Evidence map›Paper›PMID 30040846›Full record

ArticlePloS one2018

p8 deficiency leads to elevated pancreatic beta cell mass but does not contribute to insulin resistance in mice fed with high-fat diet.

Marcus Hollenbach, Nora Klöting, Ines Sommerer, Jana Lorenz, Mario Heindl, Matthias Kern, Joachim Mössner, Matthias Blüher, Albrecht Hoffmeister

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
0.7field-weighted citation impact, top 28% 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

2 citing papers in PubMed, 4 citations in OpenAlex.

  1. Review
  2. Article
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

9 authors at 2 institutions in 1 country.

Marcus HollenbachDepartment of Medicine, Neurology and Dermatology, Division of Gastroenterology and Rheumatology, University of Leipzig, Leipzig, Germany.ORCID 0000-0002-2654-3164
Nora KlötingIFB Adiposity Disease, University of Leipzig, Leipzig, Germany.
Ines SommererDepartment of Medicine, Neurology and Dermatology, Division of Gastroenterology and Rheumatology, University of Leipzig, Leipzig, Germany.
Jana LorenzDepartment of Medicine, Neurology and Dermatology, Division of Gastroenterology and Rheumatology, University of Leipzig, Leipzig, Germany.
Mario HeindlDepartment of Medicine, Neurology and Dermatology, Division of Gastroenterology and Rheumatology, University of Leipzig, Leipzig, Germany.
Matthias KernGerman Diabetes Center Leipzig, University of Leipzig, Leipzig, Germany.
Joachim MössnerDepartment of Medicine, Neurology and Dermatology, Division of Gastroenterology and Rheumatology, University of Leipzig, Leipzig, Germany.
Matthias BlüherDepartment of Medicine, Neurology and Dermatology, Division of Endocrinology and Nephrology, University of Leipzig, Leipzig, Germany.
Albrecht HoffmeisterDepartment of Medicine, Neurology and Dermatology, Division of Gastroenterology and Rheumatology, University of Leipzig, Leipzig, Germany.
Deutsches Diabetes-Zentrum e.V. · DEIFB Adiposity Diseases · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundp8 was initially described as being overexpressed in acute pancreatitis and encoding a ubiquitous stress protein. Analysis of insulin sensitivity and glucose tolerance in p8-knockout and haplodeficient mice revealed counterintuitive results. Thus, we determined glycemic control of p8 in mice fed with standard (SD) and high-fat diet (HFD).

methodsp8-/- and wild type (p8+/+) mice were used for analysis of glucagon (immunohistochemistry), insulin levels (ELISA) and beta cell mass. Hyperinsulinemic- euglycemic glucose clamp technique, i.p. glucose tolerance test (ipGTT), i.p. insulin tolerance test (ipITT) and metabolic chamber analysis were performed in SD (4% fat) and HFD (55% fat) groups.

resultsp8-/- mice showed no differences in glucagon or insulin content but higher insulin secretion from pancreatic islets upon glucose stimulation. p8 deficiency resulted in elevated beta cell mass but was not associated with increased insulin resistance in ipGTT or ipITT. Glucose clamp tests also revealed no evidence of association of p8 deficiency with insulin resistance. Metabolic chamber analysis showed equal energy expenditure in p8-/- mice and wild type animals.

conclusionp8 depletion may contribute to glucose metabolism via stress-induced insulin production and elevated beta cell mass. Nevertheless, p8 knockout showed no impact on insulin resistance in SD and HFD-fed mice.

Indexed as

AnimalsDietary FatsDiet, High-FatDNA-Binding ProteinsEnergy MetabolismFemaleGlucagonGlucoseInsulinInsulin ResistanceInsulin-Secreting CellsMaleMice, Inbred C57BLMice, KnockoutNeoplasm ProteinsDietary FatsDNA-Binding ProteinsGlucagonGlucoseInsulinNeoplasm ProteinsNupr1 protein, mouse

Identifiers

PMID30040846
PMCPMC6057664
OpenAlexW2884204026

What OpenQuestion holds

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LicenceCC BY
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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.