Evidence map›Paper›PMID 25987348›Full record

ArticleEndocrine2015

Circulating ghrelin level is higher in HNF1A-MODY and GCK-MODY than in polygenic forms of diabetes mellitus.

Natalia Nowak, Jerzy Hohendorff, Iwona Solecka, Magdalena Szopa, Jan Skupien, Beata Kiec-Wilk, Wojciech Mlynarski, Maciej T Malecki

Open access · hybridAbstract read
In one paragraph

Article in Endocrine, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed, 1 pooled it
0.9field-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

18 citing papers in PubMed, 1 synthesis or guideline pooled it, 21 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Article
  4. Review
  5. Germline and conditional ghrelin knockout increases islet size.The Journal of clinical investigation · 2023
    Article
  6. Review
  7. Article
  8. HNF1A Mutations and Beta Cell Dysfunction in Diabetes.International journal of molecular sciences · 2022
    Review
  9. Review
  10. Article
  11. Article
  12. Review
  13. Ghrelin as a Survival Hormone.Trends in endocrinology and metabolism: TEM · 2017
    Review
  14. Article
  15. Article
  16. Review
  17. Article
  18. Undiagnosed MODY: Time for Action.Current diabetes reports · 2015
    Review
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

8 authors at 3 institutions in 2 countries.

Natalia NowakDepartment of Metabolic Diseases, Jagiellonian University Medical College, 15 Kopernika Street, 31-501, Krakow, Poland.
Jerzy HohendorffDepartment of Metabolic Diseases, Jagiellonian University Medical College, 15 Kopernika Street, 31-501, Krakow, Poland.
Iwona SoleckaUniversity Hospital, Krakow, Poland.
Magdalena SzopaDepartment of Metabolic Diseases, Jagiellonian University Medical College, 15 Kopernika Street, 31-501, Krakow, Poland.
Jan SkupienDepartment of Metabolic Diseases, Jagiellonian University Medical College, 15 Kopernika Street, 31-501, Krakow, Poland.
Beata Kiec-WilkDepartment of Metabolic Diseases, Jagiellonian University Medical College, 15 Kopernika Street, 31-501, Krakow, Poland.
Wojciech MlynarskiDepartment of Pediatrics, Oncology, Hematology and Diabetology, Medical University of Lodz, Lodz, Poland.
Maciej T MaleckiDepartment of Metabolic Diseases, Jagiellonian University Medical College, 15 Kopernika Street, 31-501, Krakow, Poland. malecki_malecki@yahoo.com.
Krakow Cardiovascular Research Institute · PLJagiellonian University · PLMedical University of Lodz · PL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Ghrelin is a hormone that regulates appetite. It is likely to be involved in the pathophysiology of varying forms of diabetes. In animal studies, the ghrelin expression was regulated by the hepatocyte nuclear factor 1 alpha (HNF1A). Mutations of the HNF1A gene cause maturity onset diabetes of the young (MODY). We aimed to assess the circulating ghrelin levels in HNF1A-MODY and in other types of diabetes and to evaluate its association with HNF1A mutation status. Our cohort included 46 diabetic HNF1A gene mutation carriers, 55 type 2 diabetes (T2DM) subjects, 42 type 1 diabetes (T1DM) patients, and 31 glucokinase (GCK) gene mutation carriers with diabetes as well as 51 healthy controls. Plasma ghrelin concentration was measured using the immunoenzymatic assay with polyclonal antibody against the C-terminal fragment of its acylated and desacylated forms. Ghrelin concentrations were 0.75 ± 0.32, 0.70 ± 0.21, 0.50 ± 0.20, and 0.40 ± 0.16 ng/ml in patients with HNF1A-MODY, GCK-MODY, T1DM, and T2DM, respectively. The ghrelin levels were higher in HNF1A-MODY and GCK-MODY than in T1DM and T2DM (p < 0.001 for all comparisons) but lower than in non-diabetic controls (1.02 ± 0.29 ng/ml, p < 0.001 for both comparisons). In the multivariate linear model, the differences between both MODY groups and common diabetes types remained significant. Analysis by a HNF1A mutation type indicated that ghrelin concentration is similar in patients with different types of sequence differences. Plasma ghrelin level is higher in HNF1A-MODY and GCK-MODY than in the common polygenic forms of diabetes.

Indexed as

AdultCase-Control StudiesDiabetes Mellitus, Type 2FemaleGhrelinGlucokinaseHepatocyte Nuclear Factor 1-alphaHumansMaleMiddle AgedGhrelinGlucokinaseHepatocyte Nuclear Factor 1-alphaHNF1A protein, humanGCK–MODYGhrelinHNF1A–MODYT1DMT2DM

Identifiers

PMID25987348
PMCPMC4662709
OpenAlexW1601096267

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.