Evidence map›Paper›PMID 18563953›Full record

ReviewClinical pharmacokinetics2008

Pharmacokinetic/pharmacodynamic modelling in diabetes mellitus.

Cornelia B Landersdorfer, William J Jusko

Abstract readReview
PubMed Publisher
In one paragraph

Review in Clinical pharmacokinetics, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
42citing papers in PubMed, 1 pooled it
4.3field-weighted citation impact, top 6% 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

42 citing papers in PubMed, 1 synthesis or guideline pooled it, 93 citations in OpenAlex.

  1. Pooled it
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  8. Review
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  10. Article
  11. Insulin Signaling Pathway Model in Adipocyte Cells.Current pharmaceutical design · 2023
    Article
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  16. Review
  17. Crosstalk in transition: the translocation of Akt.Journal of mathematical biology · 2019
    Article
  18. Modeling of Diabetes and Its Clinical Impact.Journal of diabetes science and technology · 2018
    Review
  19. 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

2 authors at 1 institution in 1 country.

Cornelia B LandersdorferDepartment of Pharmaceutical Sciences, School of Pharmacy and Pharmaceutical Sciences, University at Buffalo, State University of New York, Buffalo, New York 14260, USA.
William J Jusko
University at Buffalo, State University of New York · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Diabetes mellitus is a major health risk in many countries, and the incidence rates are increasing. Diverse therapeutic agents are applied to treat this condition. Since 1960, numerous mathematical models have been developed to describe the glucose-insulin system, analyse data from diagnostic tests and quantify drug effects. This review summarizes the present state-of-the-art in diabetes modelling, with a focus on models describing drug effects, and identifies major strengths and limitations of the published models. For diagnostic purposes, the minimal model has remained the most popular choice for several decades, and numerous extensions have been developed. Use of the minimal model is limited for applications other than diagnostic tests. More mechanistic models that include glucose-insulin feedback in both directions have been applied. The use of biophase distribution models for the description of drug effects is not always appropriate. More recently, the effects of various antidiabetic agents on glucose and insulin have been modelled with indirect response models. Such models provide good curve fits and mechanistic descriptions of the effects of antidiabetic drugs on glucose-insulin homeostasis. These and other types of models were used to describe secondary drug effects on glucose and insulin, and effects on ancillary biomarkers. Modelling of disease progression in diabetes can utilize indirect response models as a disturbance of homeostasis. Future needs are to include glucose-insulin feedback more often, develop mechanistic models for new drug groups, consider dual drug effects on complementary subsystems, and incorporate elements of disease progression.

Indexed as

Models, StatisticalAnimalsBiomarkersBlood GlucoseDiabetes MellitusDisease ProgressionHumansHypoglycemic AgentsInsulinBiomarkersBlood GlucoseHypoglycemic AgentsInsulin

Identifiers

PMID18563953
OpenAlexW2009795777

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.