ArticleAmerican journal of physiology. Endocrinology and metabolism2016
Zinc transporter Slc39a14 regulates inflammatory signaling associated with hypertrophic adiposity.
Article in American journal of physiology. Endocrinology and metabolism, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers.
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Who cites it
47 citing papers in PubMed, 80 citations in OpenAlex.
- ZIP1 Is a Critical DNA Damage-Responsive Zinc Transporter Induced by Bleomycin via the TNFα-NF-κB Pathway.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026Article
- A full-length single nuclei transcriptomic atlas of human skeletal muscle insulin resistance.bioRxiv : the preprint server for biology · 2026Article
- Beneficial Role of Zinc in Metabolic Syndrome: Understanding the Underlying Pathophysiological Mechanisms.Current medicinal chemistry · 2026Review
- Genetic insights of waist-to-height ratio on the risk of steatotic and advanced liver diseases: genome-wide association study and polygenic risk score-based analyses.Human genomics · 2025Article
- Zinc and Adipose Organ Dysfunction: Molecular Insights into Obesity and Metabolic Disorders.Current nutrition reports · 2025Review
- Zrt-Irt-like Proteins (ZIP) Family Zinc Transporters: Emerging Players in Pancreatic β Cell Function and Insulin Regulation.The Journal of nutrition · 2025Review
- Impacts of zinc caproate supplementation on growth performance, intestinal health, anti-inflammatory activity, and Zn homeostasis in weaned piglets challenged with Escherichia coli K88.Journal of animal science and biotechnology · 2025Article
- Roles of zinc and zinc transporters in development, progression, and treatment of inflammatory bowel disease (IBD).Frontiers in nutrition · 2025Review
- Zinc Transporter ZnT1 mRNA Expression Is Negatively Associated with Leptin Serum Concentrations but Is not Associated with Insulin Resistance or Inflammatory Markers in Visceral Adipose Tissue.Biological trace element research · 2024Article
- The impact of solute carrier proteins on disrupting substance regulation in metabolic disorders: insights and clinical applications.Frontiers in pharmacology · 2024Review
- Absence ofAmerican journal of physiology. Endocrinology and metabolism · 2024Article
- Metal transporter SLC39A14/ZIP14 modulates regulation between the gut microbiome and host metabolism.American journal of physiology. Gastrointestinal and liver physiology · 2023Article
- Enterocyte-specific deletion of metal transporter Zip14 (Slc39a14) alters intestinal homeostasis through epigenetic mechanisms.American journal of physiology. Gastrointestinal and liver physiology · 2023Article
- Recent progress toward understanding the role of ZIP14 in regulating systemic manganese homeostasis.Computational and structural biotechnology journal · 2023Review
- Zinc homeostasis and redox alterations in obesity.Frontiers in endocrinology · 2023Review
- The Combined Partial Knockdown ofAntioxidants (Basel, Switzerland) · 2022Article
- Nitric Oxide Mobilizes Intracellular ZnInternational journal of molecular sciences · 2022Article
- The Oxidative Balance Orchestrates the Main Keystones of the Functional Activity of Cardiomyocytes.Oxidative medicine and cellular longevity · 2022Review
- The Role of Zinc Homeostasis in the Prevention of Diabetes Mellitus and Cardiovascular Diseases.Journal of atherosclerosis and thrombosis · 2021Review
- Restriction of Manganese Intake Prevents the Onset of Brain Manganese Overload inInternational journal of molecular sciences · 2021Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Zinc is a signaling molecule in numerous metabolic pathways, the coordination of which occurs through activity of zinc transporters. The expression of zinc transporter Zip14 (Slc39a14), a zinc importer of the solute carrier 39 family, is stimulated under proinflammatory conditions. Adipose tissue upregulates Zip14 during lipopolysaccharide-induced endotoxemia. A null mutation of Zip14 (KO) revealed that phenotypic changes in adipose include increased cytokine production, increased plasma leptin, hypertrophied adipocytes, and dampened insulin signaling. Adipose tissue from KO mice had increased levels of preadipocyte markers, lower expression of the differentiation marker (PPARγ), and activation of NF-κB and STAT3 pathways. Our overall hypothesis was that ZIP14 would play a role in adipocyte differentiation and inflammatory obesity. Global Zip14 KO causes systemic endotoxemia. The observed metabolic changes in adipose metabolism were reversed when oral antibiotics were administrated, indicating that circulating levels of endotoxin were in part responsible for the adipose phenotype. To evaluate a mechanism, 3T3-L1 cells were differentiated into adipocytes and treated with siRNA to knock down Zip14. These cells had an impaired ability to mobilize zinc, which caused dysregulation of inflammatory pathways (JAK2/STAT3 and NF-κB). The Zip14 deletion may limit the availability of intracellular zinc, yielding the unique phenotype of inflammation coupled with hypertrophy. Taken together, these results suggest that aberrant zinc distribution observed with Zip14 ablation impacts adipose cytokine production and metabolism, ultimately increasing fat deposition when exposed to endotoxin. To our knowledge, this is the first investigation into the mechanistic role of ZIP14 in adipose tissue regulation and metabolism.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.