Evidence map›Paper›PMID 28811499›Full record

ArticleScientific reports2017

The role of Dermcidin isoform-2 in the occurrence and severity of Diabetes.

Suman Bhattacharya, Md Mobidullah Khan, Chandradipa Ghosh, Sarbashri Bank, Smarajit Maiti

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed, 1 pooled it
0.5field-weighted citation impact, top 31% 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

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

  1. Pooled it
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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

5 authors at 2 institutions in 1 country.

Suman BhattacharyaSinha Institute of Medical Science and Technology, West Bengal, India.
Md Mobidullah KhanPG Department of Biochemistry, Cell and Molecular Therapeutics Laboratory, Oriental Institute of Science and Technology, Midnapore, West Bengal, India.
Chandradipa GhoshDepartment of Human Physiology with Community Health, Vidyasagar University, Midnapore, West Bengal, India.
Sarbashri BankSinha Institute of Medical Science and Technology, West Bengal, India.
Smarajit MaitiPG Department of Biochemistry, Cell and Molecular Therapeutics Laboratory, Oriental Institute of Science and Technology, Midnapore, West Bengal, India. maitism@rediffmail.com.
Sinha Institute of Medical Science & Technology · INVidyasagar University · IN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Diabetes is now epidemic worldwide. Several hundred-million peoples are presently suffering from this disease with other secondary-disorders. Stress, hypertension, sedentary life-style, carbohydrate/lipid metabolic-disorders due to genetic or environmental factors attributes to type-1 and/or type-2 diabetes. Present investigation demonstrates that stress-induced protein dermcidin isoform-2 (DCN-2) which appears in the serum of diabetic-patients play a key-role in this disease pathogenesis/severity. DCN-2 suppresses insulin production-release from liver/pancreas. It also increases the insulin-resistance. Stress-induction at the onset/progression of this disease is noticed as the high-level of lipid peroxides/low-level of free-thiols in association with increase of inflammatory-markers c-reactive protein and TNF-α. DCN-2 induced decrease in the synthesis of glucose-activated nitric oxide synthase (GANOS) and lower production of NO in liver has been shown here where NO is demonstrated to lower the expression of glucose trabsporter-4 (GLUT-4) and its translocation on liver membrane surface. This finally impairs glucose transport to organs from the extracellular fluid. Low level of glucose uptake further decreases glucose-induced insulin synthesis. The central role of DCN-2 has been demonstrated in type-1/type-2 diabetic individuals, in rodent hepatocytes and pancreatic-cell, tissue-slices, in-vitro and in-vivo experimental model. It can be concluded that stress-induced decrease in insulin synthesis/function, glucose transport is an interactive consequence of oxidative threats and inflammatory events.

Indexed as

AdultAnimalsBiomarkersBlood GlucoseDiabetes MellitusDiabetes Mellitus, ExperimentalDisease Models, AnimalFemaleGene ExpressionGlucoseGlucose Transporter Type 4HepatocytesHumansInsulinInsulin ResistanceMaleBiomarkersBlood GlucosedermcidinGlucoseGlucose Transporter Type 4InsulinNitric Oxide SynthasePeptidesProtein IsoformsReactive Oxygen Species

Identifiers

PMID28811499
PMCPMC5557962
OpenAlexW2743365131

What OpenQuestion holds

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Registered trials

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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.