Evidence map›Paper›PMID 20156986›Full record

ReviewEndocrine reviews2010

The role of mitochondria in the pathogenesis of type 2 diabetes.

Mary-Elizabeth Patti, Silvia Corvera

Registry-linked trialOpen access · bronzeAbstract readReview
In one paragraph

Review in Endocrine reviews, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT03323294 (Bioenergetics and Metabolism in Pediatric Populations), which is not on this map. Cited by 282 papers.

0numbers the graph read from it
0cells of the map it votes in
282citing papers in PubMed
16.0field-weighted citation impact, top 1% 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.

NCT03323294 completednot on this mapstarted 2017, after this paper: background citation

Bioenergetics and Metabolism in Pediatric Populations

TypeobservationalSponsorArkansas Children's Hospital Research InstituteRan2017 to 2024Enrolled79ConditionsObesity, Type 2 Diabetes Mellitus, Insulin Resistance
3 · Its place in the literature

Who cites it

282 citing papers in PubMed, 545 citations in OpenAlex.

  1. Trial
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  3. Statins Are Associated With Increased Insulin Resistance and Secretion.Arteriosclerosis, thrombosis, and vascular biology · 2021 · on this map
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  10. Innate immune signalling in the adipocyte.Journal of biochemistry · 2026
    Review
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222 more citing papers are in PubMed but not listed here.

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 2 institutions in 1 country.

Mary-Elizabeth PattiResearch Division, Joslin Diabetes Center, Boston, Massachusetts 02215, USA. mary.elizabeth.patti@joslin.harvard.edu
Silvia Corvera
Harvard University · USUniversity of Massachusetts Chan Medical School · US

Funding

SPECIAL ASSAY COREP30DK036836 · NIDDK · JOSLIN DIABETES CENTER · PI JEAN E. SCHAFFER · 1986 to 2026
$50.5M
Informatics for Integrating Biology/ the Bedside (RMI)U54LM008748 · NLM · BRIGHAM AND WOMEN'S HOSPITAL · PI KOHANE, ISAAC S. · 2004 to 2013
$39.0M
ZINC STATUS AND T CELL DISORDER IN MILD HUMAN ZINC DEFICIENCYM01RR001032 · NCRR · BETH ISRAEL DEACONESS MEDICAL CENTER · PI MANTZOROS, CHRISTOS S · 1985 to 2008
$32.3M
Diabetes Genome Anatomy Project (DGAP)R01DK060837 · NIDDK · JOSLIN DIABETES CENTER · PI KAHN, C RONALD · 2002 to 2006
$15.9M
PILOT AND FEASIBILITY PROGRAMP30DK032520 · NIDDK · UNIV OF MASSACHUSETTS MED SCH WORCESTER · PI CZECH, MICHAEL P · 1986 to 2010
$14.6M
Gene Expression in Prediabetes: Potential Role of PGC-1R01DK062948 · NIDDK · JOSLIN DIABETES CENTER · PI PATTI, MARY E · 2003 to 2006
$1.4M
Adipose Tissue-specific Angiogenesis and Insulin SensitivityR21DK080366 · NIDDK · UNIV OF MASSACHUSETTS MED SCH WORCESTER · PI CORVERA, SILVIA · 2008 to 2009
$450k
NCRR NIH HHS M01 RR001032NIDDK NIH HHS DK060837NIDDK NIH HHS DK062948NIDDK NIH HHS DK080366NIDDK NIH HHS DK32520NIDDK NIH HHS DK36836NIDDK NIH HHS P30 DK032520NIDDK NIH HHS P30 DK036836NIDDK NIH HHS R01 DK060837NIDDK NIH HHS R01 DK062948NIDDK NIH HHS R21 DK080366NLM NIH HHS LM008748NLM NIH HHS U54 LM008748
6 · The paper itself

Abstract

The pathophysiology of type 2 diabetes mellitus (DM) is varied and complex. However, the association of DM with obesity and inactivity indicates an important, and potentially pathogenic, link between fuel and energy homeostasis and the emergence of metabolic disease. Given the central role for mitochondria in fuel utilization and energy production, disordered mitochondrial function at the cellular level can impact whole-body metabolic homeostasis. Thus, the hypothesis that defective or insufficient mitochondrial function might play a potentially pathogenic role in mediating risk of type 2 DM has emerged in recent years. Here, we summarize current literature on risk factors for diabetes pathogenesis, on the specific role(s) of mitochondria in tissues involved in its pathophysiology, and on evidence pointing to alterations in mitochondrial function in these tissues that could contribute to the development of DM. We also review literature on metabolic phenotypes of existing animal models of impaired mitochondrial function. We conclude that, whereas the association between impaired mitochondrial function and DM is strong, a causal pathogenic relationship remains uncertain. However, we hypothesize that genetically determined and/or inactivity-mediated alterations in mitochondrial oxidative activity may directly impact adaptive responses to overnutrition, causing an imbalance between oxidative activity and nutrient load. This imbalance may lead in turn to chronic accumulation of lipid oxidative metabolites that can mediate insulin resistance and secretory dysfunction. More refined experimental strategies that accurately mimic potential reductions in mitochondrial functional capacity in humans at risk for diabetes will be required to determine the potential pathogenic role in human insulin resistance and type 2 DM.

Indexed as

AnimalsDiabetes Mellitus, Type 2HumansInsulin ResistanceMitochondriaOxidative Phosphorylation

Identifiers

PMID20156986
PMCPMC3365846
OpenAlexW2166954428

What OpenQuestion holds

Textmetadata
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.