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Major Urinary Protein-1 Increases Energy Expenditure and Improves Glucose Intolerance through Enhancing Mitochondrial Function in Skeletal Muscle of Diabetic Mice
Open accessAbstract
Major urinary protein-1 (MUP-1) is a low molecular weight secreted protein produced predominantly from the liver. Structurally it belongs to the lipocalin family, which carries small hydrophobic ligands such as pheromones. However, the physiological functions of MUP-1 remain poorly understood. Here we provide evidence demonstrating that MUP-1 is an important player in regulating energy expenditure and metabolism in mice. Both microarray and real-time PCR analysis demonstrated that the MUP-1 mRNA abundance in the liver of db/db obese mice was reduced by approximately 30-fold compared with their lean littermates, whereas this change was partially reversed by treatment with the insulin-sensitizing drug rosiglitazone. In both dietary and genetic obese mice, the circulating concentrations of MUP-1 were markedly decreased compared with the lean controls. Chronic elevation of circulating MUP-1 in db/db mice, using an osmotic pump-based protein delivery system, increased energy expenditure and locomotor activity, raised core body temperature, and decreased glucose intolerance as well as insulin resistance. At the molecular level, MUP-1-mediated improvement in metabolic profiles was accompanied by increased expression of genes involved in mitochondrial biogenesis, elevated mitochondrial oxidative capacity, decreased triglyceride accumulation, and enhanced insulin-evoked Akt signaling in skeletal muscle but not in liver. Altogether, these findings raise the possibility that MUP-1 deficiency might contribute to the metabolic dysregulation in obese/diabetic mice, and suggest that the beneficial metabolic effects of MUP-1 are attributed in part to its ability in increasing mitochondrial function in skeletal muscle.
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“Some LCN family members, including major urinary protein 1, retinol-binding protein 4, LCN2, and LCN13, have been shown to regulate energy metabolism [[254], [255], [256]].”
From Hepatokines and metabolism: Deciphering communication from the liver (2021) · cites this paper as [255]
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Metadata
- Authors
- Hui, X., Zhu, W., Wang, Y., Lam, K. S. L., Zhang, J., Wu, D., Kraegen, E. W., Li, Y., & Xu, A.
- Affiliations
- Chinese Academy of Sciences (CN)
- University of Hong Kong (HK)
- Garvan Institute of Medical Research (AU)
- Corresponding author
- Xu, Aimin
- Venue
- Journal of Biological Chemistry
- Publisher
- Elsevier BV
- Published
- 2009-05
- Volume
- 284
- Issue
- 21
- Pages
- 14050-14057
- ISSN
- 0021-9258 (ISSN-L)
- PMC
- PMC2682853
- OpenAlex
- W2069087871
- Cited by
- 130
- References
- 43
- Citations by year
- 2026: 3 · 2025: 7 · 2024: 11 · 2023: 8 · 2022: 9 · 2021: 10 · 2020: 9 · 2019: 7 · 2018: 9 · 2017: 2 · 2016: 6 · 2015: 10 · 2014: 10 · 2013: 6 · 2012: 8
- FWCI
- 5.10
- Type
- journal article
- Language
- en
- Open access
- hybrid
- doi.org
- Licence
- Locations
- Journal of Biological Chemistry (publishedVersion, cc-by)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- The HKU Scholars Hub (University of Hong Kong) (submittedVersion)
- Topics
- Health Sciences › Medicine › Physiology (medical) › Adipose Tissue and Metabolism
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Metabolism, Diabetes, and Cancer
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Adipokines, Inflammation, and Metabolic Diseases
- Keywords
- lipocalin, energy expenditure, impaired glucose tolerance, insulin resistance, mitochondrial function, skeletal muscle, mitochondrial biogenesis, obesity, type 2 diabetes, db/db mice, rosiglitazone, Akt signaling, triglyceride accumulation, locomotor activity, core body temperature
- MeSH terms
- Rosiglitazone, Animals, Diabetes Mellitus, Experimental, Dietary Fats, Energy Metabolism, Feeding Behavior, Insulin, Insulin Resistance, Liver, Mice, Inbred C57BL, Mice, Obese, Mitochondria, Motor Activity, Proteins, Recombinant Proteins, Signal Transduction, Up-Regulation, Glucose Intolerance, Muscle, Skeletal, Thiazolidinediones, Lipid Metabolism, Proto-Oncogene Proteins c-akt, Mice
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