ArticleMolecular and cellular biology2007
Aquaporin 7 is a beta-cell protein and regulator of intraislet glycerol content and glycerol kinase activity, beta-cell mass, and insulin production and secretion.
Article in Molecular and cellular biology, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 44 papers.
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Who cites it
44 citing papers in PubMed, 96 citations in OpenAlex.
- Glycerol and Glycerol-3-Phosphate: Multifaceted Metabolites in Metabolism, Cancer, and Other Diseases.Endocrine reviews · 2026Review
- Aquaporins in lipid metabolism: functions and regulation in health and disease.Lipids in health and disease · 2025Review
- LRRC8 channel complexes counterbalance KATP channels to mediate swell-secretion coupling in mouse pancreatic β cells.JCI insight · 2025Article
- Positive feedback loop between MAPK and aquaporin 7 regulates autophagy and apoptosis induced by palmitate in RIN-m5f cells.FEBS open bio · 2025Article
- The Important Role of Aquaglyceroporin 7 in Health and Disease.Biomolecules · 2024Review
- Functional Divergence in Solute Permeability between Ray-Finned Fish-Specific Paralogs of aqp10.Genome biology and evolution · 2024Article
- Aquaglyceroporins in Human Breast Cancer.Cells · 2023Article
- Review
- Cryo-EM structure supports a role of AQP7 as a junction protein.Nature communications · 2023Article
- Aquaporins in Digestive System.Advances in experimental medicine and biology · 2023Article
- Classification and Gene Structure of Aquaporins.Advances in experimental medicine and biology · 2023Article
- Aquaporins in Glandular Secretion.Advances in experimental medicine and biology · 2023Article
- Aquaporin Inhibitors.Advances in experimental medicine and biology · 2023Article
- Aquaporins in Obesity.Advances in experimental medicine and biology · 2023Review
- Glucolipotoxicity promotes the capacity of the glycerolipid/NEFA cycle supporting the secretory response of pancreatic beta cells.Diabetologia · 2022Article
- Metformin induces insulin secretion by preserving pancreatic aquaporin 7 expression in type 2 diabetes mellitus.Journal of diabetes investigation · 2022Article
- Signaling Mechanisms and Pharmacological Modulators Governing Diverse Aquaporin Functions in Human Health and Disease.International journal of molecular sciences · 2022Review
- Aquaglyceroporin Modulators as Emergent Pharmacological Molecules for Human Diseases.Frontiers in molecular biosciences · 2022Review
- Lipid-Induced Adaptations of the Pancreatic Beta-Cell to Glucotoxic Conditions Sustain Insulin Secretion.International journal of molecular sciences · 2021Review
- Metformin inhibits MAPK signaling and rescues pancreatic aquaporin 7 expression to induce insulin secretion in type 2 diabetes mellitus.The Journal of biological chemistry · 2021Article
Corrections and comments
- Erratum issued
Authors and funding
9 authors at 3 institutions in 2 countries.
Funding
Abstract
To investigate if intracellular glycerol content plays a role in the regulation of insulin secretion in pancreatic beta cells, we studied the expression of the glycerol channels, or aquaglyceroporins, encoded by the aquaporin 3 (Aqp3), Aqp7, and Aqp9 genes in mouse islets. We found expression of Aqp7 only, not that of Aqp3 or Aqp9, in the endocrine pancreas at both the mRNA (by reverse transcription-PCR) and protein (by immunohistochemistry) levels. Immunohistochemistry revealed a complete overlap between insulin and Aqp7 immunostaining in the pancreatic islet. Inactivation of Aqp7 by gene targeting produced viable and healthy mice. Aqp7-/- mice harbored an increased intraislet glycerol concentration with a concomitant increase of the glycerol kinase transcript level and enzyme activity. The islet triglyceride content in the Aqp7-/- mice was also increased compared to that in the Aqp7+/+ mice. Interestingly, Aqp7-/- mice displayed reduced beta-cell mass and insulin content but increased insulin-1 and insulin-2 mRNAs. The reduction of beta-cell mass in Aqp7-/- mice can be explained at least in part by a reduction in cell proliferation through protein kinase C and the c-myc cascade, with a reduction in the transcript levels of these two genes. Concomitantly, there was a decreased rate of apoptosis, as reflected by terminal deoxynucleotidyltransferase-mediated dUTP-biotin nick end labeling and caspase 3 and Bax expression in Aqp7-/- mice. Compared with Aqp7+/+ islets, islets isolated from Aqp7-/- mice secreted insulin at a higher rate under basal low-glucose conditions and on exposure to a high (450 mg/dl) glucose concentration. Aqp7-/- mice exhibited normal fasting blood glucose levels but elevated blood insulin levels. Their plasma glucose response to an intraperitoneal (i.p.) glucose tolerance test was normal, but their plasma insulin concentrations were higher than those of wild-type mice during the 2-h test. An i.p. insulin tolerance test showed similar plasma glucose lowering in Aqp7-/- and Aqp7+/+ mice, with no evidence of insulin resistance. In conclusion, we found that pancreatic beta cells express AQP7, which appears to be a key regulator of intraislet glycerol content as well as insulin production and secretion.
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