Akoby, “[51] Assays for differentiation of glutathione S-Transferases,” Procedures in Enzymology, vol. 77, pp. 398?05, 1981. [29] M. S. Moron, J. W. Depierre, and B. Mannervik, “Levels of glutathione, glutathione reductase and glutathione S-transferase activities in rat lung and liver,” Biochimica et Biophysica Acta, vol. 582, no. 1, pp. 67?8, 1979. [30] S. T. Omaye, J. David Turnbull, and H. E. Sauberlich, “[1] Selected strategies for the determination of ascorbic acid in animal cells, tissues, and fluids,” Approaches in Enzymology, vol. 62, pp. three?1, 1979. [31] I. D. Desai, “Vitamin E analysis procedures for animal tissues,” Techniques in Enzymology, vol. 105, pp. 138?47, 1984. [32] H. Ohkawa, N. Ohishi, and K. Yagi, “Assay for lipid peroxides in animal tissues by thiobarbituric acid reaction,” Analytical Biochemistry, vol. 95, no. two, pp. 351?58, 1979.
ORIGINAL RESEARCHAngiotensin Receptor inding Protein ATRAP/Agtrap Inhibits Metabolic Dysfunction With Visceral ObesityAkinobu Maeda, MD, PhD; Kouichi Tamura, MD, PhD; Hiromichi Wakui, MD, PhD; Toru Dejima, MD, PhD; Masato Ohsawa, MD; Kengo Azushima, MD; Tomohiko Kanaoka, MD, PhD; Kazushi Uneda, MD; Miyuki Matsuda; Akio Yamashita, PhD; Nobuko Miyazaki, MD; Keisuke Yatsu, MD, PhD; Nobuhito Hirawa, MD, PhD; Yoshiyuki Toya, MD, PhD; Satoshi Umemura, MD, PhDBackground—Metabolic issues with visceral obesity have develop into a significant medical dilemma linked using the development of hypertension, form 2 diabetes, and dyslipidemia and, ultimately, life-threatening cardiovascular and renal ailments. Adipose tissue dysfunction has been proposed as the cause of visceral obesity-related metabolic issues, moving the tissue toward a proinflammatory phenotype. Methods and Results—Here we initially report that adipose tissues from sufferers and mice with metabolic problems exhibit decreased expression of ATRAP/Agtrap, that is a precise binding modulator in the angiotensin II variety 1 receptor, in spite of its abundant expression in adipose tissues from typical human and manage mice.Methyltetrazine-Amine web Subsequently, to examine a functional part of ATRAP inside the pathophysiology of metabolic problems, we created homozygous ATRAP deficient (Agtrap?? mice, which exhibited largely typical physiological phenotype at baseline.BuyMethyl 5-bromo-1H-indole-4-carboxylate Under dietary higher fat loading, Agtrap??mice displayed systemic metabolic dysfunction, characterized by an enhanced accumulation of pad fat, hypertension, dyslipidemia, and insulin resistance, in addition to adipose tissue inflammation.PMID:23927631 Conversely, subcutaneous transplantation of donor fat pads overexpressing ATRAP derived from Agtrap transgenic mice to Agtrap??recipient mice enhanced the systemic metabolic dysfunction. Conclusions—These outcomes demonstrate that Agtrap??mice are an efficient model of metabolic problems with visceral obesity and constitute proof that ATRAP plays a protective function against insulin resistance, suggesting a new therapeutic target in metabolic issues. Identification of ATRAP as a novel receptor binding modulator of adipose tissue inflammation not merely has cardiovascular significance but might have generalized implication in the regulation of tissue function. ( J Am Heart Assoc. 2013;2: e000312 doi: 10.1161/JAHA.113.000312) Key Words: adipocyte ?angiotensin receptor ?inflammation ?insulin resistance ?transplantationPresently, patients with metabolic problems with visceral obesity are increasing worldwide. A single typical metabolic phenotypic adjust is reported to be systemic insulin resistance, and.