Evidence map›Paper›PMID 26232096›Full record

ArticleDiabetologia2015

The diabetes gene Zfp69 modulates hepatic insulin sensitivity in mice.

Bomee Chung, Mandy Stadion, Nadja Schulz, Deepak Jain, Stephan Scherneck, Hans-Georg Joost, Annette Schürmann

Open access · hybridAbstract read
In one paragraph

Article in Diabetologia, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed, 1 pooled it
0.9field-weighted citation impact, top 27% 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

17 citing papers in PubMed, 1 synthesis or guideline pooled it, 22 citations in OpenAlex.

  1. Pooled it
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  14. KRAB zinc finger proteins.Development (Cambridge, England) · 2017
    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 3 institutions in 1 country.

Bomee ChungDepartment of Experimental Diabetology, German Institute of Human Nutrition Potsdam-Rebruecke, Arthur-Scheunert-Allee 114-116, D-14558, Nuthetal, Germany.
Mandy StadionDepartment of Experimental Diabetology, German Institute of Human Nutrition Potsdam-Rebruecke, Arthur-Scheunert-Allee 114-116, D-14558, Nuthetal, Germany.
Nadja SchulzDepartment of Experimental Diabetology, German Institute of Human Nutrition Potsdam-Rebruecke, Arthur-Scheunert-Allee 114-116, D-14558, Nuthetal, Germany.
Deepak JainGerman Center for Diabetes Research (DZD), Neuherberg, Germany.
Stephan ScherneckDepartment of Experimental Diabetology, German Institute of Human Nutrition Potsdam-Rebruecke, Arthur-Scheunert-Allee 114-116, D-14558, Nuthetal, Germany.
Hans-Georg JoostDepartment of Experimental Diabetology, German Institute of Human Nutrition Potsdam-Rebruecke, Arthur-Scheunert-Allee 114-116, D-14558, Nuthetal, Germany.
Annette SchürmannDepartment of Experimental Diabetology, German Institute of Human Nutrition Potsdam-Rebruecke, Arthur-Scheunert-Allee 114-116, D-14558, Nuthetal, Germany. schuermann@dife.de.
German Center for Diabetes Research · DEHeinrich Heine University Düsseldorf · DEGerman Institute of Human Nutrition · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

aims/hypothesisZfp69 was previously identified by positional cloning as a candidate gene for obesity-associated diabetes. C57BL/6J and New Zealand obese (NZO) mice carry a loss-of-function mutation due to the integration of a retrotransposon. On the NZO background, the Zfp69 locus caused severe hyperglycaemia and loss of beta cells. To provide direct evidence for a causal role of Zfp69, we investigated the effects of its overexpression on both a lean [B6-Tg(Zfp69)] and an obese [NZO/B6-Tg(Zfp69)] background.

methodsZfp69 transgenic mice were generated by integrating the cDNA into the ROSA locus of the C57BL/6 genome and characterised.

resultsB6-Tg(Zfp69) mice were normoglycaemic, developed hyperinsulinaemia, and exhibited increased expression of G6pc and Pck1 and slightly reduced phospho-Akt levels in the liver. During OGTTs, glucose clearance was normal but insulin levels were significantly higher in the B6-Tg(Zfp69) than in control mice. The liver fat content and plasma triacylglycerol levels were significantly increased in B6-Tg(Zfp69) and NZO/B6-Tg(Zfp69) mice on a high-fat diet compared with controls. Liver transcriptome analysis of B6-Tg(Zfp69) mice revealed a downregulation of genes involved in glucose and lipid metabolism. Specifically, expression of Nampt, Lpin2, Map2k6, Gys2, Bnip3, Fitm2, Slc2a2, Ppargc1α and Insr was significantly decreased in the liver of B6-Tg(Zfp69) mice compared with wild-type animals. However, overexpression of Zfp69 did not induce overt diabetes with hyperglycaemia and beta cell loss. CONCLUSIONS/

interpretationZfp69 mediates hyperlipidaemia, liver fat accumulation and mild insulin resistance. However, it does not induce type 2 diabetes, suggesting that the diabetogenic effect of the Zfp69 locus requires synergy with other as yet unidentified genes.

Indexed as

AnimalsDiabetes Mellitus, Type 2Diet, High-FatFatty LiverHyperlipidemiasInsulin ResistanceInsulin-Secreting CellsLiverMiceMice, ObeseMice, TransgenicObesityQuantitative Trait LociTranscription FactorsTranscription FactorsZfp69 protein, mouseDiabetesHepatosteatosisInsulin resistanceLipid metabolismZfp69

Identifiers

PMID26232096
PMCPMC4572078
OpenAlexW2130654964

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.