Hepatic leptin signalling and subdiaphragmatic vagal efferents are not required for leptin-induced increases of plasma IGF binding protein-2 (IGFBP-2) in <Emphasis Type="Italic">ob/ob</Emphasis> mice |
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| Authors: | J?Levi F?K?Huynh H?C?Denroche U?H?Neumann M?M?Glavas S?D?Covey Email author" target="_blank">T?J?KiefferEmail author |
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| Institution: | (1) Department of Cellular and Physiological Sciences, Life Sciences Institute, 2350 Health Sciences Mall, University of British Columbia, Vancouver, BC, Canada, V6T 1Z3;(2) Department of Biochemistry and Molecular Biology, Life Sciences Institute, University of British Columbia, Vancouver, BC, Canada;(3) Department of Surgery, University of British Columbia, Vancouver, BC, Canada; |
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| Abstract: | Aims/hypothesis The fat-derived hormone leptin plays a crucial role in the maintenance of normal body weight and energy expenditure as well
as in glucose homeostasis. Recently, it was reported that the liver-derived protein, insulin-like growth factor binding protein-2
(IGFBP-2), is responsible for at least some of the glucose-normalising effects of leptin. However, the exact mechanism by
which leptin upregulates IGFBP-2 production is unknown. Since it is believed that circulating IGFBP-2 is predominantly derived
from the liver and leptin has been shown to have both direct and indirect actions on the liver, we hypothesised that leptin
signalling in hepatocytes or via brain–liver vagal efferents may mediate leptin control of IGFBP-2 production. |
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