Current Issue : January - March Volume : 2012 Issue Number : 1 Articles : 6 Articles
Background: There is increasing interest in the impact of diabetes mellitus on cognitive functioning. Several studies found\r\nevidence of decreased cognitive performance in type 2 diabetics (T2DM). Since the P300 component of event-related potentials\r\n(ERPs) provides valuable information concerning cognition, we studied this component of ERPs in T2DM.\r\nMethods: Auditory P300 event-related potentials (P300) were elicited in 43 T2DM patients and 29 age and sex-matched healthy\r\nvolunteers by use of the auditory oddball paradigm, taking into account the age of the subjects, disease duration and the\r\nmetabolic control.\r\nResults: Compared with controls, diabetics had significantly longer P300 latencies (F= 5.05, p= 0.026) and lower P300 amplitudes\r\nboth in Cz and Pz electrode positions (F= 8.01, p= 0.005 and F= 13.67, p= 0.000 respectively). In addition, a significant inverse\r\ncorrelation between P300 latency and amplitude was observed in diabetics both in Cz and Pz electrode positions (r= -0.43, p=\r\n0.003 and r= -0.39, p= 0.01 respectively), whereas essentially no relationship between amplitude and latency was observed for\r\nthe control group. N200 and P300 latencies and the reduction in their amplitudes in Cz and Pz leads were not related to either\r\ndisease duration or metabolic control.\r\nConclusions: The observed electrophysiological abnormalities may reflect impairment of information processing and working\r\nmemory, possibly associated with an accelerated ageing process. Our findings suggest that surface-recorded ERPs may be useful\r\nfor detecting and monitoring the changes in brain function associated with diabetes mellitus....
Type 2 diabetes mellitus (T2DM) is a progressive multisystemic disease accompanied by vascular dysfunction and a tremendous\r\nincrease in cardiovascular mortality. Numerous adipose-tissue-derived factors and beta cell dysfunction contribute to the increased\r\ncardiovascular risk in patients with T2DM. Nowadays, numerous pharmacological interventions are available to lower blood\r\nglucose levels in patients with type 2 diabetes. Beside more or less comparable glucose lowering efficacy, some of them have shown\r\nlimited or probably even unfavorable effects on the cardiovascular system and overall mortality. Recently, incretin-based therapies\r\n(GLP-1 receptor agonists and DPP-IV inhibitors) have been introduced in the treatment of T2DM. Beside the effects of GLP-1 on\r\ninsulin secretion, glucagon secretion, and gastrointestinal motility, recent studies suggested a couple of direct cardiovascular effects\r\nof GLP-1-based therapies. The goal of this paper is to provide an overview about the current knowledge of direct GLP-1 effects on\r\nendothelial and vascular function and potential consequences on the cardiovascular outcome in patients with T2DM treated with\r\nGLP-1 receptor agonists or DPP-IV inhibitors....
Diabetic nephropathy (DN) is a long-term complication of diabetes mellitus that leads to end-stage renal disease. Microalbuminuria\r\nis used for the early detection of diabetic renal damage, but such levels do not reflect the state of incipient DN precisely in type\r\n2 diabetic patients because microalbuminuria develops in other diseases, necessitating more accurate biomarkers that detect incipient\r\nDN. Isobaric tags for relative and absolute quantification (iTRAQ) were used to identify urinary proteins that were differentially\r\nexcreted in normoalbuminuric and microalbuminuric patients with type 2 diabetes where 710 and 196 proteins were identified\r\nand quantified, respectively. Some candidates were confirmed by 2-DE analysis, or validated by Western blot and multiple\r\nreaction monitoring (MRM). Specifically, some differentially expressed proteins were verified by MRM in urine from normoalbuminuric\r\nand microalbuminuric patients with type 2 diabetes, wherein alpha-1-antitrypsin, alpha-1-acid glycoprotein 1, and prostate\r\nstem cell antigen had excellent AUC values (0.849, 0.873, and 0.825, resp.). Moreover, we performed a multiplex assay using\r\nthese biomarker candidates, resulting in amerged AUC value of 0.921. Although the differentially expressed proteins in this iTRAQ\r\nstudy require further validation in larger and categorized sample groups, they constitute baseline data on preliminary biomarker\r\ncandidates that can be used to discover novel biomarkers for incipient DN....
High-fructose diet is known to produce cardiovascular and metabolic pathologies. The objective was to determine whether the\r\ntiming of high fructose (10% liquid solution) intake affect the metabolic and cardiovascular outcomes. Male C57BL mice with\r\nradiotelemetric probes were divided into four groups: (1) 24 h water (control); (2) 24 h fructose (F24); (3) 12 h fructose during\r\nthe light phase (F12L); (4) 12 h fructose during the dark phase (F12D). All fructose groups had higher fluid intake. Body weight\r\nwas increased in mice on restricted access with no difference in total caloric intake. Fasting glycemia was higher in groups with\r\nrestricted access. F24 mice showed a fructose-induced blood pressure increase during the dark period. Blood pressure circadian\r\nrhythms were absent in F12L mice. Results suggest that the timing of fructose intake is an important variable in the etiology of\r\ncardiovascular and metabolic pathologies produced by high fructose consumption....
Zinc (Zn2+) appears to be intimately involved in insulin metabolism since insulin secretion is correlated with zinc secretion in\nresponse to glucose stimulation, but little is known about the regulation of zinc homeostasis in pancreatic beta-cells. This study set\nout to identify the intracellular zinc transient by imaging free cytosolic zinc in HIT-T15 beta-cells with fluorescent zinc indicators.\nWe observed that membrane depolarization by KCl (30ââ?¬â??60mM) was able to induce a rapid increase in cytosolic concentration of\nzinc. Multiple zinc transients of similar magnitude were elicited during repeated stimulations. The amplitude of zinc responses\nwas not affected by the removal of extracellular calcium or zinc. However, the half-time of the rising slope was significantly slower\nafter removing extracellular zinc with zinc chelator CaEDTA, suggesting that extracellular zinc affect the initial rising phase of zinc\nresponse. Glucose (10mM) induced substantial and progressive increases in intracellular zinc concentration in a similar way as\nKCl, with variation in the onset and the duration of zinc mobilization. It is known that the depolarization of beta-cell membrane\nis coupled with the secretion of insulin. Rising intracellular zinc concentration may act as a critical signaling factor in insulin\nmetabolism of pancreatic beta-cells....
Background. Adverse maternal environments may predispose the offspring to metabolic syndrome in adulthoods, but the\r\nunderlying mechanism has not been fully understood. Methods. Maternal hyperglycemia was induced by streptozotocin (STZ)\r\ninjection while control (CON) rats received citrate buffer. Litters were adjusted to eight pups per dam and then weaned to standard\r\ndiet. Since 13 weeks old, a subset of offspring from STZ and CON dams were switched to high fat diet (HFD) for another 13\r\nweeks. Glucose and insulin tolerance tests (GTT and ITT) and insulin secretion assay were performed; serum levels of lipids and\r\nleptin were measured. Hepatic fat accumulation and islet area were evaluated through haematoxylin and eosin staining. Results.\r\nSTZ offspring exhibited lower survival rate, lower birth weights, and growth inhibition which persisted throughout the study.\r\nSTZ offspring on HFD showed more severe impairment in GTT and ITT, and more profound hepatic steatosis and more severe\r\nhyperlipidemia compared with CON-HFD rats. Conclusions. Offspring from diabetic dams would be prone to exhibit low birth\r\nweight and postnatal growth inhibition, but could maintain normal glucose tolerance and insulin sensitivity. HFD accelerates\r\ndevelopment of insulin resistance in the offspring of diabetic dams mainly via a compensatory response of islets....
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