In several models of obesity-induced diabetes, increased lipid accumulation in the liver has been associated with decreased diabetes susceptibility. For instance, deficiency in leptin receptor (db/db) leads to hyperphagia and obesity in both C57BL/6 and C57BLKS mice but, only on the C57BLKS background do the mice develop beta-cell loss leading to severe diabetes while C57BL/6 mice are relatively resistant. Liver triglyceride levels in the resistant C57BL/6 mice are 3 to 4 fold higher than in C57BLKS.
Systems genetics of susceptibility to obesity-induced diabetes in mice.
Sex, Age
View SamplesHigh-density lipoproteins (HDLs) protect pancreatic cells against apoptosis. This property might be related to the increased risk to develop diabetes in patients with low HDL blood levels. However, the mechanisms by which HDLs protect cells are poorly characterized. Here we use a transcriptomic approach to identify genes differentially modulated by HDLs in cells subjected to apoptotic stimuli.
Involvement of 4E-BP1 in the protection induced by HDLs on pancreatic beta-cells.
Specimen part, Cell line
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