Evidence map›Paper›PMID 20054172›Full record

ReviewObesity facts2008

Pathogenesis, risk assessment and prevention of type 2 diabetes mellitus.

Hans-Georg Joost

Abstract readReview
In one paragraph

Review in Obesity facts, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing 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

5 citing papers in PubMed.

  1. Review
  2. Article
  3. Article
  4. Review
  5. 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.

Hans-Georg JoostGerman Institute of Human Nutrition Potsdam-Rehbrucke, Nuthetal, Germany. joost@dife.de

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Type 2 diabetes mellitus is a complex, polygenic disease with a heterogeneous pathophysiology, mainly characterised by obesity-associated insulin resistance and a progressive failure of pancreatic beta-cells. Predominant risk factors for its development are abdominal obesity and age; other factors that augment the individual disease risk independent of obesity are the nutritional pattern (low consumption of fibres, high consumption of red meat, saturated and trans fat), lifestyle (smoking, low physical activity), and biomarkers such as blood pressure, HbA1c, serum adiponectin and inflammatory cytokines. These variables can provide the basis for a precise risk assessment and a personalised prevention. Genotyping for the presently known gene variants conferring an increased disease risk adds relatively little to the information provided by the phenotypic risk factors and biomarkers. However, genetic information is necessary for a personalised risk assessment and intervention that begins before phenotypic risk factors are detectable. The incidence of type 2 diabetes can significantly be lowered by reduction of the intraabdominal fat mass (by nutritional intervention and exercise), and by pharmacological control of post-prandial blood glucose excursions. Because of the high portion of non-responders to a preventive intervention, current efforts aim at the identification of phenotypic and genetic variables predicting the success of the intervention.

Indexed as

Adipose TissueAnimalsBiomarkersCytokinesDiabetes Mellitus, Type 2DietGenetic Predisposition to DiseaseHumansInflammationInsulin ResistanceInsulin-Secreting CellsLife StyleObesityPhenotypeRisk FactorsBiomarkersCytokines

Identifiers

PMID20054172
PMCPMC6452126

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.