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IDEnTIFICATIOn OF MOLECULAR MECHAnISMS AnD nEW THERAPEUTIC TARgETS
FOR DEVELOPIng PERSOnALISED EARLY InTERVEnTIOnS In DIABETES MELLITUS
For decades it had been discussed whether glycogen accumulation in beta cells of the pancreas had a major role in controlling glycaemia. By using genetic models with altered glycogen-accumulating capacity in the beta cells, we have proven that glycogen does not have a regulatory role (Mir-Coll et al., Diabetologia 2016).
Adipose tissue plays a major role in the control of energy consumption. It has been documented that selective ablation of IgFIR / IR (DKO) in brown adipose tissue induces severe atrophy of brown fat. DKO mice displayed an increase in body fat and a clear resistance to insulin, with no intolerance to glucose (Viana-Huete et al., Endocrinology 2016). These results indicate that the IgF-I receptor pathway is essential in the function of brown adipose tissue.
We have described that the activators of Heme-Regulated EIF2α kinase can revert intolerance to glucose and hepatic steatosis induced by a fat-rich diet due to its capacity to increase FgF21 (Ejaz et al., Diabetes 2016).
IDEnTIFICATIOn OF RISK PROgRESSIOn BIOMARKERS In DIABETES
A new inflammation marker has been identified in intracellular lipid droplets. Human peripheral blood monocytes contain an unusual isomer of palmitoleic acid, cis-7- hexadecenoic acid, in lipid droplets. This compound may prove useful as a biomarker of ‘foamy monocytes’ for early detection of cardiovascular diseases (Guijas et al., Cell Chem Biol 2016).
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