MicroRNA-33 regulates sterol regulatory element-binding protein 1 expression in mice
Open accessAbstract
MicroRNAs (miRs) are small non-protein-coding RNAs that bind to specific mRNAs and inhibit translation or promote mRNA degradation. Recent reports have indicated that miR-33, which is located within the intron of sterol regulatory element-binding protein (SREBP) 2, controls cholesterol homoeostasis and may be a potential therapeutic target for the treatment of atherosclerosis. Here we show that deletion of miR-33 results in marked worsening of high-fat diet-induced obesity and liver steatosis. Using miR-33−/−Srebf1+/− mice, we demonstrate that SREBP-1 is a target of miR-33 and that the mechanisms leading to obesity and liver steatosis in miR-33−/− mice involve enhanced expression of SREBP-1. These results elucidate a novel interaction between SREBP-1 and SREBP-2 mediated by miR-33 in vivo.
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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 [39]
The Results section reports increased food intake in high-fat-diet-fed miR-33 knockout mice, but its pair-feeding experiment explicitly concludes that their greater weight gain is not caused by a change in food intake. The Discussion instead attributes obesity to enhanced SREBP-1 expression. The supplied passages have no page numbers. (LLM, conf=0.90)
Checked by a reasoning model — may be wrong.
Experimental — accuracy not yet measuredA later report by the same group showed a dramatic increase in body weight and insulin resistance in miR-33−/− mice when fed a high fat (60% saturated fat) diet.
“a later report by the same group did show a dramatic increase in BW and insulin resistance in miR-33−/− mice when fed a high fat (60% saturated fat) diet (Horie et al., 2013).”
From Genetic dissection of the impact of miR-33a and miR-33b during the progression of atherosclerosis (2017) · cites this paper as Horie et al., 2013
The Results sections on obesity and insulin tolerance report markedly increased body weight and impaired insulin tolerance in miR-33−/− mice fed a high-fat diet. Our copy does not specify that the diet contained 60% saturated fat, so that detail is unsupported. (LLM, conf=0.86)
Experimental — accuracy not yet measuredMiR-33 can modulate SREBP1 expression and miR-33 knockout mice are prone to obesity and liver steatosis.
“MiR-33 can modulate SREBP1 expression and miR-33 knockout mice are prone to obesity and liver steatosis [35].”
From HIV-TAT dysregulates microglial lipid metabolism through SREBP2/miR-124 axis: Implication of lipid droplet accumulation microglia in NeuroHIV (2025) · cites this paper as [35]
Loss of miR-33 results in a predisposition to the development of obesity and insulin resistance.
“Additionally, a later report by this same group has demonstrated that loss of miR-33 results in a predisposition to the development of obesity and insulin resistance (Horie et al., 2013)”
From Genetic dissection of the impact of miR-33a and miR-33b during the progression of atherosclerosis (2017) · cites this paper as Horie et al., 2013
miR-33 knockout mice have adverse metabolic effects.
“the adverse metabolic effects reported in miR-33 knockout mice (Horie et al., 2013)”
From Genetic dissection of the impact of miR-33a and miR-33b during the progression of atherosclerosis (2017) · cites this paper as Horie et al., 2013
miR-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 [39]
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- Authors
- Horie, T., Nishino, T., Baba, O., Kuwabara, Y., Nakao, T., Nishiga, M., Usami, S., Izuhara, M., Sowa, N., Yahagi, N., Shimano, H., Matsumura, S., Inoue, K., Marusawa, H., Nakamura, T., Hasegawa, K., Kume, N., Yokode, M., Kita, T., Kimura, T., & Ono, K.
- Affiliations
- Kyoto University (JP)
- University of Tsukuba (JP)
- Kansai Medical University (JP)
- Kyoto Medical Center (JP)
- Kobe Gakuin University (JP)
- Kobe City Medical Center General Hospital (JP)
- Corresponding author
- Ono, Koh
- ORCID
- Venue
- Nature Communications
- Published
- 2013-12-03
- Volume
- 4
- Issue
- 1
- Pages
- 2883-2883
- ISSN
- 2041-1723 (ISSN-L)
- PMC
- PMC3863899
- OpenAlex
- W2167729033
- Cited by
- 230
- References
- 45
- Citations by year
- 2026: 5 · 2025: 17 · 2024: 12 · 2023: 17 · 2022: 15 · 2021: 28 · 2020: 18 · 2019: 16 · 2018: 14 · 2017: 21 · 2016: 27 · 2015: 23 · 2014: 16 · 2012: 1
- FWCI
- 7.74
- Type
- journal article
- Language
- en
- Open access
- hybrid
- doi.org
- Locations
- Nature Communications (publishedVersion, cc-by)
- Europe PMC (PubMed Central) (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- Institutional Repositories DataBase (IRDB) (submittedVersion)
- RePEc: Research Papers in Economics (submittedVersion)
- Kyoto University Research Information Repository (Kyoto University) (submittedVersion, cc-by)
- Funders
- Suzuken Memorial Foundation
- Cell Science Research Foundation
- Ministry of Education, Culture, Sports, Science and Technology
- Daiichi-Sankyo
- Otsuka Pharmaceutical
- Ono Medical Research Foundation
- Japan Society for the Promotion of Science (24790753, 23116006, 23390211, 24890094)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › MicroRNA in disease regulation
- Health Sciences › Medicine › Surgery › Cholesterol and Lipid Metabolism
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Lipid metabolism and disorders
- Keywords
- miR-33, SREBP1, SREBP2, microRNA regulation, cholesterol homeostasis, high-fat diet-induced obesity, hepatic steatosis, atherosclerosis, lipid metabolism
- MeSH terms
- Animals, Fatty Liver, Gene Expression Regulation, Humans, Introns, Male, Obesity, Mice, Knockout, MicroRNAs, Lipid Metabolism, Mice, Sterol Regulatory Element Binding Protein 1, Sterol Regulatory Element Binding Protein 2, Diet, High-Fat
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