Genetic Ablation of miR-33 Increases Food Intake, Enhances Adipose Tissue Expansion, and Promotes Obesity and Insulin Resistance
Open accessAbstract
While therapeutic modulation of miRNAs provides a promising approach for numerous diseases, the promiscuous nature of miRNAs raises concern over detrimental off-target effects. miR-33 has emerged as a likely target for treatment of cardiovascular diseases. However, the deleterious effects of long-term anti-miR-33 therapies and predisposition of miR-33 −/− mice to obesity and metabolic dysfunction exemplify the possible pitfalls of miRNA-based therapies. Our work provides an in-depth characterization of miR-33 −/− mice and explores the mechanisms by which loss of miR-33 promotes insulin resistance in key metabolic tissues. Contrary to previous reports, our data do not support a direct role for SREBP-1-mediated lipid synthesis in promoting these effects. Alternatively, in adipose tissue of miR-33 −/− mice, we observe increased pre-adipocyte proliferation, enhanced lipid uptake, and impaired lipolysis. Moreover, we demonstrate that the driving force behind these abnormalities is increased food intake, which can be prevented by pair feeding with wild-type animals.
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The obesity and insulin resistance in miR-33a knockout mice on a high-fat diet is attributed to a central nervous system phenotype, specifically an increase in food intake.
“This has been attributed to a central nervous system phenotype, specifically an increase in food intake.”
From Critical Role of microRNA-33a/b in Cardiovascular and Metabolic Disease: Molecular Mechanisms and Therapeutic Perspectives (2026) · cites this paper as [40]
The Results report that increased food intake was primarily responsible for obesity and metabolic dysfunction in high-fat-diet-fed miR-33 knockout mice: pair feeding removed the differences in weight gain and metabolic regulation. The Discussion raises a direct effect on hypothalamic neurons only as a possibility, so the paper does not establish that the increased food intake is a central nervous system phenotype. Page numbers were not provided in our copy. (LLM, conf=0.88)
Experimental — accuracy not yet measuredmiR-33a knockout mice exhibit obesity and insulin resistance when fed a high-fat diet.
“MiR-33a knockout mice exhibit obesity and insulin resistance when fed a high-fat diet 39 , 40) .”
From Critical Role of microRNA-33a/b in Cardiovascular and Metabolic Disease: Molecular Mechanisms and Therapeutic Perspectives (2026) · cites this paper as [40]
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- Authors
- Price, N. L., Singh, A. K., Rotllan, N., Goedeke, L., Wing, A., Canfrán-Duque, A., Diaz-Ruiz, A., Araldi, E., Baldán, Á., Camporez, J.-P., Suárez, Y., Rodeheffer, M. S., Shulman, G. I., de Cabo, R., & Fernández-Hernando, C.
- Affiliations
- Yale University (US)
- Saint Louis University (US)
- Howard Hughes Medical Institute (US)
- ORCID
- Venue
- Cell Reports
- Publisher
- Elsevier BV
- Published
- 2018-02
- Volume
- 22
- Issue
- 8
- Pages
- 2133-2145
- ISSN
- 2211-1247 (ISSN-L)
- PMC
- PMC5860817
- OpenAlex
- W2788393684
- Cited by
- 110
- References
- 55
- Citations by year
- 2026: 3 · 2025: 10 · 2024: 6 · 2023: 16 · 2022: 8 · 2021: 30 · 2020: 16 · 2019: 14 · 2018: 7
- FWCI
- 5.06
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Licence
- Locations
- Cell Reports (publishedVersion, cc-by-nc-nd)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion, cc-by-nc-nd)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion)
- Funders
- American Heart Association (16EIA27550005, 17SDG33110002, 16GRNT26420047)
- National Institutes of Health (R01HL135012, R35HL135820, R01HL105945, R01DK40936, 5F32DK10348902)
- American Diabetes Association (1-16-PMF-002)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › MicroRNA in disease regulation
- Health Sciences › Medicine › Epidemiology › Adipokines, Inflammation, and Metabolic Diseases
- Health Sciences › Medicine › Physiology › Adipose Tissue and Metabolism
- Keywords
- miR-33, microRNA knockout mice, obesity, insulin resistance, dietary intake, adipose tissue expansion, lipid uptake, lipolysis, SREBP1, lipogenesis, pair feeding, metabolic dysfunction
- MeSH terms
- Adipose Tissue, Animals, Eating, Enzyme Activation, Gene Expression Regulation, Germ Cells, Insulin Resistance, Cholesterol, HDL, Cholesterol, LDL, Liver, Mice, Inbred C57BL, Models, Biological, Obesity, Gene Deletion, Inflammation Mediators, Genetic Predisposition to Disease, MicroRNAs, Adiposity, Lipid Metabolism, Protein Kinase C-epsilon, Sterol Regulatory Element Binding Protein 1
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