Doktorander/Utbildningsplatser

Doktorander/Utbildningsplatser
med placering vid Sahlgrenska akademin

Sista ansökningsdag: 2010-04-20

Sahlgrenska akademin utlyser doktorandplatser med placering vid institutionen för biomedicin, institutionen för kliniska vetenskaper, institutionen för medicin och institutionen för neurovetenskap och fysiologi.

Doktorandplatserna avser två års utbildningsbidrag och två års doktorandanställning, alternativt fyra års doktorandanställning, och beräknas leda fram till doktorsexamen.

För mer information och ansökningsblankett se:
http://www.sahlgrenska.gu.se/doktorandportalen/Doktor_Fran_start_till_mal/doktorandplatser


Molecular mechanisms that link cardiac accumulation with lipotoxicity and development of insulin resistance

Application deadline: 2010-04-20

Description of the research project
Lipotoxicity refers to the consequences of delivering lipids to non-adipose tissues causing cell dysfunction or death.Lipid accumulation in non-adipose tissues likely contributes to the cellular dysfunction associated with insulin resistance and type 2 diabetes.Emerging studies also show that lipotoxicity may be involved in the pathogenesis of heart disease in humans.Furthermore, lipid accumulation in the heart has been proposed to contribute to the high mortality following infarction in subjects with type 2 diabetes.
We recently provided direct evidence for how lipid accumulation in myocardial cells promotes not only inflammation, but also insulin resistance.We identified the SNARE-protein SNAP23 as a novel link between lipid accumulation and insulin resistance (Boström et al.Nature Cell Biology, 2007).We have also identified the VLDL receptor as a novel mechanism for uptake of lipids in the heart after a myocardial infarction.
The aim of this research program is clarify the molecular mechanisms that link the cardiac lipid accumulation with lipotoxicity and development of insulin resistance.We will elucidate in detail the role of the SNARE protein SNAP23 and of the VLDL receptor, and characterize the proinflammatory lipid-derived metabolites in infarcted heart biopsies.