Evidence map›Paper›PMID 24186880›Full record

Observational studyDiabetes care2014

Clinical and genetic determinants of progression of type 2 diabetes: a DIRECT study.

Kaixin Zhou, Louise A Donnelly, Andrew D Morris, Paul W Franks, Chris Jennison, Colin Na Palmer, Ewan R Pearson

Registry-linked trialAbstract readObservational Study
In one paragraph

Observational study in Diabetes care, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT02838693 (Assessing Progression to Type-2 Diabetes), which is not on this map. Cited by 43 papers.

0numbers the graph read from it
0cells of the map it votes in
43citing 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.

NCT02838693 unknown statusnot on this mapstarted 2016, after this paper: background citation

Assessing Progression to Type-2 Diabetes (APT-2D): A Prospective Cohort Study Expanded From BRITE-SPOT (Bio-bank and Registry for StratIfication and Targeted intErventions in the Spectrum Of Type 2 Diabetes)

TypeobservationalSponsorMedicineRan2016 to 2021Enrolled2,300ConditionsPre-diabetes, DiabetesArmsNot applicable. This is an observational study.
3 · Its place in the literature

Who cites it

43 citing papers in PubMed.

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  18. Precision Medicine in Diabetes.Handbook of experimental pharmacology · 2023
    Article
  19. The impact of birthweight on subsequent phenotype of type 2 diabetes in later life.Diabetic medicine : a journal of the British Diabetic Association · 2022
    Article
  20. 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

7 authors.

Kaixin Zhou *Division of Cardiovascular & Diabetes Medicine, Medical Research Institute, University of Dundee, DD1 9SY.
Louise A Donnelly *Division of Cardiovascular & Diabetes Medicine, Medical Research Institute, University of Dundee, DD1 9SY.
Andrew D MorrisDivision of Cardiovascular & Diabetes Medicine, Medical Research Institute, University of Dundee, DD1 9SY.
Paul W FranksDepartment of Clinical Science, Genetic & Molecular Epidemiology Unit, Lund University, Malmö, Sweden; Department of Nutrition, Harvard School of Public Health, Boston, MA; Department of Public Health & Clinical Medicine, Umeå University, Umeå, Sweden.
Chris JennisonDepartment of Mathematical Sciences, University of Bath, Bath, BA2 7AY.
Colin Na PalmerDivision of Cardiovascular & Diabetes Medicine, Medical Research Institute, University of Dundee, DD1 9SY.
Ewan R PearsonDivision of Cardiovascular & Diabetes Medicine, Medical Research Institute, University of Dundee, DD1 9SY.

Funding

Chief Scientist OfficeWellcome Trust 092272Wellcome Trust 092272/Z/10/Z
6 · The paper itself

Abstract

objectiveTo identify the clinical and genetic factors that explain why the rate of diabetes progression is highly variable between individuals following diagnosis of type 2 diabetes. RESEARCH DESIGN AND

methodsWe studied 5,250 patients with type 2 diabetes using comprehensive electronic medical records in Tayside, Scotland, from 1992 onward. We investigated the association of clinical, biochemical, and genetic factors with the risk of progression of type 2 diabetes from diagnosis to the requirement of insulin treatment (defined as insulin treatment or HbA1c ≥8.5% [69 mmol/mol] treated with two or more noninsulin therapies).

resultsRisk of progression was associated with both low and high BMI. In an analysis stratified by BMI and HbA1c at diagnosis, faster progression was independently associated with younger age at diagnosis, higher log triacylglyceride (TG) concentrations (hazard ratio [HR] 1.28 per mmol/L [95% CI 1.15-1.42]) and lower HDL concentrations (HR 0.70 per mmol/L [95% CI 0.55-0.87]). A high Genetic Risk Score derived from 61 diabetes risk variants was associated with a younger age at diagnosis and a younger age when starting insulin but was not associated with the progression rate from diabetes to the requirement of insulin treatment.

conclusionsIncreased TG and low HDL levels are independently associated with increased rate of progression of diabetes. The genetic factors that predispose to diabetes are different from those that cause rapid progression of diabetes, suggesting a difference in biological process that needs further investigation.

Indexed as

Body Mass IndexCholesterol, LDLDiabetes Mellitus, Type 2Disease ProgressionFemaleGlycated HemoglobinHumansHypoglycemic AgentsInsulinMaleMiddle AgedPhenotypePolymorphism, Single NucleotideRisk FactorsScotlandTriglyceridesCholesterol, LDLGlycated HemoglobinHypoglycemic AgentsInsulinTriglycerides

Identifiers

PMID24186880
PMCPMC4038744

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

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.