Evidence map›Paper›PMID 11508279›Full record

ReviewDiabetologia2001

The accelerator hypothesis: weight gain as the missing link between Type I and Type II diabetes.

T J Wilkin

Open access · bronzeAbstract readReview
PubMed Publisher
In one paragraph

Review in Diabetologia, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 205 papers, 5 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
205citing papers in PubMed, 5 pooled it
16.5field-weighted citation impact, top 1% 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

205 citing papers in PubMed, 5 syntheses or guidelines pooled it, 617 citations in OpenAlex.

  1. Pooled it
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  4. Type 2 Diabetes: How Much of an Autoimmune Disease?Frontiers in endocrinology · 2019
    Pooled it
  5. Overweight and obesity in youth with type 1 diabetes.Annual review of nursing research · 2013
    Pooled it
  6. Trial
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  11. Review
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  15. Observational
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145 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

1 author at 1 institution in 1 country.

T J WilkinDepartment of Medicine, Postgraduate Medical School, Derriford Hospital, Plymouth, UK. T.Wilkin@plymouth.ac.uk
Derriford Hospital · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Blood glucose concentrations are controlled by a loop incorporating two components, the beta cells which secrete insulin and the insulin-sensitive tissues (liver, muscle, adipose) which respond to it. Loss of blood glucose control might result from failure of the beta cells to secrete insulin, resistance of the tissues to its action, or a combination of both. The distinctions between Type I (insulin-dependent) and Type II (non-insulin-dependent) diabetes mellitus are becoming increasingly blurred both clinically and aetiologically, where beta-cell insufficiency is the shared characteristic. The 'Accelerator Hypothesis' identifies three processes which variably accelerate the loss of beta cells through apoptosis: constitution, insulin resistance and autoimmunity. None of the accelerators leads to diabetes without excess weight gain, a trend which the 'Accelerator Hypothesis' deems central to the rising incidence of both types of diabetes in the industrially developed world. Weight gain causes an increase in insulin resistance, which results in the weakening of glucose control. The rising blood glucose (glucotoxicity) accelerates beta-cell apoptosis directly in all and, by inducing beta-cell immunogens, further accelerates it in a subset genetically predisposed to autoimmunity. Rather than overlap between two types of diabetes, the 'Accelerator Hypothesis' envisages overlay. Body mass is central to the development and rising incidence of all diabetes. Only tempo distinguishes the 'types'. The control of weight gain, and with it insulin resistance, could be the means of minimising both.

Indexed as

Models, BiologicalWeight GainApoptosisBlood GlucoseDeveloped CountriesDiabetes Mellitus, Type 1Diabetes Mellitus, Type 2HumansInsulin ResistancePhagocytosisPrevalenceRisk FactorsBlood Glucose

Identifiers

PMID11508279
OpenAlexW1966671518

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.