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MITOSENSING

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Decoding mitochondrial nutrient sensing programs in POMC neurons as key determin...

Decoding mitochondrial nutrient sensing programs in POMC neurons as key determinants of metabolic health Nutrient-sensing by POMC neurons is a critical process to monitor the metabolic status of the organism and to coordinate adaptive neuroendocrine, behavioural and metabolic effectors of energy balance. Mitochondria, as central comm... ver más

30/09/2022

FUNDACIO CLINIC PE...

2M€

Presupuesto del proyecto: 2M€

Líder del proyecto

FUNDACIO CLINIC PER A LA RECERCA BIOMEDICA No se ha especificado una descripción o un objeto social para esta compañía.

TRL 4-5 | 650K€

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Financiación concedida El organismo H2020 notifico la concesión del proyecto el día 2022-09-30

ERC-2016-COG: ERC Consolidator Grant

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2 Participantes

FUNDACIO CLINIC PER A LA REC...

2.00M€ | Lider

GOMBAU AUTOADHESIVOS SA EN L...

257.16K€ | Participante

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Duración del proyecto: 67 meses Fecha Inicio: 2017-02-22
Fecha Fin: 2022-09-30

Líder del proyecto

FUNDACIO CLINIC PER A LA RECERCA BIOMEDICA No se ha especificado una descripción o un objeto social para esta compañía.

TRL 4-5 | 650K€

Presupuesto del proyecto 2M€

Descripción del proyecto Nutrient-sensing by POMC neurons is a critical process to monitor the metabolic status of the organism and to coordinate adaptive neuroendocrine, behavioural and metabolic effectors of energy balance. Mitochondria, as central commanders of cellular energy production and primary sources of bioenergetic signals, are logical candidates to play a key role in metabolic control. However, a comprehensive understanding of the mitochondria as nutrient-sensors and modulators of systemic energy homeostasis is lacking. MITOSENSING hypothesizes that dedicated mitochondrial networks in POMC neurons are able to sense, integrate and respond to alterations in the nutritional milieu and engage physiological actions to maintain energy balance. Thus, defects in these mitochondrial nutrient-sensing programs in this subset of neurons underlie the development of metabolic conditions such as obesity and type-2 diabetes (T2D). To test it, we will pursue three aims: 1) to identify transcriptionally-modulated mitochondrial nutrient-sensing programs in POMC neurons; 2) to investigate whether disruption of specific nutrient-sensing programs in POMC neurons cause metabolic disorders; 3) to investigate whether the development of lifestyle-associated metabolic disorders are caused by defective mitochondrial nutrient-sensing programs in POMC neurons. By providing neuron-specific, integrative, functional and mechanistic in vivo strategies, MITOSENSING will represent a major step forward into the understanding of mitochondria as a nutrient-sensing entity, the gene programs involved and their physiological regulatory functions in the context of energy balance control. Adequate coordination of neuronal nutrient-sensing with energy balance control is critical to sustain life, and thus understanding the molecular mechanisms governing these physiological programs will have an enormous scientific impact and also potential therapeutical implications for obesity and T2D.

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