽  
Zhaoming Yan ◽  
...  
Keyword(s):  
Acetic Acid ◽  
Lipid Metabolism ◽  
Gut Microbiota ◽  
High Fat Diet ◽  
Control Diet ◽  
Liver Steatosis ◽  
High Fat ◽  
Acetic Acid Production ◽  
Mulberry Leaves ◽  
Brown Adipose

Here, we investigated the roles and mechanisms of flavonoids from mulberry leaves (FML) on lipid metabolism in high fat diet (HFD)-fed mice. ICR mice were fed either a control diet (Con) or HFD with or without FML (240 mg/kg/day) by oral gavage for six weeks. FML administration improved lipid accumulation, alleviated liver steatosis and the whitening of brown adipose tissue, and improved gut microbiota composition in HFD-fed mice. Microbiota transplantation from FML-treated mice alleviated HFD-induced lipid metabolic disorders. Moreover, FML administration restored the production of acetic acid in HFD-fed mice. Correlation analysis identified a significant correlation between the relative abundances of Bacteroidetes and the production of acetic acid, and between the production of acetic acid and the weight of selected adipose tissues. Overall, our results demonstrated that in HFD-fed mice, the lipid metabolism improvement induced by FML administration might be mediated by gut microbiota, especially Bacteroidetes-triggered acetic acid production.

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