Evidence map›Paper›PMID 18422469›Full record

ReviewExpert opinion on pharmacotherapy2008

Pharmacogenetics: potential role in the treatment of diabetes and obesity.

Adrian Vella, Michael Camilleri

Abstract readReview
In one paragraph

Review in Expert opinion on pharmacotherapy, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
1.6field-weighted citation impact, top 16% 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

8 citing papers in PubMed, 19 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Genetics of type 2 diabetes.Current opinion in clinical nutrition and metabolic care · 2010
    Review
  5. A model of GLP-1 action on insulin secretion in nondiabetic subjects.American journal of physiology. Endocrinology and metabolism · 2010
    Article
  6. Epigenetics and obesity.Pharmacogenomics · 2008
    Review
  7. Integrating Epigenomics into Pharmacogenomic Studies.Pharmacogenomics and personalized medicine · 2008
    Article
  8. 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.

Adrian VellaMayo Clinic, Division of Endocrinology and Metabolism, Department of Medicine, 200, First ST SW, Rochester, MN 55905, USA.
Michael Camilleri
Mayo Clinic · US

Funding

MAYO CLINIC CENTER FOR TRANSLATIONAL SCIENCE ACTIVITIESUL1RR024150 · NCRR · MAYO CLINIC ROCHESTER · PI RIZZA, ROBERT A. · 2006 to 2011
$66.4M
Physiological Characterization and Data Integration CoreP01DK068055 · NIDDK · MAYO CLINIC ROCHESTER · PI FARRUGIA, GIANRICO · 2004 to 2019
$23.8M
The regulation of fasting glucose metabolism in people with and without prediabetesR01DK078646 · NIDDK · MAYO CLINIC ROCHESTER · PI Adrian Vella · 2007 to 2026
$8.7M
Pharmacogenomics of Gastric Function &Weight in ObesityR01DK067071 · NIDDK · MAYO CLINIC ROCHESTER · PI CAMILLERI, MICHAEL L. · 2004 to 2020
$4.7M
ALPHA 2 ADRENERGIC CONTROL IN IRRITABLE BOWEL SYNDROMEK24DK002638 · NIDDK · MAYO CLINIC ROCHESTER · PI CAMILLERI, MICHAEL L. · 1999 to 2008
$1.1M
Pharmacogenomics of Gastric Function & Weight in ObesityR56DK067071 · NIDDK · MAYO CLINIC ROCHESTER · PI CAMILLERI, MICHAEL L. · 2015 to 2015
$396k
NCRR NIH HHS RR024150NIDDK NIH HHS DK02638NIDDK NIH HHS DK67071NIDDK NIH HHS P01 DK068055NIDDK NIH HHS P01-DK068055NIDDK NIH HHS R01 DK078646
6 · The paper itself

Abstract

backgroundCommon genetic variation is associated with increased risk of common metabolic diseases such as type 1 and type 2 diabetes, and obesity. Increasing experience with genetic association studies has led to an understanding of the large sample sizes required to detect a weak to moderate genetic predisposition to disease, the need to reproduce such associations in independent cohorts, and the statistical criteria required to detect a true association. This approach has been used successfully to identify disease-associated gene variation usually in representative populations of large numbers.

objectiveTo review the current understanding of how common genetic variation influences predisposition to, and treatment of, metabolic disease. METHODOLOGY: Review of scientific literature.

resultsWhile there has been progress in understanding how genetic variation predisposes to diabetes and obesity, and how candidate genes may alter drug response, several caveats limit the interpretation and significance of pharmacogenetic studies published to date: those caveats typically include relatively small numbers of participants and choice of endpoints in determining gene-associated differences in response, which may not be clinically significant or relevant as a biomarker or predictor of a desired clinical effect. The genetic variants studied at a given locus are often limited in number and may not represent a comprehensive map of the region under study.

conclusionsThe pharmacogenetic associations in diabetes and obesity that have been reported to date have had limited impact on the choice of individual treatments. We perceive, however, that this field is in its infancy in these multifactorial metabolic diseases, and with further advances and future drug intervention trials designed in a way that allows a more clear interpretation of the impact of genetic variation on differences in drug response in obesity and diabetes, it is anticipated that pharmacogenetics will have a significant impact on individualizing medical care.

Indexed as

Genetic Predisposition to DiseasePharmacogeneticsBiomarkersControlled Clinical Trials as TopicDiabetes Mellitus, Type 1Diabetes Mellitus, Type 2HumansObesityBiomarkers

Identifiers

PMID18422469
PMCPMC3901565
OpenAlexW2170397385

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.