Category: 1690-72-8

Chemistry is the experimental and theoretical study of materials on their properties at both the macroscopic and microscopic levels.In a patent， SDS of cas: 1690-72-8, Which mentioned a new discovery about 1690-72-8

A series of 3-(5-bromo-2,3-dimethoxy-phenyl)-[1, 2, 4] oxadiazole derivatives was prepared and their evaluation for anti-Parkinson’s activity was measured in vivo using albino rats. The result of the biological activity studies indicated that some of the synthesized compounds have good agonistic activity on the dopamine receptors and a few of them were also found to be free from neurotoxicity. Thus these compounds might be useful ligands for studying the functional role of dopamine receptors in vivo. The high log P value of the compounds indicates that they should easily cross the blood-brain barrier (log P > 2.6).[Figure not available: see fulltext.]

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Reference：
Piperidine – Wikipedia,
Piperidine | C5H9093N – PubChem

 

A catalyst don’t appear in the overall stoichiometry of the reaction it catalyzes, category: piperidines, but it must appear in at least one of the elementary reactions in the mechanism for the catalyzed reaction. 1690-72-8, Name is Methyl 1-methylpiperidine-3-carboxylate, molecular formula is C8H15NO2. In a Review, authors is Johnson, Patricia R.£¬once mentioned of 1690-72-8

Animal models of obesity: Genetic aspects

Among the candidate genes that have been reviewed herein, adipsin, calcitonin, cholecystokinin, G(i)alpha and G(s) subunits of G proteins, insulin I and II, and lipoprotein lipase have all been mapped to specific chromosomes in mouse or rat or both. In none of these cases is the chromosomal location syntenic with murine obesity genes db (on chromosome 4), or ob (on chromosome 6). Thus, all of these genes that code for metabolic modulators that are altered in obese animals but not in lean animals can be ruled out as possible loci of the primary genetic defect, at least for the murine models of obesity. In the case of neuropeptide Y, growth hormone, glucose transporter GLUT-4, the insulin receptor, and glyceraldehyde-3-phosphate dehydrogenase, chromosomal mapping has not yet been reported. However, in each of these cases, the evidence available strongly argues against any one of these physiologic modulators as the likely site of the primary defect for any one of the obesity mutations. Rather, in all of these cases, regardless of whether or not the gene has been mapped, the evidence suggests that posttranscriptional and/or posttranslational processes are involved in bringing about the specific alterations in level or activity of the protein product that is seen in the obese animal. Often hormonal regulation is invoked as a possible explanation for the changes observed in gene expression. The hormones most commonly identified as having a mediating effect on the particular metabolic pathways involved are insulin and/or the adrenal glucocorticoids. Since in each of the obese mutants, circulating amounts of these hormones are elevated, severely so in the case of insulin, it would not be surprising to find that they influence the levels and activities of many protein products involved in a variety of central nervous system and peripheral metabolic pathways. Glucocorticoids are known to exert direct effects on gene expression; however, with respect to adipsin gene expression, a direct effect has not been found (142). Furthermore, insulin itself has been considered as a candidate for the genetic lesion in these animals and has been ruled out by chromosomal localization. Thus, while it may certainly prove to be the case that both insulin and glucocorticoids affect these systems in some way, their effects appear to be indirect. The work by Platt and colleagues (154) in transgenic mice provides the first evidence of signal transduction between an obese mutant allele and the promoter sequence for a gene that shows significantly altered expression in the obese animal. Future studies should reveal how obese mutations exert their influence on the expression of many other structural genes in a variety of tissues that undergo significant alterations in obesity. Current data suggest that the mutant allele, in this case db, may code for a regulatory element that can interact with promoter sequences to alter gene expression in a variety of tissues. In 1982, we proposed that the fa gene may exert its influence on a fundamental cellular regulatory function pleiotropically (201). Given the information now available on numerous candidate genes that have altered levels of expression in tissues ranging from specific hypothalamic brain regions to liver, pancreas, and adipose tissue, and given the ability to construct appropriate vectors for production of transgenic animals, investigators interested in understanding genetic obesity will be able to test similar hypotheses.

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Reference£º
Piperidine – Wikipedia,
Piperidine | C5H9090N – PubChem