LIFEWITHOUTINSULIN
Metabolic actions of brain leptin receptors signaling in type 1 diabetes
| Coordinatore | UNIVERSITE DE GENEVE
Spiacenti, non ci sono informazioni su questo coordinatore. Contattare Fabio per maggiori infomrazioni, grazie. |
| Nazionalità Coordinatore | Switzerland [CH] |
| Totale costo | 1˙999˙500 € |
| EC contributo | 1˙999˙500 € |
| Programma | FP7-IDEAS-ERC
Specific programme: "Ideas" implementing the Seventh Framework Programme of the European Community for research, technological development and demonstration activities (2007 to 2013) |
| Code Call | ERC-2013-CoG |
| Funding Scheme | ERC-CG |
| Anno di inizio | 2014 |
| Periodo (anno-mese-giorno) | 2014-06-01 - 2019-05-31 |
Partecipanti
| # | ||||
|---|---|---|---|---|
| 1 |
UNIVERSITE DE GENEVE
Organization address
address: Rue du General Dufour 24 contact info |
CH (GENEVE) | hostInstitution | 1˙999˙500.00 |
| 2 |
UNIVERSITE DE GENEVE
Organization address
address: Rue du General Dufour 24 contact info |
CH (GENEVE) | hostInstitution | 1˙999˙500.00 |
Mappa
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Obiettivo del progetto (Objective)
'An established dogma is that insulin is absolutely required for survival. This notion has been supported by the fact that the sole life-saving intervention available to the millions affected by type 1 diabetes mellitus (T1DM; an illness caused by pancreatic β-cell loss and hence insulin deficiency) is insulin therapy. This treatment however does not restore normal metabolic homeostasis. In fact, the life-expectancy and -quality of T1DM people is worse compared to normal subjects. In part, this is due to challenging morbidities of T1DM, as for example heart disease and hypoglycemia, both of which are thought to be caused by insulin therapy itself. Indeed, owing to insulin’s lipogenic actions, this treatment likely contributes to the ectopic lipid deposition (i.e.: in non-adipose tissues) and extremely high incidence of coronary artery disease seen in T1DM subjects. Also, due to insulin’s potent, fast-acting, glycemia-lowering action, this therapy significantly increases the risk of hypoglycemia; a disabling and life threatening event. Because insulin therapy does not restore metabolic homeostasis in T1DM subjects, better intervention is urgently needed. To these ends, we and others have shown that the hyperglycemic and lethal consequences of insulin deficiency can be rescued by administration of the adipocyte-secreted hormone leptin. Not only these results challenge an established view, they also raise a fundamental biological and medical question: what are the mechanisms by which leptin improves hyperglycemia and permits survival in the context of insulin deficiency? This proposal aims at identifying the critical cellular and molecular components underlying the beneficial effects of leptin in the context of insulin deficiency. Once identified, manipulation of these components has the potential to improve life-expectancy and -quality of the millions affected by insulin deficiency (e.g.: T1DM and also some late-stage type 2 diabetics).'