Evidence map›Paper›PMID 21264047›Full record

ArticleMcGill journal of medicine : MJM : an international forum for the advancement of medical sciences by students2009

Pancreatic β-Cell Mass as a Pharmacologic Target in Diabetes.

Stephen Hanley

Abstract read
In one paragraph

Article in McGill journal of medicine : MJM : an international forum for the advancement of medical sciences by students, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing 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

4 citing papers in PubMed.

  1. Type 2 diabetes mellitus.Nature reviews. Disease primers · 2026
    Review
  2. Review
  3. Review
  4. 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

1 author.

Stephen Hanley

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

While the prevalence of maternal While the prevalence of diabetes mellitus reaches epidemic proportions, most available treatments still focus on the symptoms of the disease, rather than the underlying pathology. Types 1 and 2 diabetes have in common a deficit in β-cell mass. In type 1 diabetes, auto-immune β-cell destruction leads to an absolute deficit in β-cells, while in type 2 diabetes, insulin resistance and β-cell dysfunction cause a functional deficit. More recently, however, it has been suggested that type 2 diabetes is also marked by an absolute deficit in β-cell mass, although a causal relationship has not yet been established. Overall β-cell mass reflects the balance between the dynamic processes of β-cell expansion, through proliferation and neogenesis, and β-cell loss via apoptosis. Given that β-cell mass can be modified significantly by altering the rate of any of these mechanisms, therapies that modulate β-cell expansion and loss have garnered recent interest. We review herein the current therapeutics under investigation as modulators of β-cell mass dynamics, and the basic research that supports these novel therapeutic targets.

Indexed as

diabetesislet neogenesispancreasplasticityregenerationβ-cell mass

Identifiers

PMID21264047
PMCPMC2997247

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.