Changes in dominant groups of the gut microbiota do not explain cereal-fiber induced improvement of whole-body insulin sensitivity

Background

Glycated albumin (GA) is an Amadori product used as a marker of hyperglycemia. In this study, we investigated the effect of GA on insulin secretion from pancreatic β cells.

Methods

Islets were collected from male Wistar rats by collagenase digestion. Insulin secretion in the presence of non-glycated human albumin (HA) and GA was measured under three different glucose concentrations, 3 mM (G3), 7 mM (G7), and 15 mM (G15), with various stimulators. Insulin secretion was measured with antagonists of inducible nitric oxide synthetase (iNOS), and the expression of iNOS-mRNA was investigated by real-time PCR.

Results

Insulin secretion in the presence of HA and GA was 20.9 ± 3.9 and 21.6 ± 5.5 μU/3 islets/h for G3 (P = 0.920), and 154 ± 9.3 and 126.1 ± 7.3 μU/3 islets/h (P = 0.046), for G15, respectively. High extracellular potassium and 10 mM tolbutamide abrogated the inhibition of insulin secretion by GA. Glyceraldehyde, dihydroxyacetone, methylpyruvate, GLP-1, and forskolin, an activator of adenylate cyclase, did not abrogate the inhibition. Real-time PCR showed that GA did not induce iNOS-mRNA expression. Furthermore, an inhibitor of nitric oxide synthetase, aminoguanidine, and NG-nitro-L-arginine methyl ester did not abrogate the inhibition of insulin secretion.

Conclusion

GA suppresses glucose-induced insulin secretion from rat pancreatic β-cells through impairment of intracellular glucose metabolism.     

分蘖葱头和薤白对花生四烯酸代谢系列的干扰作用

分蘖葱头Allium cepa L.var.aagrogatum Don.(ACAD)和薤白(小根菜)Allium macrostemon Bunge(AMB)均为百合种植物,药用其鳞茎。江漫涛等证明分蘖葱头精油中含有甲基烯丙基三硫(MATS),二甲基噻吩,正丙基烯丙基二硫,甲基正丙基三硫等成分。薤白精油中含有乙烯撑二甲硫、MATS、二甲基三硫等成分。其主要有效成分均为MATS。并探讨了它们对血小板聚集的抑制作用还发现,薤白能有效地抑制实验性动脉粥样硬化的形成。为了进一步阐明分蘗葱头及薤白的作用机理,我们研究了它们对于花生四烯酸(AA)     

Creating an Ontology‐Based Human Phenotyping System: The Rockefeller University Bleeding History Experience

The lack of standardized methods for human phenotyping is a major obstacle in translational science. We have developed a bleeding history phenotyping system comprising an ontology, a questionnaire, a Web‐based phenotype recording instrument (PRI), and a database. The ontology facilitates transparency, collaboration, aggregation of data, and data analysis. The integrated system allows investigators worldwide to use the PRI, add their de‐identified data to the database, and query the aggregated data. Thus, this system can increase the power to detect genotype–phenotype–environment relationships and help new investigators begin their studies. We anticipate that this approach may be applicable to other disorders.     

When the heart kills the liver: acute liver failure in congestive heart failure

Congestive heart failure as a cause of acute liver failure is rarely documented with only a few cases.Although the pathophysiology is poorly understood, there is rising evidence, that low cardiac output with consecutive reduction in hepatic blood flow is a main causing factor, rather than hypotension. In the setting of acute liver failure due to congestive heart failure, clinical signs of the latter can be absent, which requires an appropriate diagnostic approach.As a reference center for acute liver failure and liver transplantation we recorded from May 2003 to December 2007 202 admissions with the primary diagnoses acute liver failure. 13/202 was due to congestive heart failure, which was associated with a mortality rate of 54%. Leading cause of death was the underlying heart failure. Asparagine transaminase (AST), bilirubin, and international normalized ratio (INR) did not differ significantly in surviving and deceased patients at admission. Despite both groups had signs of cardiogenic shock, the cardiac index (CI) was significantly higher in the survival group on admission as compared with non-survivors (2.1 L/min/m² vs. 1.6 L/min/m², p = 0.04). Central venous - and pulmonary wedge pressure did not differ significantly. Remarkable improvement of liver function was recorded in the group, who recovered from cardiogenic shock.In conclusion, patients with acute liver failure require an appropriate diagnostic approach. Congestive heart failure should always be considered as a possible cause of acute liver failure.