Enhanced Insulin Sensitivity by Adipose Tissue Browning Alters Islet Morphology and Hormone Secretion in Response to Autonomic Nervous Activation in Female Mice.
(2016) In American Journal of Physiology: Endocrinology and Metabolism 310(1). p.81-90- Abstract
- Insulin resistance results in 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 reduced insulin secretion compared to 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... (More)
- Insulin resistance results in 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 reduced insulin secretion compared to 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 the acute suppression of insulin seen in wild-type mice was absent in Foxc2TG mice suggesting impaired adrenergic signaling in 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. (Less)
Please use this url to cite or link to this publication:
https://lup.lub.lu.se/record/8243431
- author
- Omar, Bilal LU ; Kvist Reimer, Martina LU ; Enerback, Sven and Ahrén, Bo LU
- organization
- publishing date
- 2016
- type
- Contribution to journal
- publication status
- published
- subject
- in
- American Journal of Physiology: Endocrinology and Metabolism
- volume
- 310
- issue
- 1
- pages
- 81 - 90
- publisher
- American Physiological Society
- external identifiers
-
- pmid:26530152
- wos:000366597200009
- scopus:84949564058
- pmid:26530152
- ISSN
- 1522-1555
- DOI
- 10.1152/ajpendo.00296.2015
- language
- English
- LU publication?
- yes
- id
- b8f323d5-c886-4ba2-a3c9-18613c8242b3 (old id 8243431)
- alternative location
- http://www.ncbi.nlm.nih.gov/pubmed/26530152?dopt=Abstract
- date added to LUP
- 2016-04-01 10:18:16
- date last changed
- 2024-01-06 13:15:34
@article{b8f323d5-c886-4ba2-a3c9-18613c8242b3,
abstract = {{Insulin resistance results in 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 reduced insulin secretion compared to 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 the acute suppression of insulin seen in wild-type mice was absent in Foxc2TG mice suggesting impaired adrenergic signaling in 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.}},
author = {{Omar, Bilal and Kvist Reimer, Martina and Enerback, Sven and Ahrén, Bo}},
issn = {{1522-1555}},
language = {{eng}},
number = {{1}},
pages = {{81--90}},
publisher = {{American Physiological Society}},
series = {{American Journal of Physiology: Endocrinology and Metabolism}},
title = {{Enhanced Insulin Sensitivity by Adipose Tissue Browning Alters Islet Morphology and Hormone Secretion in Response to Autonomic Nervous Activation in Female Mice.}},
url = {{http://dx.doi.org/10.1152/ajpendo.00296.2015}},
doi = {{10.1152/ajpendo.00296.2015}},
volume = {{310}},
year = {{2016}},
}