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Enhanced insulin sensitivity mediated by adipose tissue browning perturbs islet morphology and hormone secretion in response to autonomic nervous activation in female mice

Journal article
Authors B. A. Omar
M. Kvist-Reimer
Sven Enerbäck
B. Ahren
Published in American Journal of Physiology-Endocrinology and Metabolism
Volume 310
Issue 1
Pages E81-E90
ISSN 0193-1849
Publication year 2016
Published at Institute of Biomedicine
Pages E81-E90
Language en
Links dx.doi.org/10.1152/ajpendo.00296.20...
Keywords insulin, glucagon, white adipose tissue, sympathetic nervous system, parasympathetic nervous, beta-cell function, high-fat diet, glucagon-secretion, glucose-tolerance, calcitonin-gene, metabolism, resistance, mouse, stimulation, obesity
Subject categories Clinical Medicine

Abstract

Insulin resistance results in a compensatory increase in insulin secretion to maintain normoglycemia. Conversely, high insulin sensitivity results in reduced insulin secretion to prevent hypoglycemia. The mechanisms for this inverse adaptation are not well understood. We utilized highly insulin-sensitive mice, due to adipocyte-specific overexpression of the FOXC2 transcription factor, to study mechanisms of the reversed islet adaptation to increased insulin sensitivity. We found that Foxc2TG mice responded to mild hyperglycemia with insulin secretion significantly lower than that of wild-type mice; however, when severe hyperglycemia was induced, Foxc2TG mice demonstrated insulin secretion equal to or greater than that of wild-type mice. In response to autonomic nervous activation by 2-deoxyglucose, the acute suppression of insulin seen in wild-type mice was absent in Foxc2TG mice, suggesting impaired sympathetic signaling to the islet. Basal glucagon was increased in Foxc2TG mice, but they displayed severely impaired glucagon responses to cholinergic and autonomic nervous stimuli. These data suggest that the autonomic nerves contribute to the islet adaptation to high insulin sensitivity, which is compatible with a neuro-adipo regulation of islet function being instrumental for maintaining glucose regulation.

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