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Lipocalin 13 Regulation of Glucose and Lipid Metabolism in Obesity
Open accessAbstract
Lipocalin (LCN) family members are small secreted proteins that bind to small hydrophobic molecules via their characteristic central β-barrels. A couple of LCN family members, including major urinary protein 1, retinol-binding protein 4, LCN2, and LCN13, have been reported to regulate insulin sensitivity and nutrient metabolism. LCN13 is expressed by multiple tissues, including the liver, pancreas, epididymis, and skeletal muscle, and is secreted into the bloodstream in mice. Obesity is associated with a downregulation of LCN13 expression and lower levels of circulating LCN13. LCN13 therapies overcome LCN13 deficiency in mice with either genetic or dietary obesity, leading to an improvement in hyperglycemia, hyperinsulinemia, insulin resistance, glucose intolerance, and hepatic steatosis. In hepatocytes, LCN13 directly suppresses hepatic gluconeogenesis and lipogenesis but increases fatty acid β oxidation. LCN13 also enhances insulin sensitivity in adipocytes. The potential mechanisms of the antidiabetes and antisteatosis actions of LCN13 are discussed.
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“both mRNA and plasma levels of LCN13 are low in mice with genetic or high-fat diet-induced obesity [254,257].”
From Hepatokines and metabolism: Deciphering communication from the liver (2021) · cites this paper as [254]
In the citing paper
“Expression and secretion of LCN13 in mice vary in response to changes in metabolic states, suggesting a role for this hepatokine in nutrient sensing and regulation [254].”
From Hepatokines and metabolism: Deciphering communication from the liver (2021) · cites this paper as [254]
In the citing paper
“LCN13 in particular is secreted from multiple tissues including the liver to regulate glucose homeostasis and improve insulin sensitivity [254].”
From Hepatokines and metabolism: Deciphering communication from the liver (2021) · cites this paper as [254]
In the citing paper
“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 [254]
In the citing paper
“it is well established that LCN13 regulates glucose metabolism in adipocytes and hepatocytes by enhancing insulin signaling, insulin-stimulated glucose uptake, and insulin suppression of glucose production [254,258].”
From Hepatokines and metabolism: Deciphering communication from the liver (2021) · cites this paper as [254]
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Metadata
- Authors
- Zhou, Y., & Rui, L.
- Affiliations
- University of Michigan (US)
- Corresponding author
- Rui, Liangyou
- ORCID
- Rui, Liangyou
- Venue
- Vitamins & Hormones
- Publisher
- Elsevier
- Published
- 2013
- Volume
- 91
- Pages
- 369-383
- ISSN
- 0083-6729 (ISSN-L)
- PMC
- PMC4020521
- OpenAlex
- W2177781559
- Cited by
- 28
- References
- 63
- Citations by year
- 2026: 2 · 2024: 5 · 2023: 3 · 2022: 10 · 2021: 2 · 2020: 1 · 2017: 1 · 2016: 1 · 2015: 2 · 2014: 1
- FWCI
- 5.43
- Type
- book chapter
- Language
- en
- Open access
- green
- europepmc.org
- Locations
- Vitamins and hormones (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institutes of Health
- National Institute of Diabetes and Digestive and Kidney Diseases (R01DK065122)
- Topics
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Adipokines, Inflammation, and Metabolic Diseases
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Peroxisome Proliferator-Activated Receptors
- Life Sciences › Neuroscience › Endocrine and Autonomic Systems › Regulation of Appetite and Obesity
- Keywords
- obesity, glucose metabolism, lipid metabolism, insulin resistance, hepatic steatosis, hepatic gluconeogenesis, lipogenesis, fatty acid beta-oxidation, adipocytes, antidiabetic therapy, retinol-binding protein 4, neutrophil gelatinase-associated lipocalin
- MeSH terms
- Animals, Blood Glucose, Gene Expression Regulation, Lipid Metabolism, Mice, Lipocalins
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