Key result
Fasting plasma adiponectin concentrations were not associated with glucose-, GLP-1-, or arginine-stimulated insulin secretion in normal glucose-tolerant subjects (all P > 0.42).
Why the study?
Does adiponectin affect insulin secretion or beta-cell apoptosis in human islets or normal glucose-tolerant subjects?
Cross-Sectional (n=65)
Does adiponectin affect insulin secretion or beta-cell apoptosis in human islets or normal glucose-tolerant subjects?
p-value: p=> 0.42
Although adiponectin receptors are expressed and functionally active in human islets, adiponectin does not directly influence insulin secretion or protect against fatty acid-induced beta-cell apoptosis.
Adiponectin effects on human islets remain hypothesis-generating; clinical studies needed before physiological relevance.
CONTEXT: The adipokine adiponectin has insulin-sensitizing, antiatherogenic, and antiinflammatory properties. Mouse and human adiponectin receptor-1 and -2 have been cloned, both of which are expressed in various tissues and mediate effects of globular and full-length adiponectin. Whether adiponectin affects insulin secretion and beta-cell apoptosis and whether plasma adiponectin is associated with beta-cell function in humans is under investigation. DESIGN AND METHODS: In human islets from multiorgan donors, we investigated expression of adiponectin receptor-1 and -2. Furthermore, glucose-stimulated insulin secretion was determined by RIA. In addition, we investigated fatty acid-induced beta-cell apoptosis by terminal dUTP nick end labeling and flow-cytometric cell cycle analysis (sub-G1 formation). In humans in vivo, insulin secretory function was measured during hyperglycemic clamps in 65 normal glucose-tolerant subjects. We determined first and second phase of glucose-stimulated, glucagon-like peptide-1-stimulated, and arginine-stimulated insulin secretion. RESULTS: Adiponectin receptor-1 and -2 are expressed in human islets at the mRNA and protein level. Moreover, full-length adiponectin induces phosphorylation of acetyl coenzyme A carboxylase. However, adiponectin did not affect basal or glucose-stimulated insulin secretion or basal or fatty acid-induced beta-cell apoptosis. In vivo, fasting plasma adiponectin concentrations were not associated with glucose-stimulated first- and second-phase insulin secretion or with glucagon-like peptide-1- or arginine-stimulated insulin secretion (all P > 0.42). CONCLUSIONS: These data support a regulatory role of adiponectin in human islets; however, adiponectin does not seem to affect insulin secretion or basal/fatty acid-induced beta-cell apoptosis in humans.
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Staiger et al. (2005) conducted a cross-sectional in Normal glucose tolerance (n=65). Fasting plasma adiponectin was evaluated on Glucose-stimulated, glucagon-like peptide-1-stimulated, and arginine-stimulated insulin secretion (p=> 0.42). Fasting plasma adiponectin concentrations were not associated with glucose-, GLP-1-, or arginine-stimulated insulin secretion in normal glucose-tolerant subjects (all P > 0.42).