LEPTINT1DM

Unraveling the mechanism underlying the anti-diabetic action of leptin

Coordinatore	UNIVERSITE DE GENEVE    more  Organization address address: Rue du General Dufour 24 city: GENEVE postcode: 1211 contact info Titolo: Prof. Nome: Dominique Cognome: Belin Email: send email Telefono: 410224000000
Nazionalità Coordinatore	Switzerland [CH]
Totale costo	100˙000 €
EC contributo	100˙000 €
Programma	FP7-PEOPLE Specific programme "People" implementing the Seventh Framework Programme of the European Community for research, technological development and demonstration activities (2007 to 2013)
Code Call	FP7-PEOPLE-2012-CIG
Funding Scheme	MC-CIG
Anno di inizio	2012
Periodo (anno-mese-giorno)	2012-12-01   -   2016-11-30

 Partecipanti

#	participant	country	role	EC contrib. [€]
1	UNIVERSITE DE GENEVE  Organization address address: Rue du General Dufour 24 city: GENEVE postcode: 1211 contact info Titolo: Prof. Nome: Dominique Cognome: Belin Email: send email Telefono: 410224000000	CH (GENEVE)	coordinator	100˙000.00

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 Obiettivo del progetto (Objective)

'Type 1 diabetes mellitus (T1DM) is caused by pancreatic β-cell loss. The sole life-saving intervention available to the millions affected by T1DM is insulin therapy. Unfortunately, this therapy does not restore normal metabolic homeostasis and as a result the life-expectancy and -quality of T1DM people is worse than the ones of 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, better anti-T1DM intervention is urgently needed. Recent findings in rodents strongly indicate that administration of leptin (a slow-acting, glycemia-lowering hormone) reverses the lethal consequences and many of the metabolic defects caused by insulin deficiency. Because leptin exerts lipolytic action and does not cause hypoglycemia, this hormone represents an attractive alternative and/or adjuvant to current T1DM therapy. Yet, the mechanism underlying leptin’s anti-T1DM action is unknown. Here, the hypothesis that hypothalamic neurons mediate leptin’s anti-T1DM action will be directly tested by assessing the efficacy of leptin therapy in T1DM mice lacking or expressing leptin receptor only in specific hypothalamic neurons. Results from these studies will establish the mechanism underlying leptin’s anti-T1DM action and hence bring us closer to develop better anti-T1DM strategies without the risks of hypoglycemia and cardiovascular disease.'