Circulating insulin stimulates fatty acid retention in white adipose tissue via KATP channel activation in the central nervous system only in insulin-sensitive mice
Insulin signaling in the central nervous system (CNS) is required for the inhibitory effect of insulin on glucose production. Our aim was to determine whether the CNS is also involved in the stimulatory effect of circulating insulin on the tissue-specific retention of fatty acid (FA) from plasma. In...
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doaj-e28774ae54384d0baefe6731789094a92021-04-28T06:03:24ZengElsevierJournal of Lipid Research0022-22752011-09-0152917121722Circulating insulin stimulates fatty acid retention in white adipose tissue via KATP channel activation in the central nervous system only in insulin-sensitive miceClaudia P. Coomans0Janine J. Geerling1Bruno Guigas2Anita M. van den Hoek3Edwin T. Parlevliet4D. Margriet Ouwens5Hanno Pijl6Peter J. Voshol7Patrick C.N. Rensen8Louis M. Havekes9Johannes A. Romijn10To whom correspondence should be addressed; Departments of Endocrinology and Metabolic Diseases, Leiden University Medical CenterDepartments of Endocrinology and Metabolic Diseases, Leiden University Medical CenterDepartments of Molecular Cell Biology, Leiden University Medical CenterDepartments of Endocrinology and Metabolic Diseases, Leiden University Medical Center; Netherlands Organization for Applied Scientific Research - BioSciences, Gaubius Laboratory, LeidenDepartments of Endocrinology and Metabolic Diseases, Leiden University Medical CenterDepartments of Molecular Cell Biology, Leiden University Medical CenterDepartments of Endocrinology and Metabolic Diseases, Leiden University Medical CenterDepartments of Endocrinology and Metabolic Diseases, Leiden University Medical CenterDepartments of Endocrinology and Metabolic Diseases, Leiden University Medical Center; Departments of General Internal Medicine, Leiden University Medical CenterDepartments of General Internal Medicine, Leiden University Medical Center; Departments of Cardiology, Leiden University Medical Center; Netherlands Organization for Applied Scientific Research - BioSciences, Gaubius Laboratory, LeidenDepartments of Endocrinology and Metabolic Diseases, Leiden University Medical Center; Department of Medicine, Academic Medical Center, Amsterdam, The NetherlandsInsulin signaling in the central nervous system (CNS) is required for the inhibitory effect of insulin on glucose production. Our aim was to determine whether the CNS is also involved in the stimulatory effect of circulating insulin on the tissue-specific retention of fatty acid (FA) from plasma. In wild-type mice, hyperinsulinemic-euglycemic clamp conditions stimulated the retention of both plasma triglyceride-derived FA and plasma albumin-bound FA in the various white adipose tissues (WAT) but not in other tissues, including brown adipose tissue (BAT). Intracerebroventricular (ICV) administration of insulin induced a similar pattern of tissue-specific FA partitioning. This effect of ICV insulin administration was not associated with activation of the insulin signaling pathway in adipose tissue. ICV administration of tolbutamide, a KATP channel blocker, considerably reduced (during hyperinsulinemic-euglycemic clamp conditions) and even completely blocked (during ICV administration of insulin) WAT-specific retention of FA from plasma. This central effect of insulin was absent in CD36-deficient mice, indicating that CD36 is the predominant FA transporter in insulin-stimulated FA retention by WAT. In diet-induced insulin-resistant mice, these stimulating effects of insulin (circulating or ICV administered) on FA retention in WAT were lost. In conclusion, in insulin-sensitive mice, circulating insulin stimulates tissue-specific partitioning of plasma-derived FA in WAT in part through activation of KATP channels in the CNS. Apparently, circulating insulin stimulates fatty acid uptake in WAT but not in BAT, directly and indirectly through the CNS.http://www.sciencedirect.com/science/article/pii/S0022227520408624braininsulin resistancelipid metabolismlipoprotein lipasetriglyceridesbrown adipose tissue |
collection |
DOAJ |
language |
English |
format |
Article |
sources |
DOAJ |
author |
Claudia P. Coomans Janine J. Geerling Bruno Guigas Anita M. van den Hoek Edwin T. Parlevliet D. Margriet Ouwens Hanno Pijl Peter J. Voshol Patrick C.N. Rensen Louis M. Havekes Johannes A. Romijn |
spellingShingle |
Claudia P. Coomans Janine J. Geerling Bruno Guigas Anita M. van den Hoek Edwin T. Parlevliet D. Margriet Ouwens Hanno Pijl Peter J. Voshol Patrick C.N. Rensen Louis M. Havekes Johannes A. Romijn Circulating insulin stimulates fatty acid retention in white adipose tissue via KATP channel activation in the central nervous system only in insulin-sensitive mice Journal of Lipid Research brain insulin resistance lipid metabolism lipoprotein lipase triglycerides brown adipose tissue |
author_facet |
Claudia P. Coomans Janine J. Geerling Bruno Guigas Anita M. van den Hoek Edwin T. Parlevliet D. Margriet Ouwens Hanno Pijl Peter J. Voshol Patrick C.N. Rensen Louis M. Havekes Johannes A. Romijn |
author_sort |
Claudia P. Coomans |
title |
Circulating insulin stimulates fatty acid retention in white adipose tissue via KATP channel activation in the central nervous system only in insulin-sensitive mice |
title_short |
Circulating insulin stimulates fatty acid retention in white adipose tissue via KATP channel activation in the central nervous system only in insulin-sensitive mice |
title_full |
Circulating insulin stimulates fatty acid retention in white adipose tissue via KATP channel activation in the central nervous system only in insulin-sensitive mice |
title_fullStr |
Circulating insulin stimulates fatty acid retention in white adipose tissue via KATP channel activation in the central nervous system only in insulin-sensitive mice |
title_full_unstemmed |
Circulating insulin stimulates fatty acid retention in white adipose tissue via KATP channel activation in the central nervous system only in insulin-sensitive mice |
title_sort |
circulating insulin stimulates fatty acid retention in white adipose tissue via katp channel activation in the central nervous system only in insulin-sensitive mice |
publisher |
Elsevier |
series |
Journal of Lipid Research |
issn |
0022-2275 |
publishDate |
2011-09-01 |
description |
Insulin signaling in the central nervous system (CNS) is required for the inhibitory effect of insulin on glucose production. Our aim was to determine whether the CNS is also involved in the stimulatory effect of circulating insulin on the tissue-specific retention of fatty acid (FA) from plasma. In wild-type mice, hyperinsulinemic-euglycemic clamp conditions stimulated the retention of both plasma triglyceride-derived FA and plasma albumin-bound FA in the various white adipose tissues (WAT) but not in other tissues, including brown adipose tissue (BAT). Intracerebroventricular (ICV) administration of insulin induced a similar pattern of tissue-specific FA partitioning. This effect of ICV insulin administration was not associated with activation of the insulin signaling pathway in adipose tissue. ICV administration of tolbutamide, a KATP channel blocker, considerably reduced (during hyperinsulinemic-euglycemic clamp conditions) and even completely blocked (during ICV administration of insulin) WAT-specific retention of FA from plasma. This central effect of insulin was absent in CD36-deficient mice, indicating that CD36 is the predominant FA transporter in insulin-stimulated FA retention by WAT. In diet-induced insulin-resistant mice, these stimulating effects of insulin (circulating or ICV administered) on FA retention in WAT were lost. In conclusion, in insulin-sensitive mice, circulating insulin stimulates tissue-specific partitioning of plasma-derived FA in WAT in part through activation of KATP channels in the CNS. Apparently, circulating insulin stimulates fatty acid uptake in WAT but not in BAT, directly and indirectly through the CNS. |
topic |
brain insulin resistance lipid metabolism lipoprotein lipase triglycerides brown adipose tissue |
url |
http://www.sciencedirect.com/science/article/pii/S0022227520408624 |
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