Evidence map›Paper›PMID 30603372›Full record

ArticleDiabetology international2018

Pathophysiological significance of hepatokine overproduction in type 2 diabetes.

Hirofumi Misu

Open access · bronzeAbstract read
In one paragraph

Article in Diabetology international, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
0.8field-weighted citation impact, top 29% 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

9 citing papers in PubMed, 15 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

1 author at 1 institution in 1 country.

Hirofumi Misu1Department of Endocrinology and Metabolism, Kanazawa University Graduate School of Medical Sciences, 13-1 Takara-machi, Kanazawa, Ishikawa 920-8641 Japan.ORCID 0000-0003-3286-8464
Kanazawa University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Currently, many studies draw attention to novel secretory factors, such as adipokines or myokines, derived from the tissues that were not originally recognized as endocrine organs. The liver may contribute to the onset of various kinds of pathologies of type 2 diabetes by way of the production of secretory proteins "hepatokines." Using the comprehensive gene expression analyses in human livers, we have rediscovered selenoprotein P and LECT2 as hepatokines involved in the onset of dysregulated glucose metabolism. Overproduction of selenoprotein P, previously reported as a transport protein of selenium, induces insulin resistance and hyperglycemia in type 2 diabetic condition. Selenoprotein P also contributes to vascular complications of type 2 diabetes directly by inducing VEGF resistance in vascular endothelial cells. Notably, selenoprotein P impairs health-promoting effects of exercise by inhibiting ROS/AMPK/PGC-1α pathway in the skeletal muscle through its receptor LRP1. Overproduction of LECT2, previously reported as a neutrophil chemotactic protein, links obesity to insulin resistance in the skeletal muscle. Further studies would develop novel diagnostic or therapeutic procedures targeting hepatokines to combat over-nutrition-related diseases such as type 2 diabetes.

Indexed as

HepatokinesInsulin resistanceLECT2Selenoprotein P

Identifiers

PMID30603372
PMCPMC6224882
OpenAlexW2886510241

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.