Knauf 2008 Endocrinology: Difference between revisions
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energy expenditure by reducing metabolic thermogenesis and | energy expenditure by reducing metabolic thermogenesis and | ||
ambulatory activity. | ambulatory activity. | ||
|mipnetlab= | |mipnetlab=FR Toulouse Casteilla L | ||
|discipline=Biomedicine | |discipline=Biomedicine | ||
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{{Labeling | {{Labeling | ||
| | |tissues=Nervous system | ||
|diseases=Diabetes | |diseases=Diabetes | ||
|couplingstates=OXPHOS | |couplingstates=OXPHOS | ||
|instruments=Oxygraph-2k | |||
|discipline=Biomedicine | |discipline=Biomedicine | ||
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Revision as of 14:10, 27 March 2015
Knauf C, Cani PD, Ait-Belgnaoui A, Benani A, Dray C, Cabou C, Colom A, Uldry M, Rastrelli S, Sabatier E, Godet N, Waget A, PΓ©nicaud L, Valet P, Burcelin R (2008) Brain glucagon-like peptide 1 signaling controls the onset of high-fat diet-induced insulin resistance and reduces energy expenditure. Endocrinol 149:4768-77. |
Knauf C, Cani PD, Ait-Belgnaoui A, Benani A, Dray C, Cabou C, Colom A, Uldry M, Rastrelli S, Sabatier E, Godet N, Waget A, Penicaud L, Valet P, Burcelin R (2008) Endocrinol
Abstract: Glucagon-like peptide-1 (GLP-1) is a peptide released by the intestine and the brain. We previously demonstrated that brain GLP-1 increases glucose-dependent hyperinsulinemia and insulin resistance. These two features are major characteristics of the onset of type 2 diabetes. Therefore, we investigated whether blocking brain GLP-1 signaling would prevent high-fat diet (HFD)-induced diabetes in the mouse. Our data show that a 1-month chronic blockage of brain GLP-1 signaling by exendin-9 (Ex9), totally prevented hyperinsulinemia and insulin resistance in HFD mice. Furthermore, food intake was dramatically increased, but body weight gain was unchanged, showing that brain GLP-1 controlled energy expenditure. Thermogenesis, glucose utilization, oxygen consumption, carbon dioxide production, muscle glycolytic respiratory index, UCP2 expression in muscle, and basal ambulatory activity were all increased by the exendin-9 treatment. Thus,wehave demonstrated that in response to a HFD, brain GLP-1 signaling induces hyperinsulinemia and insulin resistance and decreases energy expenditure by reducing metabolic thermogenesis and ambulatory activity.
β’ O2k-Network Lab: FR Toulouse Casteilla L
Labels:
Pathology: Diabetes
Tissue;cell: Nervous system
Coupling state: OXPHOS
HRR: Oxygraph-2k