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Exploring the underlying mechanIsms of partial leptin reduction towards a non in...

Exploring the underlying mechanIsms of partial leptin reduction towards a non invasive obesity therapy Leptin regulates energy balance by functioning as a satiety signal. When identified 26 years ago, expectations were high that leptin therapies could be used for the treatment of obesity. In contrast to the successful use of leptin... ver más

31/03/2025

HVL

284K€

Presupuesto del proyecto: 284K€

Líder del proyecto

HOGSKULEN PA VESTLANDET No se ha especificado una descripción o un objeto social para esta compañía.

Fecha límite participación Sin fecha límite de participación.

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Financiación concedida El organismo H2020 notifico la concesión del proyecto el día 2021-03-01

MSCA-IF-2020: Individual Fellowships

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3 Participantes

HVL

284.35K€ | Lider

THE UNIVERSITY OF TEXAS SYST...

177.27K€ | Participante

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Duración del proyecto: 48 meses Fecha Inicio: 2021-03-01
Fecha Fin: 2025-03-31

Líder del proyecto

HOGSKULEN PA VESTLANDET No se ha especificado una descripción o un objeto social para esta compañía.

Presupuesto del proyecto 284K€

Fecha límite de participación Sin fecha límite de participación.

Descripción del proyecto Leptin regulates energy balance by functioning as a satiety signal. When identified 26 years ago, expectations were high that leptin therapies could be used for the treatment of obesity. In contrast to the successful use of leptin for treatment of individuals with lipodystrophy and complete leptin deficiency, pharmacological approaches using leptin therapy for the treatment of diet-induced obesity have been widely unsuccessful. Injecting recombinant leptin in the context of obesity, associated with elevated leptin levels, remains ineffective as central neurons become leptin resistant. Interestingly, Scherer et al. recently published a series of findings that encourages for a conceptual shift. They reported that a partial reduction of circulating leptin levels in the obese state prompts an unexpected systemic response resulting in weight loss, reduced food intake, improved glucose and insulin tolerance and increased energy expenditure - all consistent with leptin re-sensitization in central neurons. The systemic physiological benefits of partial leptin reduction have already been demonstrated. The overall goal of this proposal is therefore to determine the underlying molecular mechanisms that are induced by leptin reduction and trigger leptin re-sensitization. Understanding of these conceptual steps should lead us to explore partial leptin reduction as a viable avenue for anti-obesity and anti-diabetic therapy in the near future. We aim to determine the peripheral effects of leptin reduction using neutralizing leptin antibodies and advanced mouse genetics. Moreover, we will determine downstream signaling events that are affected in peripheral tissues upon leptin depletion using imaging mass cytometry and transcriptional regulation by single cell RNAseq. Finally, we will also determine whether leptin lowering offers synergistic effects with existing weight loss approaches and whether anti-diabetic interventions rely on leptin lowering independent of weight loss.

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