Effect of oral arginine supplementation on GH secretion and lipid metabolism in Wistar trained rats

The Oral Arginine Supplementation (OAS) and exercise are able to modify the secretion of the Growth Hormone (GH) that stimulates the lipid metabolism. The aim of the study was to verify the effect of the OAS, the aerobic exercise and the combination of the OAS with the aerobic exercise on the GH secretion and lipid metabolism in rats. The sample was composted for 40 male wistar rats, divided in four groups: Sedentary control (SC), sedentary arginine (SA), trained control (TC) and trained arginine (TA). The AS and AT received the oral supplementation in alternated days and the groups CT and AT realized swimming exercise for 1hour/day with overload equivalent to 5% of body mass five days per week during 4 weeks. The concentrations of GH were significantly difference between the sedentary groups (SC and AS) and (TC and AT) and the lipid metabolism did not change throughout all groups. In conclusions, aerobic physical training did not modify the lipid metabolism and diminishes the values of GH concentration and the OAS did not modify the concentration of GH in Wistar rats

Guidelines for the use and interpretation of assays for monitoring autophagy

In 2008 we published the first set of guidelines for standardizing research in autophagy. Since then, research on this topic has continued to accelerate, and many new scientists have entered the field. Our knowledge base and relevant new technologies have also been expanding. Accordingly, it is important to update these guidelines for monitoring autophagy in different organisms. Various reviews have described the range of assays that have been used for this purpose. Nevertheless, there continues to be confusion regarding acceptable methods to measure autophagy, especially in multicellular eukaryotes. A key point that needs to be emphasized is that there is a difference between measurements that monitor the numbers or volume of autophagic elements (e.g., autophagosomes or autolysosomes) at any stage of the autophagic process vs. those that measure flux through the autophagy pathway (i.e., the complete process); thus, a block in macroautophagy that results in autophagosome accumulation needs to be differentiated from stimuli that result in increased autophagic activity, defined as increased autophagy induction coupled with increased delivery to, and degradation within, lysosomes (in most higher eukaryotes and some protists such as Dictyostelium) or the vacuole (in plants and fungi). In other words, it is especially important that investigators new to the field understand that the appearance of more autophagosomes does not necessarily equate with more autophagy. In fact, in many cases, autophagosomes accumulate because of a block in trafficking to lysosomes without a concomitant change in autophagosome biogenesis, whereas an increase in autolysosomes may reflect a reduction in degradative activity. Here, we present a set of guidelines for the selection and interpretation of methods for use by investigators who aim to examine macroautophagy and related processes, as well as for reviewers who need to provide realistic and reasonable critiques of papers that are focused on these processes. These guidelines are not meant to be a formulaic set of rules, because the appropriate assays depend in part on the question being asked and the system being used. In addition, we emphasize that no individual assay is guaranteed to be the most appropriate one in every situation, and we strongly recommend the use of multiple assays to monitor autophagy. In these guidelines, we consider these various methods of assessing autophagy and what information can, or cannot, be obtained from them. Finally, by discussing the merits and limits of particular autophagy assays, we hope to encourage technical innovation in the field. © 2012 Landes Bioscience

Guidelines for the use and interpretation of assays for monitoring autophagy (3rd edition)

[[sponsorship]]生物化學研究所[[note]]已出版;[SCI];有審查制度;具代表性[[note]]http://gateway.isiknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcAuth=Drexel&SrcApp=hagerty_opac&KeyRecord=1554-8627&DestApp=JCR&RQ=IF_CAT_BOXPLO