scholarly journals Maternal High-Fat Diet Promotes Body Length Increases and Insulin Insensitivity in Second-Generation Mice

Endocrinology ◽  
2009 ◽  
Vol 150 (11) ◽  
pp. 4999-5009 ◽  
Author(s):  
Gregory A. Dunn ◽  
Tracy L. Bale
Keyword(s):  
Body Length ◽  
High Fat Diet ◽  
Maternal Obesity ◽  
Maternal Diet ◽  
Somatic Growth ◽  
High Fat ◽  
Length Increase ◽  
Two Generations ◽  
Igf Binding ◽  
Diet Exposure

Maternal obesity and diet consumption during pregnancy have been linked to offspring adiposity, cardiovascular disease, and impaired glucose metabolism. Furthermore, nutrition during development is clearly linked to somatic growth. However, few studies have examined whether phenotypes derived from maternal high-fat diet exposure can be passed to subsequent generations and by what mechanisms this may occur. Here we report the novel finding of a significant body length increase that persisted across at least two generations of offspring in response to maternal high-fat diet exposure. This phenotype is not attributable to altered intrauterine conditions or maternal feeding behavior because maternal and paternal lineages were able to transmit the effect, supporting a true epigenetic manner of inheritance. We also detected a heritable feature of reduced insulin sensitivity across two generations. Alterations in the GH secretagogue receptor (GHSR), the GHSR transcriptional repressor AF5q31, plasma IGF-I concentrations, and IGF-binding protein-3 (IGFBP3) suggest a contribution of the GH axis. These studies provide evidence that the heritability of body length and glucose homeostasis are modulated by maternal diet across multiple generations, providing a mechanism where length can increase rapidly in concert with caloric availability.

scholarly journals Alteration of the Early Development Environment by Maternal Diet and the Occurrence of Autistic-like Phenotypes in Rat Offspring

2021 ◽  
Vol 22 (18) ◽  
pp. 9662
Author(s):  
Kinga Gawlińska ◽  
Dawid Gawliński ◽  
Ewelina Kowal-Wiśniewska ◽  
Małgorzata Jarmuż-Szymczak ◽  
Małgorzata Filip
Keyword(s):  
High Fat Diet ◽  
Maternal Obesity ◽  
Maternal Diet ◽  
Repetitive Behavior ◽  
Autism Spectrum ◽  
High Fat ◽  
Development Environment ◽  
Rat Offspring ◽  
Adolescent Offspring ◽  
Pregnancy And Lactation

Epidemiological and preclinical studies suggest that maternal obesity increases the risk of autism spectrum disorder (ASD) in offspring. Here, we assessed the effects of exposure to modified maternal diets limited to pregnancy and lactation on brain development and behavior in rat offspring of both sexes. Among the studied diets, a maternal high-fat diet (HFD) disturbed the expression of ASD-related genes (Cacna1d, Nlgn3, and Shank1) and proteins (SHANK1 and TAOK2) in the prefrontal cortex of male offspring during adolescence. In addition, a maternal high-fat diet induced epigenetic changes by increasing cortical global DNA methylation and the expression of miR-423 and miR-494. As well as the molecular changes, behavioral studies have shown male-specific disturbances in social interaction and an increase in repetitive behavior during adolescence. Most of the observed changes disappeared in adulthood. In conclusion, we demonstrated the contribution of a maternal HFD to the predisposition to an ASD-like phenotype in male adolescent offspring, while a protective effect occurred in females.

RYGB Is More Effective than VSG at Protecting Mice from Prolonged High-Fat Diet Exposure: An Occasion to Roll Up Our Sleeves?

2021 ◽  
Author(s):  
Matthew Stevenson ◽  
Ankita Srivastava ◽  
Jenny Lee ◽  
Christopher Hall ◽  
Thomas Palaia ◽  
...  
Keyword(s):  
High Fat Diet ◽  
High Fat ◽  
Diet Exposure

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 Telomere Dysfunction in Oocytes and Embryos From Obese Mice

2021 ◽  
Vol 9 ◽  
Author(s):  
Juan Ge ◽  
Congyang Li ◽  
Hongzheng Sun ◽  
Yongan Xin ◽  
Shuai Zhu ◽  
...  
Keyword(s):  
Embryo Development ◽  
High Frequency ◽  
High Fat Diet ◽  
Maternal Obesity ◽  
Oocyte Quality ◽  
Telomere Dysfunction ◽  
Obese Mice ◽  
High Fat ◽  
Telomere Shortening ◽  
Early Embryos

Maternal obesity impairs oocyte quality and embryo development. However, the potential molecular pathways remain to be explored. In the present study, we examined the effects of obesity on telomere status in oocytes and embryos obtained from mice fed with high-fat diet (HFD). Of note, telomere shortening was observed in both oocytes and early embryos from obese mice, as evidenced by the reduced expression of telomerase reverse transcriptase and activity of telomerase. Moreover, quantitative analysis of telomere dysfunction-induced foci (TIFs) revealed that maternal obesity induces the defective telomeres in oocytes and embryos. Meanwhile, the high frequency of aneuploidy was detected in HFD oocytes and embryos as compared to controls, accompanying with the increased incidence of apoptotic blastocysts. In conclusion, these results indicate that telomere dysfunction might be a molecular pathway mediating the effects of maternal obesity on oocyte quality and embryo development.

scholarly journals Astroglial Regulation of Caloric Intake Following Acute High‐Fat Diet Exposure

2021 ◽  
Vol 35 (S1) ◽  
Author(s):  
Courtney Clyburn ◽  
R. Alberto Travagli ◽  
Kirsteen Browning
Keyword(s):  
High Fat Diet ◽  
Caloric Intake ◽  
High Fat ◽  
Diet Exposure

132 Early Establishment of the Human Gut Microbiome—a Tale of Moms, Their Diets, and Babes Guts

2021 ◽  
Vol 99 (Supplement_3) ◽  
pp. 68-68
Author(s):  
Kjersti M Aagaard
Keyword(s):  
Gut Microbiome ◽  
Maternal Obesity ◽  
Maternal Diet ◽  
Dietary Exposure ◽  
Metabolic Phenotype ◽  
Strong Impact ◽  
High Fat ◽  
Lower Genital Tract ◽  
And Function ◽  
The Impact

Abstract Human microbial communities are characterized by their metagenomic and metabolic diversity, which varies by distinct body sites and influences human physiology. We are only beginning to characterize the complex set of interactions which alters both community membership and function in early development. With respect to the potential source of microbiota at birth, it has been generally assumed that the majority of seeding microbes originate from the maternal lower genital tract, with microbiota ascending into the otherwise sterile intrauterine. However, we and subsequently others have recently demonstrated that (1) the vaginal and gut microbiome communities are distinctly structured in pregnancy, and (2) the intrauterine environment and the fetus is in fact not sterile, but rather harbors a low-abundance microbiome which varies by several measured exposures, and (3) the maternal diet during both gestation and lactation, and notably a high fat diet, has a particularly strong impact on the developing and early in life microbial community structure. We have taken two dynamic approaches to answering these questions in our studies. First, we use large and robust longitudinal cohorts of maternal-infant dyads collected across gestation and into infancy to gain deeper insight into both source and sink of the early developmental microbiome and its role on determining length of gestation. Second, we utilize our well established primate models of maternal high fat dietary exposure, both in the absence and presence of maternal obesity, to determine the impact of maternal diet on both the microbiome and the resultant offspring metabolic phenotype.

scholarly journals Neonatal administration of kaempferol does not alter satiety but increases somatic growth and reduces adiposity in offspring of high-fat diet dams

Life Sciences ◽  
2020 ◽  
Vol 259 ◽  
pp. 118224
Author(s):  
Wenicios Ferreira Chaves ◽  
Isabeli Lins Pinheiro ◽  
Luana Olegário da Silva ◽  
Débora Priscila Lima-Oliveira ◽  
Gisélia de Santana Muniz ◽  
...  
Keyword(s):  
High Fat Diet ◽  
Somatic Growth ◽  
High Fat ◽  
Neonatal Administration

scholarly journals Maternal High Fat Diet and in-Utero Metformin Exposure Significantly Impact upon the Fetal Renal Proteome of Male Mice

2019 ◽  
Vol 8 (5) ◽  
pp. 663 ◽  
Author(s):  
Eva Nüsken ◽  
Eva-Maria Turnwald ◽  
Gregor Fink ◽  
Jenny Voggel ◽  
Christopher Yosy ◽  
...  
Keyword(s):  
High Fat Diet ◽  
Maternal Obesity ◽  
Laser Microdissection ◽  
Kidney Tissue ◽  
Standard Diet ◽  
High Fat ◽  
Proteomic Screen ◽  
Eicosanoid Metabolism ◽  
Associated Conditions ◽  
Underlying Mechanisms

There is accumulating evidence for fetal programming of later kidney disease by maternal obesity or associated conditions. We performed a hypothesis-generating study to identify potentially underlying mechanisms. Female mice were randomly split in two groups and fed either a standard diet (SD) or high fat diet (HFD) from weaning until mating and during pregnancy. Half of the dams from both groups were treated with metformin ((M), 380 mg/kg), resulting in four experimental groups (SD, SD-M, HFD, HFD-M). Caesarean section was performed on gestational day 18.5. Fetal kidney tissue was isolated from cryo-slices using laser microdissection methods and a proteomic screen was performed. For single proteins, a fold change ≥1.5 and q-value <0.05 were considered to be statistically significant. Interestingly, HFD versus SD had a larger effect on the proteome of fetal kidneys (56 proteins affected; interaction clusters shown for proteins concerning transcription/translation, mitochondrial processes, eicosanoid metabolism, H2S-synthesis and membrane remodeling) than metformin exposure in either SD (29 proteins affected; clusters shown for proteins involved in transcription/translation) or HFD (6 proteins affected; no cluster). By further analysis, ATP6V1G1, THY1, PRKCA and NDUFB3 were identified as the most promising candidates potentially mediating reprogramming effects of metformin in a maternal high fat diet.

Sign in / Sign up

Export Citation Format

Share Document