Abstract | OBJECTIVE: METHODS: RESULTS:
Leptin ameliorated STZ-induced hyperglycemia in both intact and vagotomised mice. Similarly, mice with a partial chemical sympathectomy did not have an attenuated response to leptin-mediated glucose lowering relative to sham controls, and showed intact leptin-induced Ucp1 expression in BAT. Although leptin activated BAT thermogenesis in STZ-diabetic mice, the anti-diabetic effect of leptin was not blunted in Ucp1 (-/-) mice. CONCLUSIONS: These results suggest that leptin lowers blood glucose in insulin-deficient diabetes through a manner that does not require parasympathetic or sympathetic innervation, and thus imply that leptin lowers blood glucose through an alternative CNS-mediated mechanism or redundant target tissues. Furthermore, we conclude that the glucose lowering action of leptin is independent of UCP1-dependent thermogenesis.
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Authors | Heather C Denroche, Michelle M Kwon, Maria M Glavas, Eva Tudurí, Marion Philippe, Whitney L Quong, Timothy J Kieffer |
Journal | Molecular metabolism
(Mol Metab)
Vol. 5
Issue 8
Pg. 716-724
(Aug 2016)
ISSN: 2212-8778 [Print] Germany |
PMID | 27656409
(Publication Type: Journal Article)
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