Evidence map›Paper›PMID 29296001›Full record

ArticleNature communications2018

Sirt2 facilitates hepatic glucose uptake by deacetylating glucokinase regulatory protein.

Hitoshi Watanabe, Yuka Inaba, Kumi Kimura, Michihiro Matsumoto, Shuichi Kaneko, Masato Kasuga, Hiroshi Inoue

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 papers.

0numbers the graph read from it
0cells of the map it votes in
53citing papers in PubMed
3.6field-weighted citation impact, top 7% 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

53 citing papers in PubMed, 103 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

7 authors at 2 institutions in 1 country.

Hitoshi WatanabeMetabolism and Nutrition Research Unit, Institute for Frontier Science Initiative, Kanazawa University, Kanazawa, Ishikawa, 920-8641, Japan.
Yuka InabaMetabolism and Nutrition Research Unit, Institute for Frontier Science Initiative, Kanazawa University, Kanazawa, Ishikawa, 920-8641, Japan.
Kumi KimuraMetabolism and Nutrition Research Unit, Institute for Frontier Science Initiative, Kanazawa University, Kanazawa, Ishikawa, 920-8641, Japan.
Michihiro MatsumotoDepartment of Molecular Metabolic Regulation, Diabetes Research Center, Research Institute, National Center for Global Health and Medicine, Tokyo, 162-8655, Japan.
Shuichi KanekoDepartment of System Biology, Kanazawa University Graduate School of Medical Sciences, Kanazawa, Ishikawa, 920-8641, Japan.
Masato KasugaNational Center for Global Health and Medicine, Tokyo, 162-8655, Japan.
Hiroshi InoueMetabolism and Nutrition Research Unit, Institute for Frontier Science Initiative, Kanazawa University, Kanazawa, Ishikawa, 920-8641, Japan. inoue-h@staff.kanazawa-u.ac.jp.
Kanazawa University · JPNational Center for Global Health and Medicine · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Impaired hepatic glucose uptake (HGU) causes postprandial hyperglycemia in type 2 diabetes. Here, we show that diminished hepatic Sirt2 activity impairs HGU in obese diabetic mice. Hepatic Sirt2 overexpression increases HGU in high-fat diet (HFD)-fed obese diabetic mice and mitigates their impaired glucose tolerance. Hepatic Sirt2 knockdown in non-diabetic mice reduces HGU and causes impaired glucose tolerance. Sirt2 promotes glucose-dependent HGU by deacetylating K126 of glucokinase regulatory protein (GKRP). Glucokinase and GKRP glucose-dependent dissociation is necessary for HGU but is inhibited in hepatocytes derived from obese diabetic mice, depleted of Sirt2 or transfected with GKRP acetylation-mimicking mutants. GKRP deacetylation-mimicking mutants dissociate from glucokinase in a glucose concentration-dependent manner in obese diabetic mouse-derived hepatocytes and increase HGU and glucose tolerance in HFD-induced or db/db obese diabetic mice. We demonstrate that Sirt2-dependent GKRP deacetylation improves impaired HGU and suggest that it may be a therapeutic target for type 2 diabetes.

Indexed as

Adaptor Proteins, Signal TransducingAnimalsBiological TransportCarrier ProteinsDiabetes Mellitus, Type 2Gene Expression RegulationGene Knockdown TechniquesGlucoseIntracellular Signaling Peptides and ProteinsLiverMiceMice, ObeseMutationSirtuin 2Adaptor Proteins, Signal TransducingCarrier ProteinsGckr protein, mouseGlucoseIntracellular Signaling Peptides and ProteinsSirt2 protein, mouseSirtuin 2

Identifiers

PMID29296001
PMCPMC5750207
OpenAlexW2779749520

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.