Evidence map›Paper›PMID 27770396›Full record

ArticleEndocrine2016

Insulin resistance elicited in postpubertal primate offspring deprived of estrogen in utero.

Gerald J Pepe, Adina Maniu, Graham Aberdeen, Terrie J Lynch, Soon Ok Kim, Jerry Nadler, Eugene D Albrecht

Abstract read
In one paragraph

Article in Endocrine, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
1.2field-weighted citation impact, top 16% 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

11 citing papers in PubMed, 14 citations in OpenAlex.

  1. Article
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  4. Microvascular Skeletal-Muscle Crosstalk in Health and Disease.International journal of molecular sciences · 2023
    Review
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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

7 authors at 2 institutions in 1 country.

Gerald J PepeDepartment of Physiological Sciences, Eastern Virginia Medical School, Norfolk, VA, USA. PEPEGJ@EVMS.EDU.
Adina ManiuDepartment of Obstetrics/Gynecology/Reproductive Sciences, University of Maryland School of Medicine, Baltimore, MD, USA.
Graham AberdeenDepartment of Obstetrics/Gynecology/Reproductive Sciences, University of Maryland School of Medicine, Baltimore, MD, USA.
Terrie J LynchDepartment of Physiological Sciences, Eastern Virginia Medical School, Norfolk, VA, USA.
Soon Ok KimDepartment of Physiological Sciences, Eastern Virginia Medical School, Norfolk, VA, USA.
Jerry NadlerDepartment of Internal Medicine, Eastern Virginia Medical School, Norfolk, VA, USA.
Eugene D AlbrechtDepartments of Obstetrics/Gynecology/Reproductive Sciences and Physiology, University of Maryland School of Medicine, Baltimore, MD, USA.
Eastern Virginia Medical School · USUniversity of Maryland, Baltimore · US

Funding

Primate Fetal Adrenal Development: Impact on Physiological Processes After BirthR01DK093950 · NIDDK · UNIVERSITY OF MARYLAND BALTIMORE · PI ALBRECHT, EUGENE D. · 2013 to 2016
$2.3M
NIDDK NIH HHS R01 DK093950
6 · The paper itself

Abstract

We recently demonstrated that offspring delivered to baboons deprived of estrogen during the second half of gestation exhibited insulin resistance prior to onset of puberty. Because gonadal hormones have a profound effect on insulin action and secretion in adults, we determined whether insulin resistance is retained after initiation of gonadal secretion of testosterone and estradiol. Glucose tolerance tests were performed in postpubertal baboon offspring of untreated and letrozole-treated animals (serum estradiol reduced >95 %). Basal fasting levels of insulin (P < 0.05) and peak 1 min and 1 + 3 + 5 min levels of glucose after glucose tolerance tests challenge (P < 0.03) were greater in offspring delivered to letrozole-treated, estrogen-deprived baboons than untreated animals. Moreover, the value for the HOMA-IR, an accepted index of insulin resistance, was 2-fold greater (P < 0.05) in offspring delivered to baboons treated with letrozole than in untreated animals. Collectively these results support the proposal that estrogen normally has an important role in programming mechanisms in utero within the developing fetus that lead to insulin sensitivity after birth.

Indexed as

Insulin ResistancePrenatal Exposure Delayed EffectsSexual MaturationAnimalsAromatase InhibitorsEstradiolFemaleGlucose Tolerance TestLetrozoleNitrilesPapio anubisPregnancyTriazolesAromatase InhibitorsEstradiolLetrozoleNitrilesTriazolesEstrogenInsulin sensitivityOffspringPrimate

Identifiers

PMID27770396
PMCPMC6038696
OpenAlexW2539442405

What OpenQuestion holds

Textmetadata
LicenceTDM
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 OpenQuestion graph.