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SUMMARY:Mitofusin 2 in POMC Neurons Connects ER Stress with Leptin Resista
 nce and Energy Imbalance
DTSTART:20140403T103000
DTEND:20140403T113000
DTSTAMP:20260506T002454Z
UID:c29d6e1354d2637e9254f9743f3dae8eaaddce95183194d036415730
CATEGORIES:Conferences - Seminars
DESCRIPTION:Marc Schneeberger Pané\, August Pi i Sunyer Biomedical Resear
 ch Institute (IDIBAPS)\, Barcelona (E)\nSEMINAR of the LAUSANNE INTEGRATIV
 E METABOLISM and NUTRITION ALLIANCE (LIMNA)Abstract:\nMitofusin 2 (MFN2) p
 lays critical roles in both mitochondrial fusion and the establishment of 
 mitochondria-endoplasmic reticulum (ER) interactions. Hypothalamic ER stre
 ss has emerged as a causative factor for the development of leptin resista
 nce\, but the underlying mechanisms are largely unknown. Here\, we show th
 at mitochondria-ER contacts in anorexigenic pro-opiomelanocortin (POMC) ne
 urons in the hypothalamus are decreased in diet-induced obesity. POMC-spec
 ific ablation of Mfn2 resulted in loss of mitochondria-ER contacts\, de
 fective POMC processing\, ER stress-induced leptin resistance\, hyperphagi
 a\, reduced energy expenditure\, and obesity. Pharmacological relieve of h
 ypothalamic ER stress reversed these metabolic alterations. Our data estab
 lish MFN2 in POMC neurons as an essential regulator of systemic energy b
 alance by fine-tuning the mitochondrial-ER axis homeostasis and function. 
 This previously unrecognized role for MFN2 argues for a crucial involvem
 ent in mediating ER stress-induced leptin resistance.Bio:\n2010-Present: 
   PhD Student:\, August Pi i Sunyer Biomedical Research Institute (IDIBAP
 S)\, Barcelona (E)\n(Neuroscience research in hypothalamic POMC neurons)\n
 2009-   Departament de Biologia Molecular\, Universitat de Barcelona\nUnd
 ergraduate:\nUniversitat de Barcelona\, Bell-Lloc del Pla
LOCATION:AI 1153 https://plan.epfl.ch/?room==AI%201153
STATUS:CONFIRMED
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