Hertle, E.; Greevenbroek, M.; Stehouwer, C.
doi: 10.1007/s00125-012-2462-zpmid: 22282163
C3 is the central component of the complement system and activation of C3 via any of the three major activation pathways—the classical, the lectin and the alternative pathways—results in initiation of the terminal complement pathway and release of the anaphylatoxin C3a. Both terminal pathway activation and signalling of C3a and its inactivation product C3a-desarg via the C3a receptor and C5a-like receptor 2, respectively, can induce inflammatory, immunomodulatory and metabolic responses. C3 has been implicated in metabolic disorders, notably adiposity, dyslipidaemia, insulin resistance, liver dysfunction and diabetes, and C3 is increasingly recognised as a cardiometabolic risk factor. C3 may play a role in the macrovascular, as well as microvascular, complications of diabetes. Moreover, C3 may interact with the coagulation system and as such also contribute to a procoagulant, hypofibrinolytic and, ultimately, prothrombotic state. Recent data suggest a diabetes-dependent incorporation of C3 into fibrin clots, with concomitant effects on clot characteristics. Taken together, epidemiological and experimental evidence concordantly point to a role of complement C3 in metabolic, atherosclerotic/atherothrombotic and microangiopathic processes and further research should be directed towards the elucidation of complement function and activation in cardiometabolic disorders.
Carstensen, B.; Witte, D.; Friis, S.
doi: 10.1007/s00125-011-2381-4pmid: 22120574
The observed duration effects suggest that both increased surveillance for cancer in the first years after diagnosis of diabetes, and reverse causation, where undiagnosed cancers increase the likelihood of diabetes diagnosis, play a role. For longer durations, a combination of common causes for diabetes and cancer, as well as the effects of diabetes and insulin exposure per se, may play a role in the association between diabetes and some cancers.
Gray, L.; Davies, M.; Hiles, S.; Taub, N.; Webb, D.; Srinivasan, B.; Khunti, K.
doi: 10.1007/s00125-011-2432-xpmid: 22231125
The score can be used to reliably identify those with undiagnosed IGR and type 2 diabetes in multiethnic populations. This is the first score developed taking into account HbA 1c in the diagnosis of type 2 diabetes.
Gkrania-Klotsas, E.; Langenberg, C.; Tauriainen, S.; Sharp, S.; Luben, R.; Forouhi, N.; Khaw, K.; Hyöty, H.; Wareham, N.
doi: 10.1007/s00125-011-2443-7pmid: 22231126
The presence of antibodies against any of five serotypes of Coxsackievirus B was not associated with incident type 2 diabetes.
Hunt, K.; Marlow, N.; Gebregziabher, M.; Ellerbe, C.; Mauldin, J.; Mayorga, M.; Korte, J.
doi: 10.1007/s00125-011-2430-zpmid: 22237686
These data suggest that the negative effects of GDM combined with obesity during pregnancy may be greater in NHB than in NHW individuals.
Fava, E.; Dehghany, J.; Ouwendijk, J.; Müller, A.; Niederlein, A.; Verkade, P.; Meyer-Hermann, M.; Solimena, M.
doi: 10.1007/s00125-011-2438-4pmid: 22252472
A major reason for the lower mean granule number/rat beta cell relative to previous accounts is a reduced estimation of the mean beta cell volume. These findings imply that each granule contains about twofold more insulin, while its exocytosis increases membrane capacitance about twofold less than assumed previously. Our integrated approach defines new standards for quantitative image analysis of beta cells and could be applied to other cellular systems.
Favaro, E.; Granata, R.; Miceli, I.; Baragli, A.; Settanni, F.; Cavallo Perin, P.; Ghigo, E.; Camussi, G.; Zanone, M.
doi: 10.1007/s00125-011-2423-ypmid: 22231124
Showing 1 to 10 of 18 Articles
doi: 10.1007/s00125-012-2450-3pmid: 22278338
The results for the novel GWA study-identified loci are genuine and not due to population stratification. The next step, namely correlation of the most disease-associated genotypes with phenotypes, such as RNA and protein expression analyses for the candidate genes within or near each of the susceptibility regions, can now proceed.
doi: 10.1007/s00125-011-2400-5pmid: 22189485
Although contributing marginally to glucose-induced insulin secretion, compound exocytosis becomes quantitatively significant under conditions associated with global elevation of cytoplasmic calcium. These findings suggest that compound exocytosis is a major contributor to the augmentation of glucose-induced insulin secretion by muscarinic receptor activation.
The ghrelin gene-derived peptides and Ex-4 exert cytoprotective effects in islet MECs. The anti-apoptotic effects involve phosphoinositide 3-kinase (PI3K)/Akt, ERK1/2 and cAMP/PKA pathways. These peptides could therefore represent a potential tool to improve islet vascularisation and, indirectly, islet cell function.