Evidence map›Paper›PMID 35111136›Full record

ArticleFrontiers in endocrinology2021

Maternal High-Fat Diet During Pre-Conception and Gestation Predisposes Adult Female Offspring to Metabolic Dysfunction in Mice.

Brian Akhaphong, Brigid Gregg, Doga Kumusoglu, Seokwon Jo, Kanakadurga Singer, Joshua Scheys, Jennifer DelProposto, Carey Lumeng, Ernesto Bernal-Mizrachi, Emilyn U Alejandro

Open access · goldAbstract read
In one paragraph

Article in Frontiers in endocrinology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
8.4field-weighted citation impact, top 2% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

15 citing papers in PubMed, 22 citations in OpenAlex.

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  14. Parental obesity-induced changes in developmental programming.Frontiers in cell and developmental biology · 2022
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

10 authors at 5 institutions in 1 country.

Brian AkhaphongDepartment of Integrative Biology & Physiology, University of Minnesota, Minneapolis, MN, United States.
Brigid GreggDepartment of Pediatrics, Division of Diabetes, Endocrinology, and Metabolism, University of Michigan Medical School, Ann Arbor, MI, United States.
Doga KumusogluDepartment of Internal Medicine, Division of Metabolism, Endocrinology and Diabetes, Brehm Center for Diabetes Research, Ann Arbor, United States.
Seokwon JoDepartment of Integrative Biology & Physiology, University of Minnesota, Minneapolis, MN, United States.
Kanakadurga SingerDepartment of Pediatrics, Division of Diabetes, Endocrinology, and Metabolism, University of Michigan Medical School, Ann Arbor, MI, United States.
Joshua ScheysDepartment of Internal Medicine, Division of Metabolism, Endocrinology and Diabetes, Brehm Center for Diabetes Research, Ann Arbor, United States.
Jennifer DelPropostoDepartment of Pediatrics, Division of Diabetes, Endocrinology, and Metabolism, University of Michigan Medical School, Ann Arbor, MI, United States.
Carey LumengDepartment of Pediatrics, Division of Diabetes, Endocrinology, and Metabolism, University of Michigan Medical School, Ann Arbor, MI, United States.
Ernesto Bernal-MizrachiDepartment of Internal Medicine, Division of Metabolism, Endocrinology and Diabetes, Brehm Center for Diabetes Research, Ann Arbor, United States.
Emilyn U AlejandroDepartment of Integrative Biology & Physiology, University of Minnesota, Minneapolis, MN, United States.
University of Michigan–Ann Arbor · USIowa Diabetes and Endocrinology Research Center · USUniversity of Minnesota · USIntegra (United States) · USVA Ann Arbor Healthcare System · US

Funding

Regulation of Adipose Tissue Inflammation By Antigen Presenting CellsR01DK090262 · NIDDK · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI LUMENG, CAREY N · 2011 to 2024
$5.3M
AKT/mTOR Signaling and Regulation of Cell Cycle in beta CellsR01DK073716 · NIDDK · WASHINGTON UNIVERSITY · PI BERNAL-MIZRACHI, ERNESTO · 2006 to 2022
$4.6M
The role of O-linked N-Acetylglucosamine Homeostasis in Pancreatic Beta-cell Development and FunctionR01DK115720 · NIDDK · UNIVERSITY OF MINNESOTA · PI ALEJANDRO, EMILYN · 2018 to 2022
$1.9M
Programming of beta-cells and Glucose Homeostasis by Maternal Metformin ExposureK08DK102526 · NIDDK · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI GREGG, BRIGID ELLEN · 2015 to 2021
$797k
Mechanisms of Developmental Programing of beta-cell Susceptibility to GlucolipotoxicityK01DK103823 · NIDDK · UNIVERSITY OF MINNESOTA · PI ALEJANDRO, EMILYN · 2014 to 2017
$572k
Innate Immune Complement System and Developmental Programming of Functional β Cell MassR21HD100840 · NICHD · UNIVERSITY OF MINNESOTA · PI ALEJANDRO, EMILYN, REGAL, JEAN F. · 2020 to 2021
$425k
Role of placental nutrient-sensor protein mTOR on fetal programming of beta-cell dysfunction and susceptibility to type 2 diabetesR03DK114465 · NIDDK · UNIVERSITY OF MINNESOTA · PI ALEJANDRO, EMILYN · 2018 to 2019
$360k
NICHD NIH HHS R21 HD100840NIDDK NIH HHS K01 DK103823NIDDK NIH HHS K08 DK102526NIDDK NIH HHS R01 DK073716NIDDK NIH HHS R01 DK090262NIDDK NIH HHS R01 DK115720NIDDK NIH HHS R03 DK114465
6 · The paper itself

Abstract

The risk of obesity in adulthood is subject to programming in the womb. Maternal obesity contributes to programming of obesity and metabolic disease risk in the adult offspring. With the increasing prevalence of obesity in women of reproductive age there is a need to understand the ramifications of maternal high-fat diet (HFD) during pregnancy on offspring's metabolic heath trajectory. In the present study, we determined the long-term metabolic outcomes on adult male and female offspring of dams fed with HFD during pregnancy. C57BL/6J dams were fed either Ctrl or 60% Kcal HFD for 4 weeks before and throughout pregnancy, and we tested glucose homeostasis in the adult offspring. Both Ctrl and HFD-dams displayed increased weight during pregnancy, but HFD-dams gained more weight than Ctrl-dams. Litter size and offspring birthweight were not different between HFD-dams or Ctrl-dams. A significant reduction in random blood glucose was evident in newborns from HFD-dams compared to Ctrl-dams. Islet morphology and alpha-cell fraction were normal but a reduction in beta-cell fraction was observed in newborns from HFD-dams compared to Ctrl-dams. During adulthood, male offspring of HFD-dams displayed comparable glucose tolerance under normal chow. Male offspring re-challenged with HFD displayed glucose intolerance transiently. Adult female offspring of HFD-dams demonstrated normal glucose tolerance but displayed increased insulin resistance relative to controls under normal chow diet. Moreover, adult female offspring of HFD-dams displayed increased insulin secretion in response to high-glucose treatment, but beta-cell mass were comparable between groups. Together, these data show that maternal HFD at pre-conception and during gestation predisposes the female offspring to insulin resistance in adulthood.

Indexed as

Diet, High-FatInsulin SecretionMaternal ExposureAnimalsAnimals, NewbornBirth WeightBlood GlucoseFemaleGlucose IntoleranceInsulin-Secreting CellsLitter SizeMaleMiceOrgan SizePregnancyPregnancy in ObesityBlood Glucosediabetesfetal programminghigh-fat dietinflammationmaternal obesitymetabolic dysfunctionsex dimorphismWestern-diet

Identifiers

PMID35111136
PMCPMC8801938
OpenAlexW4206778154

What Socratic holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.