Acute or chronic upregulation of mitochondrial fatty acid oxidation has no net effect on whole-body energy expenditure or adiposity

Hoehn, Kyle L.; Turner, Nigel; Swarbrick, Michael M.; Wilks, Donna; Preston, Elaine; Phua, Yuwei; Joshi, Himani; Furler, Stuart M.; Larance, Mark; Hegarty, Bronwyn D.; Leslie, Simon J.; Pickford, Russell; Hoy, Andrew J.; Kraegen, Edward W.; James, David E.; Cooney, Gregory J.

doi:10.1016/j.cmet.2009.11.008

Cited by 158Metabolism, Diabetes, and CancerAdipose Tissue and MetabolismPeroxisome Proliferator-Activated Receptors

Acute or chronic upregulation of mitochondrial fatty acid oxidation has no net effect on whole-body energy expenditure or adiposity

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Hoehn, Kyle L., Turner, Nigel, Swarbrick, Michael M., Wilks, Donna, Preston, Elaine, Phua, Yuwei, Joshi, Himani, Furler, Stuart M. +8 more·2010·Cell Metabolism

DOI 10.1016/j.cmet.2009.11.008PMC PMC2824926

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Abstract

Activation of AMP-activated protein kinase (AMPK) is thought to convey many of the beneficial effects of exercise via its inhibitory effect on acetyl-CoA carboxylase 2 (ACC2) and promotion of fatty acid oxidation. Hence, AMPK and ACC have become major drug targets for weight loss and improved insulin action. However, it remains unclear whether or how activation of the fatty acid oxidation pathway without a concomitant increase in energy expenditure could be beneficial. Here, we have used either pharmacological (administration of the AMPK agonist 5(') aminoimidazole-4-carboxamide-riboside) or genetic means (mutation of the ACC2 gene in mice) to manipulate fatty acid oxidation to determine whether this is sufficient to promote leanness. Both of these strategies increased whole-body fatty acid oxidation without altering energy expenditure or adiposity. We conclude that negative energy balance is a prerequisite for weight reduction, and increased fatty acid oxidation per se has little, if any, effect to reduce adiposity.

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Two other groups generated whole-body and muscle-specific ACC2 knockout models and found no effect of gene deletion on body weight, food intake, body composition, or susceptibility to diet-induced obesity and glucose intolerance.
“Intriguingly however, two other groups have recently generated whole body- and muscle-specific ACC2 knockout models and found no effect of the gene deletion on body weight, food intake, body composition and susceptibility to diet-induced obesity and glucose intolerance (Hoehn et al., 2010; Olson et al., 2010).”
From Lipid-Induced Mitochondrial Stress and Insulin Action in Muscle (2012) · cites this paper as Hoehn et al., 2010
In second-generation ACC2 knockout models, the switch to fat catabolism was offset by diminished glucose oxidation and a reciprocal rise in de novo lipogenesis.
“Instead, the genetically engineered switch to fat catabolism was offset by diminished glucose oxidation and a reciprocal rise in de novo lipogenesis.”
From Lipid-Induced Mitochondrial Stress and Insulin Action in Muscle (2012) · cites this paper as Hoehn et al., 2010
In second-generation ACC2 models, total energy expenditure was either unaffected or only slightly increased.
“In these second generation models total energy expenditure was either unaffected (Hoehn et al., 2010) or only slightly increased (Olson et al., 2010).”
From Lipid-Induced Mitochondrial Stress and Insulin Action in Muscle (2012) · cites this paper as Hoehn et al., 2010
A shift in substrate preference, without an increase in total energy expenditure, will not protect against fat-induced insulin resistance.
“Together, these data suggest that a shift in substrate preference, without an increase in total energy expenditure, will not protect against fat-induced insulin resistance.”
From Lipid-induced insulin resistance: unravelling the mechanism (2010) · cites this paper as [54]

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Authors: Hoehn, K. L., Turner, N., Swarbrick, M. M., Wilks, D., Preston, E., Phua, Y., Joshi, H., Furler, S. M., Larance, M., Hegarty, B. D., Leslie, S. J., Pickford, R., Hoy, A. J., Kraegen, E. W., James, D. E., & Cooney, G. J.
Affiliations: Garvan Institute of Medical Research (AU)
UNSW Sydney (AU)
Corresponding author: James, David E.
ORCID: Hoehn, Kyle L.
Turner, Nigel
Swarbrick, Michael M.
Larance, Mark
Hegarty, Bronwyn D.
Pickford, Russell
Hoy, Andrew J.
James, David E.
Cooney, Gregory J.
Venue: Cell Metabolism
Publisher: Elsevier BV
Published: 2010-01
Volume: 11
Issue: 1
Pages: 70-76
ISSN: 1550-4131 (ISSN-L)
DOI: 10.1016/j.cmet.2009.11.008
PMC: PMC2824926
OpenAlex: W2084320367
Cited by: 156
References: 23
Citations by year: 2026: 2 · 2025: 4 · 2024: 3 · 2023: 5 · 2022: 4 · 2021: 6 · 2020: 8 · 2019: 8 · 2018: 8 · 2017: 7 · 2016: 15 · 2015: 12 · 2014: 14 · 2013: 13 · 2012: 18
FWCI: 7.82
Type: journal article
Language: en
Open access: bronze
doi.org
Licence: www.elsevier.com/tdm/userlicense/1.0/ (tdm)
www.elsevier.com/open-access/userlicense/1.0/ (vor, 1293 d)
Locations: Cell Metabolism (publishedVersion)
PubMed (publishedVersion)
Discovery Research Portal (University of Dundee) (publishedVersion)
Europe PMC (PubMed Central) (acceptedVersion)
PubMed Central (acceptedVersion)
Funders: National Institute of Diabetes and Digestive and Kidney Diseases (R01DK067509, DK-067509, F32DK075249)
Topics: Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Metabolism, Diabetes, and Cancer
Health Sciences › Medicine › Physiology › Adipose Tissue and Metabolism
Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Peroxisome Proliferator-Activated Receptors
Keywords: mitochondrial fatty acid oxidation, AMPK, acetyl-CoA carboxylase 2, energy expenditure, adiposity, weight loss, negative energy balance, physical activity
MeSH terms: Acetyl-CoA Carboxylase, Animals, Energy Metabolism, Fatty Acids, Mitochondria, Oxidation-Reduction, Up-Regulation, Adiposity, Mice, AMP-Activated Protein Kinases

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Acute or chronic upregulation of mitochondrial fatty acid oxidation has no net effect on whole-body energy expenditure or adiposity

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