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Cited by 258Adipokines, Inflammation, and Metabolic DiseasesAdipose Tissue and MetabolismRegulation of Appetite and Obesity

The DOI matches its Crossref record; 23 of the 23 references it cites were found in a registry or an index.

The release of the adipocytokine visfatin is regulated by glucose and insulin

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Haider, D. G., Schaller, G., Kapiotis, S., Maier, C., Luger, A., Wolzt, M.·2006·Diabetologia
DOI 10.1007/s00125-006-0303-7
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Abstract

Aims/hypothesis The novel insulin-mimetic adipocytokine visfatin has been linked to the metabolic syndrome, but its regulation has not been characterised to date. Since insulin-mimetic actions of visfatin may be part of the feedback regulation of glucose homeostasis, we hypothesised that visfatin concentrations are influenced by glucose or insulin blood levels in humans.Subjects, materials and methods In this randomised, double-blind, placebo-controlled crossover study, nine healthy male subjects (age 26+/-6 years) attended three different study days. On each day, systemic glucose concentrations of 5.0, 8.3 and 11.1 mmol/l were attained by stepwise increases in i.v. infusions of glucose, representing fasting and postprandial conditions. Visfatin plasma concentrations were studied during concomitant exogenous hyperinsulinaemia, inhibition of endogenous insulin production by somatostatin infusion, and placebo time control. Additionally, human adipocytes were cultured to study visfatin release and mRNA expression in vitro.Results Glucose concentrations of 8.3 and 11.1 mmol/l increased circulating visfatin from baseline concentrations of 0.5+/-0.0 ng/ml to 0.9+/-0.1 and 2.1+/-0.3 ng/ml, respectively (p<0.01). Glucose-induced elevation of visfatin was prevented by co-infusion of insulin or somatostatin (p<0.05). Cultured subcutaneous and visceral adipocytes released an equivalent amount of visfatin upon glucose-concentration- and time-dependent stimulation. Visfatin secretion involved the phosphatidylinositol 3-kinase (PI3-kinase) and protein kinase B (AKT) pathways. The mRNA expression pattern of visfatin was consistent with this altered protein release.Conclusions/interpretation Circulating visfatin concentrations are increased by hyperglycaemia. This effect is suppressed by exogenous hyperinsulinaemia or somatostatin infusion. Glucose signalling for visfatin release in adipocytes involves the PI3-kinase/AKT pathway.

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Metadata

Authors
Haider, D. G., Schaller, G., Kapiotis, S., Maier, C., Luger, A., & Wolzt, M.
Affiliations
Medical University of Vienna (AT)
Corresponding author
Wolzt, M.
ORCID
Wolzt, M.
Venue
Diabetologia
Publisher
Springer Science and Business Media LLC
Published
2006-05-31
Volume
49
Issue
8
Pages
1909-1914
ISSN
  • 0012-186X (ISSN-L)
  • 1432-0428
DOI
10.1007/s00125-006-0303-7
OpenAlex
W1985941542
Cited by
258
References
23
Citations by year
2026: 1 · 2025: 2 · 2024: 4 · 2023: 12 · 2022: 8 · 2021: 9 · 2020: 8 · 2019: 5 · 2018: 9 · 2017: 5 · 2016: 11 · 2015: 18 · 2014: 14 · 2013: 20 · 2012: 14
FWCI
18.55
Type
journal article
Language
en
Open access
Licence
www.springer.com/tdm (tdm)
Locations
  • Diabetologia (publishedVersion)
  • PubMed (publishedVersion)
  • 8th European Congress of Endocrinology incorporating the British Endocrine Societies
Topics
  • Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Adipokines, Inflammation, and Metabolic Diseases
  • Health Sciences › Medicine › Physiology (medical) › Adipose Tissue and Metabolism
  • Life Sciences › Neuroscience › Endocrine and Autonomic Systems › Regulation of Appetite and Obesity
Keywords
visfatin, adipokines, glucose homeostasis, hyperinsulinemia, hyperglycemia, somatostatin, adipocytes, PI3K/Akt signaling, insulin signaling, metabolic syndrome
MeSH terms
Insulin Secretion, Adult, Blood Glucose, Double-Blind Method, Glucose, Humans, Hyperinsulinism, Infusions, Intravenous, Insulin, Male, Placebos, Reference Values, Somatostatin, Cytokines, Adipocytes, Cross-Over Studies, Nicotinamide Phosphoribosyltransferase

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