Evidence map›Paper›PMID 28242267›Full record

ReviewJournal of diabetes and its complications2017

The undoing and redoing of the diabetic β-cell.

Wei Wang, Chune Liu, Maria Jimenez-Gonzalez, Woo-Jin Song, Mehboob A Hussain

Abstract readReview
In one paragraph

Review in Journal of diabetes and its complications, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
–field-weighted citation impact
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

8 citing papers in PubMed.

  1. Article
  2. Review
  3. Review
  4. Article
  5. Article
  6. Ion Channels of the Islets in Type 2 Diabetes.Journal of molecular biology · 2020
    Review
  7. Article
  8. Article
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.

Wei WangMetabolism Division, Departments of Pediatrics, Medicine and Biological Chemistry, Johns Hopkins University School of Medicine, 600 N Wolfe Street, CMSC 10-113, Baltimore, MD 21287.
Chune LiuMetabolism Division, Departments of Pediatrics, Medicine and Biological Chemistry, Johns Hopkins University School of Medicine, 600 N Wolfe Street, CMSC 10-113, Baltimore, MD 21287.
Maria Jimenez-GonzalezMetabolism Division, Departments of Pediatrics, Medicine and Biological Chemistry, Johns Hopkins University School of Medicine, 600 N Wolfe Street, CMSC 10-113, Baltimore, MD 21287.
Woo-Jin SongMetabolism Division, Departments of Pediatrics, Medicine and Biological Chemistry, Johns Hopkins University School of Medicine, 600 N Wolfe Street, CMSC 10-113, Baltimore, MD 21287.
Mehboob A HussainMetabolism Division, Departments of Pediatrics, Medicine and Biological Chemistry, Johns Hopkins University School of Medicine, 600 N Wolfe Street, CMSC 10-113, Baltimore, MD 21287. Electronic address: mhussai4@jhmi.edu.

Funding

JHU-UMD Diabetes Research CenterP30DK079637 · NIDDK · JOHNS HOPKINS UNIVERSITY · PI AHIMA, REXFORD S. · 2013 to 2017
$9.7M
Beta-cell ProliferationR01DK081472 · NIDDK · JOHNS HOPKINS UNIVERSITY · PI HUSSAIN, MEHBOOB A, WONDISFORD, FREDRIC E. · 2009 to 2013
$2.1M
Hepatic endocrine suppression of the pancreatic beta-cellR01DK101591 · NIDDK · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI HUSSAIN, MEHBOOB A, WOLFE, ANDREW M · 2014 to 2017
$2.0M
The AMP-Activated Protein Kinase (AMPK) Antagonizes Inflammation Through SIRT1R01DK084172 · NIDDK · WAKE FOREST UNIVERSITY HEALTH SCIENCES · PI SHI, HANG · 2009 to 2012
$1.2M
NIDDK NIH HHS P30 DK079637NIDDK NIH HHS R01 DK081472NIDDK NIH HHS R01 DK084172NIDDK NIH HHS R01 DK101591
6 · The paper itself

Abstract

A hallmark of type 2 diabetes (T2DM) is the reduction in functional β-cell mass, which is considered at least in part to result from an imbalance of β-cell renewal and apoptosis, with the latter being accelerated during metabolic stress. More recent studies, however, suggest that the loss of functional β-cell mass is not as much due to β-cell death but rather to de-differentiation of β-cells when these cells are exposed to metabolic stressors, opening the possibility to re-differentiate and restore functional β-cell mass by therapeutic intervention. In parallel, clinical observations suggest that temporary intensive insulin therapy in early diagnosed humans with T2DM, so as to "rest" endogenous β-cells, allows these patients to regain adequate insulin secretion and to maintain euglycemia for prolonged periods free of continued pharmacotherapy. Whether observations made in (mostly rodent) models of diabetes mellitus and in clinical trials are revealing identical mechanisms and therapeutic opportunities remains a tantalizing possibility. Our intention is for this review to serve as an overview of the field and commentary of this particularly exciting field of research.

Indexed as

Down-RegulationAnimalsApoptosisCell DedifferentiationCell DifferentiationDiabetes Mellitus, Type 2HumansHypoglycemic AgentsInsulinInsulin ResistanceInsulin-Secreting CellsInsulin SecretionHypoglycemic AgentsInsulin

Identifiers

PMID28242267
PMCPMC5450161

What OpenQuestion holds

Textmetadata
LicenceTDM
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.