CoChat
Sign Up
Cited by 502Mitochondrial Function and PathologyCardiovascular Function and Risk FactorsCardiac Ischemia and Reperfusion

The DOI matches its Crossref record; 31 of the 31 references it cites were found in a registry or an index.

Reduced Mitochondrial Oxidative Capacity and Increased Mitochondrial Uncoupling Impair Myocardial Energetics in Obesity

Boudina, Sihem, Sena, Sandra, O’Neill, Brian T., Tathireddy, Prakash, Young, Martin E., Abel, E. Dale·2005·Circulation
DOI 10.1161/circulationaha.105.554360
Open this paper in CoChat — free account

Abstract

Background— Obesity is a risk factor for cardiovascular disease and is strongly associated with insulin resistance and type 2 diabetes. Recent studies in obese humans and animals demonstrated increased myocardial oxygen consumption (MV̇ o 2 ) and reduced cardiac efficiency (CE); however, the underlying mechanisms remain unclear. The present study was performed to determine whether mitochondrial dysfunction and uncoupling are responsible for reduced cardiac performance and efficiency in ob/ob mice. Methods and Results— Cardiac function, MV̇ o 2 , mitochondrial respiration, and ATP synthesis were measured in 9-week-old ob/ob and control mouse hearts. Contractile function and MV̇ o 2 in glucose-perfused ob/ob hearts were similar to controls under basal conditions but were reduced under high workload. Perfusion of ob/ob hearts with glucose and palmitate increased MV̇ o 2 and reduced CE by 23% under basal conditions, and CE remained impaired at high workload. In glucose-perfused ob/ob hearts, mitochondrial state 3 respirations were reduced but ATP/O ratios were unchanged. In contrast, state 3 respiration rates were similar in ob/ob and control mitochondria from hearts perfused with palmitate and glucose, but ATP synthesis rates and ATP/O ratios were significantly reduced in ob/ob , which suggests increased mitochondrial uncoupling. Pyruvate dehydrogenase activity and protein levels of complexes I, III, and V were reduced in obese mice. Conclusions— These data indicate that reduced mitochondrial oxidative capacity may contribute to cardiac dysfunction in ob/ob mice. Moreover, fatty acid but not glucose-induced mitochondrial uncoupling reduces CE in obese mice by limiting ATP production and increasing MV̇ o 2 .

Overview

Integrity signals

Registry

Crossref · 10.1161/circulationaha.105.554360

Cites

31 of 31 references verified0 citation errors · 0 not checkable

Statistics

Recomputing p-values needs the paper’s full text.

Verification

Claims the paper makes

This paper’s full text isn’t openly available, so its claims and self-check weren’t run. The registry and citation checks still apply.

Claims other papers make about this one

Each is checked against this paper’s own text: does it say what the citing paper says it does?

Citations

Cites

Flagged first, then by citations

Cited by

Sorted by citations

See all 502

Related

See all

Metadata

Authors
Boudina, S., Sena, S., O’Neill, B. T., Tathireddy, P., Young, M. E., & Abel, E. D.
Affiliations
  • Baylor College of Medicine (US)
  • From the Division of Endocrinology, Metabolism and Diabetes and Program in Human Molecular Biology and Genetics (S.B., S.S., B.T.O., P.T., E.D.A.), University of Utah School of Medicine, Salt Lake City, Utah, and USDA/ARS Children’s Nutrition Research Center and Department of Pediatrics (M.E.Y.), Baylor College of Medicine, Houston, Tex.
ORCID
Venue
Circulation
Publisher
Ovid Technologies (Wolters Kluwer Health)
Published
2005-10-25
Volume
112
Issue
17
Pages
2686-2695
ISSN
  • 0009-7322 (ISSN-L)
  • 1524-4539
DOI
10.1161/circulationaha.105.554360
OpenAlex
W2160331251
Cited by
502
References
31
Citations by year
2026: 7 · 2025: 12 · 2024: 20 · 2023: 17 · 2022: 22 · 2021: 23 · 2020: 23 · 2019: 16 · 2018: 20 · 2017: 29 · 2016: 25 · 2015: 42 · 2014: 48 · 2013: 39 · 2012: 33
FWCI
6.15
Type
journal article
Language
en
Update notices
correction (2021-12-06)
Open access
closed
Locations
  • Circulation (publishedVersion)
  • PubMed (publishedVersion)
Funders
  • American Diabetes Association
  • American Heart Association
  • National Institutes of Health
  • National Heart, Lung, and Blood Institute (R01HL073167, R01-HL-73167, UO1HL70525, U01HL070525)
  • National Institute of Diabetes and Digestive and Kidney Diseases (R01DK092065)
Topics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Mitochondrial Function and Pathology
  • Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Cardiovascular Function and Risk Factors
  • Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Cardiac Ischemia and Reperfusion
Keywords
obesity, mitochondrial uncoupling, mitochondrial oxidative capacity, myocardial oxygen consumption, cardiac efficiency, cardiac energetics, ob/ob mice, palmitate, fatty acid metabolism, pyruvate dehydrogenase, mitochondrial respiration, ATP production, insulin resistance, type 2 diabetes, cardiac contractile function
MeSH terms
Adenosine Triphosphate, Animals, Energy Metabolism, Mice, Inbred C57BL, Mice, Obese, Mitochondria, Heart, Myocardium, Obesity, Oxidative Phosphorylation, Oxygen Consumption, Mice

About these checks

Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.

Statistics and arithmetic are recomputed, not judged.

Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.

What counts as a claim ›How we measure confidence ›How we check this ›

Are you an author, or do you see a problem with this page? Request a review