Evidence map›Paper›PMID 21903749›Full record

ArticleThe Journal of pharmacology and experimental therapeutics2011

Modeling diabetes disease progression and salsalate intervention in Goto-Kakizaki rats.

Yanguang Cao, Debra C Dubois, Hao Sun, Richard R Almon, William J Jusko

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of pharmacology and experimental therapeutics, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
2.6field-weighted citation impact, top 11% 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

19 citing papers in PubMed, 26 citations in OpenAlex.

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  13. Diabetes disease progression in Goto-Kakizaki rats: effects of salsalate treatment.Diabetes, metabolic syndrome and obesity : targets and therapy · 2014
    Article
  14. A review of rodent models of type 2 diabetic skeletal fragility.Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research · 2014
    Review
  15. Article
  16. Article
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  18. Pharmacokinetic/pharmacodynamic modeling in inflammation.Critical reviews in biomedical engineering · 2012
    Review
  19. 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

5 authors at 3 institutions in 3 countries.

Yanguang CaoDepartment of Pharmaceutical Sciences, School of Pharmacy and Pharmaceutical Sciences, State University of New York, Buffalo, NY 14260, USA.
Debra C Dubois
Hao Sun
Richard R Almon
William J Jusko
Pharmaceutical Biotechnology (Czechia) · CZDepartment of Biological Sciences · RUUniversity at Buffalo, State University of New York · US

Funding

MATHEMATICAL MODELS IN PHARMACODYNAMICSR01GM057980 · NIGMS · STATE UNIVERSITY OF NEW YORK AT BUFFALO · PI JUSKO, WILLIAM J., KRZYZANSKI, WOJCIECH · 1998 to 2013
$3.4M
NIGMS NIH HHS GM57980NIGMS NIH HHS R01 GM057980
6 · The paper itself

Abstract

Type 2 diabetes mellitus (T2DM) arises owing to insulin resistance and β-cell dysfunction. Chronic inflammation is widely identified as a cause of T2DM. The Goto-Kakizaki (GK) rat is a spontaneous rodent model for T2DM with chronic inflammation. The purpose of this study was to characterize diabetes progression in GK rats and evaluate the potential role of the anti-inflammatory agent salsalate. The GK rats were divided into control groups (n = 6) and salsalate treatment groups (n = 6), which were fed a salsalate-containing diet from 5 to 21 weeks of age. Blood glucose and salicylate concentrations were measured once a week. Glucose concentrations showed a biphasic increase in which the first phase started at approximately 5 weeks, resulting in an increase by 15 to 25 mg/dl and a second phase at 14 to 15 weeks with an upsurge of more than 100 mg/dl. A mechanism-based model was proposed to describe the natural diabetes progression and salsalate pharmacodynamics by using a population method in S-ADAPT. Two transduction cascades were applied to mimic the two T2DM components: insulin resistance and β-cell dysfunction. Salsalate suppressed both disease factors by a fraction of 0.622 on insulin resistance and 0.134 on β-cell dysfunction. The substantial alleviation of diabetes by salsalate supports the hypothesis that chronic inflammation is a pathogenic factor of diabetes in GK rats. In addition, body weight and food intake were measured and further modeled by a mechanism-based growth model. Modeling results suggest that salsalate reduces weight gain by enhancing metabolic rate and energy expenditure in both GK and Wister-Kyoto rats.

Indexed as

SoftwareAnimalsAnti-Inflammatory Agents, Non-SteroidalBlood GlucoseBody WeightDiabetes Mellitus, Type 2Disease Models, AnimalDisease ProgressionMaleModels, BiologicalRandom AllocationRatsRats, Inbred WKYSalicylatesSodium SalicylateAnti-Inflammatory Agents, Non-SteroidalBlood GlucoseSalicylatessalicylsalicylic acidSodium Salicylate

Identifiers

PMID21903749
PMCPMC3226370
OpenAlexW2109255059

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.