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Enhanced PIP3 signaling in POMC neurons causes diet-sensitive obesity as the consequence of neuronal silencing via KATP channel activation

L Plum, X Ma, B Hampel, H Münzberg, M Shanabrough, E Rother, L Koch, R Janoschek, J Alber, BF Belgardt, W Krone, TL Horvath, FM Ashcroft, JC Brüning · Diabetologie und Stoffwechsel · Ausgabe 06/2006

DOI 10.1055/s-2006-943791

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Autor:innenL Plum, X Ma, B Hampel, H Münzberg, M Shanabrough, E Rother, L Koch, R Janoschek, J Alber, BF Belgardt, W Krone, TL Horvath, FM Ashcroft, JC Brüning
ZeitschriftDiabetologie und Stoffwechsel
Ausgabe06/2006
Jahrgang / SeitenNicht angegeben

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Abstract-Vorschau

Leptin and insulin have been identified as fuel sensors acting in part through their hypothalamic receptors to inhibit food intake and stimulate energy expenditure. Both insulin and leptin receptors efficiently activate insulin receptor substrate-dependent signaling leading to activation of the phosphatidyl-inositol (PI) 3-kinase and subsequent generation of PI3,4,5-trisphosphate (PIP3). We directly addressed the ro…

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Zitierempfehlung

L Plum, X Ma, B Hampel, H Münzberg, M Shanabrough, E Rother, L Koch, R Janoschek, J Alber, BF Belgardt, W Krone, TL Horvath, FM Ashcroft, JC Brüning (2006) Enhanced PIP3 signaling in POMC neurons causes diet-sensitive obesity as the consequence of neuronal silencing via KATP channel activation. Diabetologie und Stoffwechsel (06). https://doi.org/10.1055/s-2006-943791

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