Please use this identifier to cite or link to this item: https://repositorio.uca.edu.ar/handle/123456789/8679
Título : Transient receptor potential canonical 3 (TRPC3) channels are required for hypothalamic glucose detection and energy homeostasis
Autor : Chrétien, Chloé 
Fenech, Claire 
Liénard, Fabienne 
Grall, Sylvie 
Chevalier, Charlène 
Chaudy, Sylvie 
Brenachot, Xavier 
Berges, Raymond 
Louche, Katie 
Stark, Romana 
Nédélec, Emmanuelle 
Laderrière, Amélie 
Andrews, Zane B. 
Benani, Alexandre 
Flockerzi, Veit 
Gascuel, Jean 
Hartmann, Jana 
Moro, Cédric 
Birnbaumer, Lutz 
Leloup, Corinne 
Pénicaud, Luc 
Fioramonti, Xavier 
Palabras clave : GLUCOSA HIPOTALAMICAHOMEOSTASIS ENERGETICATRPC3CANALES IONICOS
Fecha de publicación : 2017
Editorial : American Diabetes Association
Cita : Chrétien, C. et al. Transient receptor potential canonical 3 (TRPC3) channels are required for hypothalamic glucose detection and energy homeostasis [en línea]. En Diabetes 66:314–324, 2017. Disponible en: https://repositorio.uca.edu.ar/handle/123456789/8679
Resumen : The mediobasal hypothalamus (MBH) contains neurons capable of directly detecting metabolic signals such as glucose to control energy homeostasis. Among them, glucose-excited (GE) neurons increase their electrical activity when glucose rises. In view of previous work, we hypothesized that transient receptor potential canonical type 3 (TRPC3) channels are involved in hypothalamic glucose detection and the control of energy homeostasis. To investigate the role of TRPC3, we used constitutive and conditional TRPC3-deficient mouse models. Hypothalamic glucose detection was studied in vivo by measuring food intake and insulin secretion in response to increased brain glucose level. The role of TRPC3 in GE neuron response to glucose was studied by using in vitro calcium imaging on freshly dissociated MBH neurons. We found that whole-body and MBH TRPC3-deficient mice have increased body weight and food intake. The anorectic effect of intracerebroventricular glucose and the insulin secretory response to intracarotid glucose injection are blunted in TRPC3-deficient mice. TRPC3 loss of function or pharmacological inhibition blunts calcium responses to glucose in MBH neurons in vitro. Together, the results demonstrate that TRPC3 channels are required for the response to glucose of MBH GE neurons and the central effect of glucose on insulin secretion and food intake.
URI : https://repositorio.uca.edu.ar/handle/123456789/8679
Disciplina: MEDICINA
DOI: 10.2337/db16-1114
Derechos: Acceso abierto
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