Kent-Olov Jonsson suggest a rather unspecific process. The fact that AEA is highly lipophilic, makes diffusion through the lipid layer a distinct possibility. The importance of FAAH in driving accumulation was suggested by Deutsch et al. 2001 ; who showed that FAAH transfected cells accumulated AEA to a larger extent than wild type cells with low FAAH activity, although it was still present in untransfected cells. Evidence against a separate membrane protein responsible for AEA accumulation was presented by Glaser et al. 2003 ; . They showed that AEA transport inhibitors were not able to inhibit AEA uptake when using short incubation times 1 min ; , but instead a saturable uptake was seen using longer incubation times. These authors indicated FAAH as the protein responsible for the saturable inhibition of uptake, and attributed the crossing over the plasma membrane as simple diffusion driven by the concentration gradient. In contrast to these results, Fegley et al. 2004 ; showed that there was no difference upon AEA uptake between neurons from FAAH ; and FAAH + + ; mice, indicating a lack of effect of FAAH. These results are in line with other studies identifying compounds that lack effects on FAAH but still can inhibit AEA uptake Ortar et al., 2003; Lpez-Rodrguez et al., 2003; Fegley et al., 2004 ; . Furthermore, Fegley et al. 2004 ; reported that the prototypical AEA uptake inhibitor AM404 was still pharmacologically active in vivo when given to FAAH ; mice. Hillard & Jarrahian 2003 ; proposed that AEA is taken over the cell membrane by simple diffusion, and thereafter intracellularly sequestered or bound to proteins, in which the second process is the saturable part in AEA uptake. This model was proposed by the finding that radiolabelled AEA reaches higher intracellular concentrations than found extracellularly. An alternative to sequestration is the presence of intracellular shuttling protein s ; , which take the AEA from the inside of the plasma membrane to the endoplasmic reticulum, where the FAAH is located Fowler et al., 2004; Ortega-Gutirrez et al., 2004 ; . Since uptake inhibitors like AM404 and the closely related VDM11 can inhibit AEA binding to plastic wells Karlsson et al., 2004; Fowler et al., 2004; Ortega-Gutirrez et al., 2004; see also Paper I of this thesis ; , the structural requirements of such binding proteins may not need to be that stringent. In the fourth model, McFarland & Barker 2004 ; proposed that the sequestration of AEA was due to a caveolae-related endocytic process. Caveolae are flask shaped invaginations of the plasma membrane, and their model involves the binding of AEA to a protein located on. There are three critical areas that should be assessed in determining the causes of nonphysiologic weight loss in older adults: 1 ; social environmental 2 ; psychological, and 3 ; medical table 1 and neurontin.
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