Evidence map›Paper›PMID 19756484›Full record

ArticleDiabetologia2009

Beta cell (dys)function in non-diabetic offspring of diabetic patients.

M Stadler, G Pacini, J Petrie, A Luger, C Anderwald, RISC Investigators

Open access · bronzeAbstract read
PubMed Publisher
In one paragraph

Article in Diabetologia, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
7.7field-weighted citation impact, top 2% 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

29 citing papers in PubMed, 69 citations in OpenAlex.

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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

6 authors at 3 institutions in 3 countries.

M Stadler3rd Medical Department of Metabolic Diseases and Nephrology, Hietzing Hospital, Vienna, Austria.
G PaciniMetabolic Unit, Institute of Biomedical Engineering, ISIB-CNR, Padova, Italy.
J PetrieSection of Diabetes, Division of Medicine and Therapeutics, Ninewells Hospital and Medical School, University of Dundee, Dundee, UK.
A LugerDivision of Endocrinology and Metabolism, Department of Internal Medicine III, Medical University of Vienna, Vienna, Austria.
C AnderwaldDivision of Endocrinology and Metabolism, Department of Internal Medicine III, Medical University of Vienna, Vienna, Austria. christian-heinz.anderwald@meduniwien.ac.at.
RISC Investigators
Klinik Hietzing · ATMedical University of Vienna · ATUniversity of Dundee · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

aims/hypothesisThe first-degree offspring of patients with type 2 diabetes are prone to develop type 2 diabetes, and have both insulin resistance and beta cell impairment. However, it is still unclear whether both pathophysiological features are inseparably combined and which is the outstanding determinant in the offspring.

methodsGlucose metabolism, insulin sensitivity (calculated as M value divided by insulin [M/I]) and beta cell function were studied in the offspring of individuals with type 2 diabetes (n = 187; 57% females; age 43.8 +/- 8.1 years; BMI 26.8 +/- 4.5 kg/m(2)) and in individuals without a family history of type 2 diabetes (controls, n = 519, 55% females; age 43.4 +/- 8.2 years; BMI 26.4 +/- 3.7 kg/m(2), no significant differences between the groups for any characteristic) by performance of 75 g OGTT and 2 h hyperinsulinaemic (40 mU min(-1) m(-2))-isoglycaemic clamp tests. Beta cell function was evaluated by calculating insulinogenic index (IGI) from C-peptide AUC:glucose AUC ratios from the first hour of OGTT (IGI[60 min]) and from the total OGTT (IGI[120 min]).

resultsDuring the OGTT, the offspring of individuals with type 2 diabetes showed 4-14% higher plasma glucose from 30 to 120 min (p < 0.05) and 20-29% higher serum insulin from 90 to 120 min, but decreased IGI(60 min) and IGI(120 min) (p < 0.05). M/I was 11% lower in the offspring of affected individuals than in controls (p < 0.01). To study the offspring of patients with type 2 diabetes with insulin sensitivity similar to that of the control group, the offspring of affected patients were divided into M/I quartiles. Those in the third M/I quartile showed M/I values and major anthropometric characteristics similar to those of the controls, but insulin AUC and C-peptide AUC values were lower in the first hour and the total OGTT (p < 0.05). The third M/I quartile had lower IGI values at 60 min and 120 min: 11% and 14% lower, respectively (p < 0.02). CONCLUSIONS/

interpretationThe first-degree offspring of type 2 diabetic patients show insulin resistance and beta cell dysfunction in response to oral glucose challenge. Beta cell impairment exists in insulin-sensitive offspring of patients with type 2 diabetes, suggesting beta cell dysfunction to be a major defect determining diabetes development in diabetic offspring.

Indexed as

AdultBlood GlucoseBody Mass IndexChildChild of Impaired ParentsDiabetes Mellitus, Type 2FemaleGlucose Clamp TechniqueGlucose Tolerance TestHumansInsulin-Secreting CellsMaleMedical History TakingMiddle AgedBlood Glucose

Identifiers

PMID19756484
OpenAlexW2139847728

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.