Xu, J.; Han, J.; Long, Y.; Lock, J.; Weir, G.; Epstein, P.; Liu, Y.
doi: 10.1007/s00125-008-1155-0pmid: 18802677
Mouse islets contain ME, which plays a significant role in regulating insulin secretion.
Bakhtadze, E.; Cervin, C.; Lindholm, E.; Borg, H.; Nilsson, P.; Arnqvist, H.; Bolinder, J.; Eriksson, J.; Gudbjörnsdottir, S.; Nyström, L.; Agardh, C.-D.; Landin-Olsson, M.; Sundkvist, G.; Groop, L.
Sjögren, M.; Lyssenko, V.; Jonsson, A.; Berglund, G.; Nilsson, P.; Groop, L.; Orho-Melander, M.
doi: 10.1007/s00125-008-1151-4pmid: 18853134
Polymorphisms in susceptibility genes for type 2 diabetes ( TCF7L2 , WFS1 , IGF2BP2 ) and obesity ( FTO ) predispose to the metabolic syndrome by increasing the risk of one specific component of the metabolic syndrome. The findings argue against a unifying genetic component for the metabolic syndrome.
Casas, S.; Novials, A.; Reimann, F.; Gomis, R.; Gribble, F.
doi: 10.1007/s00125-008-1111-zpmid: 18751967
Alterations in (Ca 2+ ) i play a key role in hIAPP-induced beta cell cytotoxicity. By electron microscopy, we detected extracellular hIAPP aggregates adjacent to irregular invaginated regions of the plasma membrane. We propose that TRPV4 channels may sense physical changes in the plasma membrane induced by hIAPP aggregation, enabling Ca 2+ entry, membrane depolarisation and activation of L-type Ca 2+ channels. Decreasing the activity of TRPV4 prevented hIAPP-induced (Ca 2+ ) i changes, reduced hIAPP-triggered ER stress and improved cell viability.
Zhang, Y.; Zhang, N.; Gyulkhandanyan, A.; Xu, E.; Gaisano, H.; Wheeler, M.; Wang, Q.
doi: 10.1007/s00125-008-1166-xpmid: 18850083
These results suggest a potential role for HCN channels in regulation of glucagon secretion via modulating Ca 2+ and Na + channel activities.
doi: 10.1007/s00125-008-1154-1pmid: 18806995
The current review revealed a detrimental association of psychosocial factors with the prognosis of both type 1 and type 2 diabetes. However, any aetiological effect of adverse psychosocial factors remains elusive as a result of the small number of individuals enrolled in the cohorts studied.
Zillikens, M.; Yazdanpanah, M.; Pardo, L.; Rivadeneira, F.; Aulchenko, Y.; Oostra, B.; Uitterlinden, A.; Pols, H.; Duijn, C.
doi: 10.1007/s00125-008-1163-0pmid: 18839131
Sex-specific genetic effects underlie sexual dimorphism in several body composition traits. The findings are relevant for studies on the relationship of body composition with common diseases like cardiovascular disease and type 2 diabetes and for genetic association studies.
Kawasaki, E.; Uga, M.; Nakamura, K.; Kuriya, G.; Satoh, T.; Fujishima, K.; Ozaki, M.; Abiru, N.; Yamasaki, H.; Wenzlau, J.; Davidson, H.; Hutton, J.; Eguchi, K.
doi:
Varona-Santos, J.; Pileggi, A.; Molano, R.; Sanabria, N.; Ijaz, A.; Atsushi, M.; Ichii, H.; Pastori, R.; Inverardi, L.; Ricordi, C.; Fornoni, A.
doi: 10.1007/s00125-008-1169-7pmid: 18853132
Showing 1 to 10 of 19 Articles
doi: 10.1007/s00125-008-1161-2pmid: 18839133
Common variants in the TCF7L2 gene help to differentiate young but not middle-aged GADA-positive and GADA-negative diabetic patients, suggesting that young GADA-negative patients have type 2 diabetes and that middle-aged GADA-positive patients are different from their young GADA-positive counterparts and share genetic features with type 2 diabetes.
These results indicate that variant residue at amino acid 325 is a key determinant of humoral autoreactivity to ZnT8 and that the SLC30A8 genotype is an important determinant of autoantibody specificity.
We have shown a deleterious effect of JNK2 deficiency on islet graft outcome, most likely related to JNK1 activation, suggesting that specific JNK1 blockade may be superior to general JNK inhibition, particularly when administered to transplant recipients.