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Most relevant scientific articles
• García-Aguilar A., Guillén C., Nellist M., Bartolomé A., Benito M. TSC2 n-terminal lysine acetylation status affects to its stability modulating mTORC1 signaling and autophagy. Biochimica et Biophysica Acta - Molecular Cell Research. 2016;1863(11):2658-2667.
• Díaz-Castroverde S., Baos S., Luque M., Di Scala M., González-Aseguinolaza G., Gómez-Hernández A. et al. Prevalent role of the insulin receptor isoform A in the regulation of hepatic glycogen metabolism in hepatocytes and in mice. Diabetologia. 2016;:1-9.
• Viana-Huete V, Guillén C, García-Aguilar A, García G, Fernández S, Kahn CR et al. Essential role of IgFIR in the onset of male brown fat thermogenic function: Regulation of glucose homeostasis by differential organ-specific insulin sensitivity.Endocrinology. 2016; en20151623.
• Beneit N, Fernández-García CE, Martín-Ventura JL, Perdomo L, Escribano Ó, Michel JB et al. Expression of insulin receptor (IR) A and B isoforms, IGF-IR, and IR/IGF-IR hybrid receptors in vascular smooth muscle cells and their role in cell migration in atherosclerosis. Cardiovascular diabetology. 2016;15(1):161.
• Díaz-Castroverde S., Gómez-Hernández A., Fernández S., García-Gómez G., Di Scala M., González- Aseguinolaza G. et al. Insulin receptor isoform A ameliorates long-term glucose intolerance in diabetic mice. DMM Disease Models and Mechanisms. 2016;9(11):1271-1281.
Highlights
Regarding to the ethiopathogenesis of type 2 diabetes, human amylin, but not rat amylin, through agregates formation in insulinoma cells overexpressing human amilin inhibited autophagy and enhanced the apoptosis susceptibility in response to induced ER stress. On the other hand, brown adipose tissue- specific knockout of IGFIR/IR (BATIGFIRDKO) induced a severe brown fat atrophy and mitochondrial crystae disruption, which turned out in an impaired cold-induced Drp-1-phophrylation fission mechanism, Overall DKO mice under HFD for 8 weeks showed an increased total body fat mass by NMR, overweight, a manifest insulin resistance, without glucose intolerance, a compensatory insulin secretion and finally, a severe hyperinsulinemia.
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