A novel adipose-specific gene deletion model demonstrates potential pitfalls of existing methods
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Adipose-specific gene deletion in mice is crucial in determining gene function in adipocyte homeostasis and the development of obesity. We noted 100% mortality when the Hdac3 gene was conditionally deleted using Fabp4-Cre mice, the most commonly used model of adipose-targeted Cre recombinase. However, this surprising result was not reproduced using other models of adipose targeting of Cre, including a novel Retn-Cre mouse. These findings underscore the need for caution when interpreting data obtained using Fabp4-Cre mice and should encourage the use of additional or alternative adipose-targeting Cre mouse models before drawing conclusions about in vivo adipocyte-specific functions.
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The aP2/Fabp4 promoter used to drive adipocyte-specific Cre expression is known to have problems with mosaicism and also drive expression in skeletal muscle and brain.
“However, this work utilized an aP2/Fabp4 promoter to drive adipocyte-specific Cre expression, which is known to have problems with mosaicism and also drive expression in skeletal muscle and brain, highlighting the pitfalls of this model for adipose-specific targeting [27].”
From Antibody blockade of activin type II receptors preserves skeletal muscle mass and enhances fat loss during GLP-1 receptor agonism (2024) · cites this paper as [27]
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The widely used Ucp1-Cre Evdr transgene elicits complex developmental and metabolic phenotypesPreprint
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- Authors
- Mullican, S. E., Tomaru, T., Gaddis, C. A., Peed, L. C., Sundaram, A., & Lazar, M. A.
- Affiliations
- University of Pennsylvania (US)
- Corresponding author
- Lazar, Mitchell A.
- Venue
- Molecular Endocrinology
- Publisher
- The Endocrine Society
- Published
- 2013-01-01
- Volume
- 27
- Issue
- 1
- Pages
- 127-134
- ISSN
- 0888-8809 (ISSN-L)
- 1944-9917
- PMC
- PMC3545212
- OpenAlex
- W2169845602
- Cited by
- 83
- References
- 48
- Citations by year
- 2025: 2 · 2024: 4 · 2023: 3 · 2022: 4 · 2021: 5 · 2020: 6 · 2019: 7 · 2018: 9 · 2017: 9 · 2016: 11 · 2015: 8 · 2014: 11 · 2013: 4
- FWCI
- 4.93
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Molecular Endocrinology (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- University of Pennsylvania
- National Institutes of Health
- Perelman School of Medicine, University of Pennsylvania
- Japan Society for the Promotion of Science (24790906)
- National Cancer Institute
- National Institute of Diabetes and Digestive and Kidney Diseases (R37DK43806, P01-DK49210, P01DK049210, R37DK043806, P30DK019525)
- Topics
- Health Sciences › Medicine › Physiology › Adipose Tissue and Metabolism
- Health Sciences › Medicine › Epidemiology › Adipokines, Inflammation, and Metabolic Diseases
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Peroxisome Proliferator-Activated Receptors
- Keywords
- HDAC3, obesity, mouse model
- MeSH terms
- Histone Deacetylase 3, Adipose Tissue, Animals, Disease Models, Animal, Epididymis, Genes, Lethal, Genetic Engineering, Histone Deacetylases, Male, Mice, Transgenic, Obesity, Organ Specificity, Phenotype, Gene Deletion, Fatty Acid-Binding Proteins, Mice
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