Difference between revisions of "Knauf 2008 Endocrinology"
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{{Publication | {{Publication | ||
|title=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, Pénicaud 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. | |title=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, Pénicaud 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. Endocrinology 149:4768-77. | ||
|info=[http://www.ncbi.nlm.nih.gov/pubmed/18556349 PMID: 18556349] | |info=[http://www.ncbi.nlm.nih.gov/pubmed/18556349 PMID: 18556349] | ||
|authors=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 | |authors=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 | ||
|year=2008 | |year=2008 | ||
|journal= | |journal=Endocrinology | ||
|abstract=Glucagon-like peptide-1 (GLP-1) is a peptide released by the | |abstract=Glucagon-like peptide-1 (GLP-1) is a peptide released by the | ||
intestine and the brain. We previously demonstrated that | intestine and the brain. We previously demonstrated that | ||
Line 25: | Line 25: | ||
energy expenditure by reducing metabolic thermogenesis and | energy expenditure by reducing metabolic thermogenesis and | ||
ambulatory activity. | ambulatory activity. | ||
|mipnetlab= | |mipnetlab=FR Toulouse Casteilla L, FR Toulouse Dray C | ||
|discipline=Biomedicine | |discipline=Biomedicine | ||
}} | }} | ||
{{Labeling | {{Labeling | ||
|area=Respiration | |||
|diseases=Diabetes | |||
|tissues=Nervous system | |||
|couplingstates=OXPHOS | |||
|instruments=Oxygraph-2k | |instruments=Oxygraph-2k | ||
|discipline=Biomedicine | |discipline=Biomedicine | ||
}} | }} |
Latest revision as of 17:00, 26 March 2018
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, Pénicaud 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. Endocrinology 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) Endocrinology
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.
• O2k-Network Lab: FR Toulouse Casteilla L, FR Toulouse Dray C
Labels: MiParea: Respiration
Pathology: Diabetes
Tissue;cell: Nervous system
Coupling state: OXPHOS
HRR: Oxygraph-2k