ArticleDiabetologia2016
Adipose-derived lipocalin 14 alleviates hyperglycaemia by suppressing both adipocyte glycerol efflux and hepatic gluconeogenesis in mice.
Article in Diabetologia, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 11 citations in OpenAlex.
- The novel adipokine Placin regulates glucose homeostasis via insulin secretion and IGF1 receptor signaling.Molecular therapy : the journal of the American Society of Gene Therapy · 2026Article
- Epigen-mediated mechanisms to alleviate glucose homeostasis disruptions in diet-induced obese and STZ-induced diabetic mice.Molecular therapy : the journal of the American Society of Gene Therapy · 2025Article
- Amelioration of non-alcoholic fatty liver disease by targeting adhesion G protein-coupled receptor F1 (eLife · 2023Article
- Lipocalin family proteins and their diverse roles in cardiovascular disease.Pharmacology & therapeutics · 2023Review
- Article
- Adipose-Derived Lipid-Binding Proteins: The Good, the Bad and the Metabolic Diseases.International journal of molecular sciences · 2021Review
- Lipocalin 13 enhances insulin secretion but is dispensable for systemic metabolic control.Life science alliance · 2021Article
- The role of adipokines in skeletal muscle inflammation and insulin sensitivity.Journal of inflammation (London, England) · 2018Review
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
aims/hypothesisGrowing evidence supports that dysregulation of adipose tissue-derived factors contributes to the pathogenesis of diabetes and its complications. Since our global gene profiling analysis has identified lipocalin-14 (LCN14)-a secretory protein with lipid-binding properties-as a potential adipokine highly expressed in white adipose tissue (WAT), this study aims to explore the metabolic roles of LCN14 in obese mice, and to investigate the functional mechanisms involved.
methodsImmunoassays and western blotting were performed to determine the circulating level and tissue distribution of LCN14, respectively. Recombinant adeno-associated virus (rAAV)-mediated gene delivery was used to overexpress LCN14 in diet-induced obese (DIO) mice and the effects on glucose and lipid metabolism were examined.
resultsLCN14 is expressed predominantly in WAT. Both circulating levels of LCN14 and its expression in adipose tissues are repressed in DIO and genetically inherited diabetic (db/db) mice. Overexpression of LCN14 by rAAV-mediated gene delivery in DIO mice significantly increased insulin sensitivity in major metabolic tissues and ameliorated hyperglycaemia by inhibiting hepatic gluconeogenesis. The reduced hepatic glucose production is attributed to the suppressive effects of LCN14 on the expression of gluconeogenic genes and on glycerol efflux in adipocytes, possibly by reducing the expression of aquaporin-7. CONCLUSIONS/
interpretationReduced LCN14 expression is involved in the pathogenesis of obesity-related metabolic dysregulation. LCN14 exerts its beneficial effects on glucose homeostasis and insulin sensitivity via its actions in both adipocytes and hepatocytes.
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