Evidence map›Paper›PMID 26650569›Full record

ArticleEndocrinology2016

Developmental Programming: Impact of Gestational Steroid and Metabolic Milieus on Adiposity and Insulin Sensitivity in Prenatal Testosterone-Treated Female Sheep.

Rodolfo C Cardoso, Almudena Veiga-Lopez, Jacob Moeller, Evan Beckett, Anthony Pease, Erica Keller, Vanessa Madrigal, Gregorio Chazenbalk, Daniel Dumesic, Vasantha Padmanabhan

Open access · bronzeAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Endocrinology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.

0numbers the graph read from it
0cells of the map it votes in
38citing papers in PubMed
8.4field-weighted citation impact, top 3% 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

38 citing papers in PubMed, 67 citations in OpenAlex.

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  10. Leptin as a key regulator of the adipose organ.Reviews in endocrine & metabolic disorders · 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 3 institutions in 1 country.

Rodolfo C CardosoDepartment of Pediatrics (R.C.C., A.V.-L., J.M., E.B., V.P.), University of Michigan, Ann Arbor, Michigan 48109; Department of Small Animal Clinical Sciences (A.P.), Michigan State University, East Lansing, Michigan 48824; and Department of Obstetrics and Gynecology (E.K., V.M., G.C., D.D.), David Geffen School of Medicine at University of California, Los Angeles, Los Angeles, California 90095.
Almudena Veiga-LopezDepartment of Pediatrics (R.C.C., A.V.-L., J.M., E.B., V.P.), University of Michigan, Ann Arbor, Michigan 48109; Department of Small Animal Clinical Sciences (A.P.), Michigan State University, East Lansing, Michigan 48824; and Department of Obstetrics and Gynecology (E.K., V.M., G.C., D.D.), David Geffen School of Medicine at University of California, Los Angeles, Los Angeles, California 90095.
Jacob MoellerDepartment of Pediatrics (R.C.C., A.V.-L., J.M., E.B., V.P.), University of Michigan, Ann Arbor, Michigan 48109; Department of Small Animal Clinical Sciences (A.P.), Michigan State University, East Lansing, Michigan 48824; and Department of Obstetrics and Gynecology (E.K., V.M., G.C., D.D.), David Geffen School of Medicine at University of California, Los Angeles, Los Angeles, California 90095.
Evan BeckettDepartment of Pediatrics (R.C.C., A.V.-L., J.M., E.B., V.P.), University of Michigan, Ann Arbor, Michigan 48109; Department of Small Animal Clinical Sciences (A.P.), Michigan State University, East Lansing, Michigan 48824; and Department of Obstetrics and Gynecology (E.K., V.M., G.C., D.D.), David Geffen School of Medicine at University of California, Los Angeles, Los Angeles, California 90095.
Anthony PeaseDepartment of Pediatrics (R.C.C., A.V.-L., J.M., E.B., V.P.), University of Michigan, Ann Arbor, Michigan 48109; Department of Small Animal Clinical Sciences (A.P.), Michigan State University, East Lansing, Michigan 48824; and Department of Obstetrics and Gynecology (E.K., V.M., G.C., D.D.), David Geffen School of Medicine at University of California, Los Angeles, Los Angeles, California 90095.
Erica KellerDepartment of Pediatrics (R.C.C., A.V.-L., J.M., E.B., V.P.), University of Michigan, Ann Arbor, Michigan 48109; Department of Small Animal Clinical Sciences (A.P.), Michigan State University, East Lansing, Michigan 48824; and Department of Obstetrics and Gynecology (E.K., V.M., G.C., D.D.), David Geffen School of Medicine at University of California, Los Angeles, Los Angeles, California 90095.
Vanessa MadrigalDepartment of Pediatrics (R.C.C., A.V.-L., J.M., E.B., V.P.), University of Michigan, Ann Arbor, Michigan 48109; Department of Small Animal Clinical Sciences (A.P.), Michigan State University, East Lansing, Michigan 48824; and Department of Obstetrics and Gynecology (E.K., V.M., G.C., D.D.), David Geffen School of Medicine at University of California, Los Angeles, Los Angeles, California 90095.
Gregorio ChazenbalkDepartment of Pediatrics (R.C.C., A.V.-L., J.M., E.B., V.P.), University of Michigan, Ann Arbor, Michigan 48109; Department of Small Animal Clinical Sciences (A.P.), Michigan State University, East Lansing, Michigan 48824; and Department of Obstetrics and Gynecology (E.K., V.M., G.C., D.D.), David Geffen School of Medicine at University of California, Los Angeles, Los Angeles, California 90095.
Daniel DumesicDepartment of Pediatrics (R.C.C., A.V.-L., J.M., E.B., V.P.), University of Michigan, Ann Arbor, Michigan 48109; Department of Small Animal Clinical Sciences (A.P.), Michigan State University, East Lansing, Michigan 48824; and Department of Obstetrics and Gynecology (E.K., V.M., G.C., D.D.), David Geffen School of Medicine at University of California, Los Angeles, Los Angeles, California 90095.
Vasantha PadmanabhanDepartment of Pediatrics (R.C.C., A.V.-L., J.M., E.B., V.P.), University of Michigan, Ann Arbor, Michigan 48109; Department of Small Animal Clinical Sciences (A.P.), Michigan State University, East Lansing, Michigan 48824; and Department of Obstetrics and Gynecology (E.K., V.M., G.C., D.D.), David Geffen School of Medicine at University of California, Los Angeles, Los Angeles, California 90095.
University of Michigan–Ann Arbor · USUniversity of California, Los Angeles · USMichigan State University · US

Funding

Regional Pilot And Feasibility Study Grants ProgramP30DK020572 · NIDDK · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI Mehboob A Hussain · 2013 to 2026
$24.3M
PROJECT 4: ANDROGEN EXCESS IN ADIPOGENIC DYSFUNCTION IN PCOS WOMENP50HD071836 · NICHD · OREGON HEALTH & SCIENCE UNIVERSITY · PI DUMESIC, DANIEL A · 2014 to 2021
$14.7M
STEROIDAL AND METABOLIC MEDIATION OF NEUROENDOCRINE CIRCUITRYP01HD044232 · NICHD · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI PADMANABHAN, VASANTHA · 2004 to 2015
$12.9M
NICHD NIH HHS P01 HD044232NICHD NIH HHS P01 HD44232NICHD NIH HHS P50 HD071836NIDDK NIH HHS P30 DK020572
6 · The paper itself

Abstract

Prenatally testosterone (T)-treated sheep present metabolic disruptions similar to those seen in women with polycystic ovary syndrome. These females exhibit an increased ratio of small to large adipocytes, which may be the earliest event in the development of adult insulin resistance. Additionally, our longitudinal studies suggest the existence of a period of compensatory adaptation during development. This study tested whether 1) in utero cotreatment of prenatally T-treated sheep with androgen antagonist (flutamide) or insulin sensitizer (rosiglitazone) prevents juvenile insulin resistance and adult changes in adipocyte size; and 2) visceral adiposity and insulin sensitivity are both unaltered during early adulthood, confirming the predicted developmental trajectory in this animal model. Insulin sensitivity was tested during juvenile development and adipose tissue distribution, adipocyte size, and concentrations of adipokines were determined during early adulthood. Prenatal T-treated females manifested juvenile insulin resistance, which was prevented by prenatal rosiglitazone cotreatment. Neither visceral adiposity nor insulin sensitivity differed between groups during early adulthood. Prenatal T-treated sheep presented an increase in the relative proportion of small adipocytes, which was not substantially prevented by either prenatal intervention. A large effect size was observed for increased leptin concentrations in prenatal T-treated sheep compared with controls, which was prevented by prenatal rosiglitazone. In conclusion, gestational alterations in insulin-glucose homeostasis likely play a role in programming insulin resistance, but not adipocyte size distribution, in prenatal T-treated sheep. Furthermore, these results support the notion that a period of compensatory adaptation of the metabolic system to prenatal T exposure occurs between puberty and adulthood.

Indexed as

Insulin ResistanceAdiposityAnimalsDisease Models, AnimalEmbryonic DevelopmentFemaleFlutamideObesityPolycystic Ovary SyndromePregnancyPrenatal Exposure Delayed EffectsRosiglitazoneSheepTestosteroneThiazolidinedionesFlutamideRosiglitazoneTestosteroneThiazolidinediones

Identifiers

PMID26650569
PMCPMC4733129
OpenAlexW2226969145

What OpenQuestion holds

Textmetadata
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.