Evidence map›Paper›PMID 30303709›Full record

ArticleAmerican journal of physiology. Regulatory, integrative and comparative physiology2018

Reduced uterine perfusion pressure causes loss of pancreatic β-cell area but normal function in fetal rat offspring.

Brian Akhaphong, Amber Lockridge, Seokwon Jo, Ramkumar Mohan, Jacob A Wilcox, Cameron R Wing, Jean F Regal, Emilyn U Alejandro

Open access · bronzeAbstract read
In one paragraph

Article in American journal of physiology. Regulatory, integrative and comparative physiology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed, 1 pooled it
4.4field-weighted citation impact, top 6% 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

13 citing papers in PubMed, 1 synthesis or guideline pooled it, 21 citations in OpenAlex.

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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

8 authors at 2 institutions in 1 country.

Brian AkhaphongDepartment of Integrative Biology & Physiology, University of Minnesota: Twin Cities, Minnesota.
Amber LockridgeDepartment of Integrative Biology & Physiology, University of Minnesota: Twin Cities, Minnesota.
Seokwon JoDepartment of Integrative Biology & Physiology, University of Minnesota: Twin Cities, Minnesota.
Ramkumar MohanDepartment of Integrative Biology & Physiology, University of Minnesota: Twin Cities, Minnesota.
Jacob A WilcoxDepartment of Biomedical Sciences, University of Minnesota Medical School, Duluth Campus, Duluth, Minnesota.
Cameron R WingDepartment of Biomedical Sciences, University of Minnesota Medical School, Duluth Campus, Duluth, Minnesota.
Jean F RegalDepartment of Biomedical Sciences, University of Minnesota Medical School, Duluth Campus, Duluth, Minnesota.
Emilyn U AlejandroDepartment of Integrative Biology & Physiology, University of Minnesota: Twin Cities, Minnesota.ORCID 0000-0002-7941-8439
University of Minnesota · USUniversity of Minnesota, Duluth · US

Funding

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
Complement Activation in Pregnancy and HypertensionR15HL109843 · NHLBI · UNIVERSITY OF MINNESOTA DULUTH · PI REGAL, JEAN F. · 2011 to 2015
$1.3M
O-linked-N-acetylglucosamine Post-translational Modification in Pancreatic Beta-cells Regulating ER Stress and Mitochondrial FunctionR21DK112144 · NIDDK · UNIVERSITY OF MINNESOTA · PI ALEJANDRO, EMILYN · 2017 to 2019
$576k
Mechanisms of Developmental Programing of beta-cell Susceptibility to GlucolipotoxicityK01DK103823 · NIDDK · UNIVERSITY OF MINNESOTA · PI ALEJANDRO, EMILYN · 2014 to 2017
$572k
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
NHLBI NIH HHS R15 HL109843NIDDK NIH HHS K01 DK103823NIDDK NIH HHS R01 DK115720NIDDK NIH HHS R03 DK114465NIDDK NIH HHS R21 DK112144
6 · The paper itself

Abstract

Maternal hypertension during pregnancy is a major risk factor for intrauterine growth restriction (IUGR), which increases susceptibility to cardiovascular and metabolic disease in adulthood through unclear mechanisms. The aim of this study was to characterize the pancreatic β-cell area and function in the fetal rat offspring of a reduced uterine perfusion pressure (RUPP) model of gestational hypertension. At embryonic day 19.5, RUPP dams exhibited lower body weight, elevated mean blood pressure, reduced litter size, and higher blood glucose compared with sham-operated controls. In RUPP placental lysates, a nonsignificant change in mammalian target of rapamycin (mTOR) activity markers, phosphorylated S6 at serine 240, and phosphorylated AKT (at S473) was observed. RUPP offspring showed significantly reduced β-cell-to-pancreas area and increased β-cell death but normal insulin levels in serum. Isolated islets had normal insulin content and secretory function in response to glucose and palmitate. Fetal pancreatic lysates showed a tendency for reduced insulin levels, with a significant reduction in total mTOR protein with RUPP surgery. In addition, its downstream complex 2 targets phosphorylation of AKT at S473, and pAKT at Thr

Indexed as

AnimalsBlood PressureDiabetes Mellitus, Type 2FemaleFetal Growth RetardationHypertension, Pregnancy-InducedInsulin-Secreting CellsPlacentaPre-EclampsiaPregnancyRats, Sprague-DawleyUterusintrauterine growth restrictionisletsmTORplacentaβ-cell

Identifiers

PMID30303709
PMCPMC6425640
OpenAlexW2897469252

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.