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完整後設資料紀錄
DC 欄位 | 值 | 語言 |
---|---|---|
dc.contributor.advisor | 陳靜宜(Ching-Yi Chen) | |
dc.contributor.author | Miao-Ju Chien | en |
dc.contributor.author | 簡妙如 | zh_TW |
dc.date.accessioned | 2021-06-17T06:59:54Z | - |
dc.date.available | 2022-07-31 | |
dc.date.copyright | 2019-08-06 | |
dc.date.issued | 2019 | |
dc.date.submitted | 2019-08-02 | |
dc.identifier.citation | 李欣瑾。2013。探討西方飼糧對李宋豬代謝異常與內質網壓力之影響。台灣大學動物科學技術學系碩士論文。54-56。
鄭位明、王珮華、張浩宏與宋永義。1999。小耳種李宋系迷你豬乳齒萌發順序之研究。中國畜牧會誌。28:347-358。 Aydin, S., A. Aksoy, S. Aydin, M. Kalayci, M. Yilmaz, T. Kuloglu, C. Citil, and Z. Catak. 2014. Today's and yesterday's of pathophysiology: biochemistry of metabolic syndrome and animal models. Nutrition.30 :1-9. Becker, G. J., and T. D. Hewitson. 2013. Animal models of chronic kidney disease: useful but not perfect Nephrol Dial Transplant. 28:2432-2438. Bhargava, P., and R. G. Schnellmann. 2017. Mitochondrial energetics in the kidney. Nature reviews. Nephrology. 13:629-646. Bhupathiraju, S. N., and F. B. Hu. 2016. Epidemiology of Obesity and Diabetes and Their Cardiovascular Complications. Circ Res. 118:1723-1735. Bobulescu, I. A., Y. Lotan, J. Zhang, T. R. Rosenthal, J. T. Rogers, B. Adams-Huet, K. Sakhaee, and O. W. Moe. 2014. Triglycerides in the human kidney cortex: relationship with body size. PloS one. 9:e101285. Boden, G. 1997. Role of fatty acids in the pathogenesis of insulin resistance and NIDDM. Diabetes. 46:3-10. Brand, M. D., C. Affourtit, T. C. Esteves, K. Green, A. J. Lambert, S. Miwa, J. L. Pakay, and N. Parker. 2004. Mitochondrial superoxide: production, biological effects, and activation of uncoupling proteins. Free Radic Biol Med. 37:755-767. Brooks, C., Q. Wei, S. G. Cho, and Z. Dong. 2009. Regulation of mitochondrial dynamics in acute kidney injury in cell culture and rodent models. J Clin Invest. 119:1275-1285. Chen, M. S., and S. H. Chen. 2018. A data-driven assessment of the metabolic syndrome criteria for adult health management in Taiwan. Int J Environ Res Public Health.16. Cho, J., H. Hong, S. Park, S. Kim, and H. Kang. 2017. Insulin resistance and its association with metabolic syndrome in korean children. Biomed Res Int. 2017:8728017. Chu, N. F., H. C. Chin, and S. C. Wang. 2011. Prevalence and anthropometric risk of metabolic syndrome in taiwanese adolescents. ISRN Cardiol. 2011:743640. Cioffi, F., R. Senese, P. Lasala, A. Ziello, A. Mazzoli, R. Crescenzo, G. Liverini, A. Lanni, F. Goglia, and S. Iossa. 2017. Fructose-rich diet affects mitochondrial DNA damage and repair in rats. Nutrients. 9 : E323. Cobbs, A., X. Chen, Y. Zhang, J. George, M.-b. Huang, V. Bond, W. Thompson, and X. Zhao. 2019. Saturated fatty acid stimulates production of extracellular vesicles by renal tubular epithelial cells. Mol Cell Biochem.458:113-124. Cornier, M. A., D. Dabelea, T. L. Hernandez, R. C. Lindstrom, A. J. Steig, N. R. Stob, R. E. Van Pelt, H. Wang, and R. H. Eckel. 2008. The metabolic syndrome. Endocr Rev. 29:777-822. Cullen-McEwen, L., M. R. Sutherland, and M. J. Black. 2016. Chapter 3 - The human kidney: parallels in structure, spatial development, and timing of nephrogenesis. In: M. H. Little, editor, Kidney Development, Disease, Repair and Regeneration. Academic Press, San Diego. 27-40. Czernichow, S., A. P. Kengne, E. Stamatakis, M. Hamer, and G. D. Batty. 2011. Body mass index, waist circumference and waist-hip ratio: which is the better discriminator of cardiovascular disease mortality risk?: evidence from an individual-participant meta-analysis of 82 864 participants from nine cohort studies. Obes Rev. 12:680-687. De Lucia Rolfe, E., A. Sleigh, F. M. Finucane, S. Brage, R. P. Stolk, C. Cooper, S. J. Sharp, N. J. Wareham, and K. K. Ong. 2010. Ultrasound measurements of visceral and subcutaneous abdominal thickness to predict abdominal adiposity among older men and women. Obesity. 18:625-631. Deeds, M. C., J. M. Anderson, A. S. Armstrong, D. A. Gastineau, H. J. Hiddinga, A. Jahangir, N. L. Eberhardt, and Y. C. Kudva. 2011. Single dose streptozotocin-induced diabetes: considerations for study design in islet transplantation models. Lab Anim. 45:131-140. Després, J.-P. 2006. Abdominal obesity: the most prevalent cause of the metabolic syndrome and related cardiometabolic risk. Arterioscler Thromb Vasc Biol. 6:1309-42. Després, J.-P., and I. Lemieux. 2006. Abdominal obesity and metabolic syndrome. Nature. 444:881-887. Felizardo, R. J., M. B. da Silva, C. F. Aguiar, and N. O. Câmara. 2014. Obesity in kidney disease: a heavyweight opponent. World J Nephrol. 3:50-63. Forbes, J. M., M. T. Coughlan, and M. E. Cooper. 2008. Oxidative stress as a major culprit in kidney disease in diabetes. Diabetes. 57:1446-1454. Fotheringham, J., N. Weatherley, B. Kawar, D. G. Fogarty, and T. Ellam. 2014. The body composition and excretory burden of lean, obese, and severely obese individuals has implications for the assessment of chronic kidney disease. Kidney Int. 86:1221-1228. Frank, A. P., R. de Souza Santos, B. F. Palmer, and D. J. Clegg. 2018. Determinants of body fat distribution in humans may provide insight about obesity-related health risks. Journal of lipid research. J Lipid Res.10. Fuchs, T., M. P. Loureiro, L. E. Macedo, D. Nocca, M. Nedelcu, and T. A. Costa-Casagrande. 2018. Animal models in metabolic syndrome. Rev Col Bras Cir. 45:e1975. Funk, J. A., and R. G. Schnellmann. 2013. Accelerated recovery of renal mitochondrial and tubule homeostasis with SIRT1/PGC-1alpha activation following ischemia-reperfusion injury. Toxicol Appl Pharmacol. 273:345-354. Galvan, D. L., N. H. Green, and F. R. Danesh. 2017. The hallmarks of mitochondrial dysfunction in chronic kidney disease. Kidney Int. 92:1051-1057. Gardner, B. M., D. Pincus, K. Gotthardt, C. M. Gallagher, and P. Walter. 2013. Endoplasmic reticulum stress sensing in the unfolded protein response. Cold Spring Harb Perspect Biol. 5:a013169. Gentile, G., and G. Remuzzi. 2016. Novel biomarkers for renal diseases? none for the moment (but one). J Biomol Screen. 21:655-670. Gersch, M. S., W. Mu, P. Cirillo, S. Reungjui, L. Zhang, C. Roncal, Y. Y. Sautin, R. J. Johnson, and T. Nakagawa. 2007. Fructose, but not dextrose, accelerates the progression of chronic kidney disease. Am J Physiol Renal Physiol. 293:F1256-1261. Ghasemi, A., S. Khalifi, and S. Jedi. 2014. Streptozotocin-nicotinamide-induced rat model of type 2 diabetes (review). Acta Physiol Hung. 101:408-420. Giraud, S., F. Favreau, N. Chatauret, R. Thuillier, S. Maiga, and T. Hauet. 2011.Contribution of large pig for renal ischemia-reperfusion and transplantation studies: the preclinical model J Biomed Biotechnol. 2011:532127. Glastras, S. J., H. Chen, R. Teh, R. T. McGrath, J. Chen, C. A. Pollock, M. G. Wong, and S. Saad. 2016. Mouse models of diabetes, obesity and related kidney disease. PloS one. 11:e0162131. Grundy, S. M. 2008. Metabolic syndrome pandemic. Arterioscler Thromb Vasc Biol. 28:629-636. Guo, X., M. Kesimer, G. Tolun, X. Zheng, Q. Xu, J. Lu, J. K. Sheehan, J. D. Griffith, and X. Li. 2012. The NAD(+)-dependent protein deacetylase activity of SIRT1 Contribution of large pig for renal ischemia-reperfusion and transplantation studies: the preclinical model is regulated by its oligomeric status. Sci Rep.2:640. Hariharan, D., K. Vellanki, and H. Kramer. 2015. The western diet and chronic kidney disease. Curr Hypertens Rep. 17:16. Herget-Rosenthal, S., A. Bokenkamp, and W. Hofmann. 2007. How to estimate GFR-serum creatinine, serum cystatin C or equations? Clin Biochem. 40:153-161. Higgins, G. C., and M. T. Coughlan. 2014. Mitochondrial dysfunction and mitophagy: the beginning and end to diabetic nephropathy? Br J Pharmacol. 171:1917-1942. Holmstrom, K. M., and T. Finkel. 2014. Cellular mechanisms and physiological consequences of redox-dependent signalling. Nat Rev Mol Cell Biol. 15:411-421. Huang, K. C., L. T. Lee, C. Y. Chen, and P. K. Sung. 2008. All-cause and cardiovascular disease mortality increased with metabolic syndrome in Taiwanese. Obesity (Silver Spring). 16:684-689. Ibrahim, M. M. 2010. Subcutaneous and visceral adipose tissue: structural and functional differences. Obes Rev. 11:11-18. Isomaa, B. 2003. A major health hazard: the metabolic syndrome. Life Sci. 73:2395-2411. Jorgensen, W., K. A. Rud, O. H. Mortensen, L. Frandsen, N. Grunnet, and B. Quistorff. 2017. Your mitochondria are what you eat: a high-fat or a high-sucrose diet eliminatesmetabolic flexibility in isolated mitochondria from rat skeletal muscle. Physiol Rep. 5 : e13207. Kahn, S. E., R. L. Hull, and K. M. Utzschneider. 2006. Mechanisms linking obesity to insulin resistance and type 2 diabetes. Nature. 444:840-846. Kang, H. M., S. H. Ahn, P. Choi, Y. A. Ko, S. H. Han, F. Chinga, A. S. Park, J. Tao, K. Sharma, J. Pullman, E. P. Bottinger, I. J. Goldberg, and K. Susztak. 2015. Defective fatty acid oxidation in renal tubular epithelial cells has a key role in kidney fibrosis development. Nat Med. 21:37-46. Kang, J. X. 2003. The importance of omega-6/omega-3 fatty acid ratio in cell function. The gene transfer of omega-3 fatty acid desaturase. World Rev Nutr Diet. 92:23-36. Kaur, J. 2014. A comprehensive review on metabolic syndrome. Cardiol Res Pract. 2014:943162. Kennedy, A. J., K. L. Ellacott, V. L. King, and A. H. Hasty. 2010. Mouse models of the metabolic syndrome. Dis Model Mech. 3:156-166. Khairoun, M., M. van den Heuvel, B. M. van den Berg, O. Sorop, R. de Boer, N. S. van Ditzhuijzen, I. M. Bajema, H. J. Baelde, M. Zandbergen, D. J. Duncker, T. J. Rabelink, M. E. J. Reinders, W. J. van der Giessen, and J. I. Rotmans. 2015. Early systemic microvascular damage in pigs with atherogenic diabetes mellitus coincides with renal angiopoietin dysbalance. PloS one. 10:e0121555. Kim, B. H., E. S. Lee, R. Choi, J. Nawaboot, M. Y. Lee, E. Y. Lee, H. S. Kim, and C. H. Chung. 2016. Protective effects of curcumin on renal oxidative stress and lipid metabolism in a rat model of type 2 diabetic nephropathy. Yonsei Med J. 57:664-673. King, A. J. 2012. The use of animal models in diabetes research. Br J Pharmacol. 166:877-894. Lemoine, S., F. Guebre-Egziabher, F. Sens, M. S. Nguyen-Tu, L. Juillard, L. Dubourg, and A. Hadj-Aissa. 2014. Accuracy of GFR estimation in obese patients. Clin J Am Soc Nephrol. 9:720-727. Li, S. J., S. T. Ding, H. J. Mersmann, C. H. Chu, C. D. Hsu, and C. Y. Chen. 2016. A nutritional nonalcoholic steatohepatitis minipig model. J Nutr Biochem. 28:51-60. Li, S. J., C. H. Liu, C. W. Chang, H. P. Chu, K. J. Chen, H. J. Mersmann, S. T. Ding, C. H. Chu, and C. Y. Chen. 2015. Development of a dietary-induced metabolic syndrome model using miniature pigs involvement of AMPK and SIRT1. Eur J Clin Invest. 45:70-80. Li, X. 2013. SIRT1 and energy metabolism. Acta Biochim Biophys Sin (Shanghai). 45:51-60. Li, Z., J. R. Woollard, S. Wang, M. J. Korsmo, B. Ebrahimi, J. P. Grande, S. C. Textor, A. Lerman, and L. O. Lerman. 2011. Increased glomerular filtration rate in early metabolic syndrome is associated with renal adiposity and microvascular proliferation. Am J Physiol Renal Physiol. 301:F1078-1087. Liu, B. C., T. T. Tang, L. L. Lv, and H. Y. Lan. 2018. Renal tubule injury: a driving force toward chronic kidney disease. Kidney Int. 93:568-579. Liu, Y. 2006. Renal fibrosis: new insights into the pathogenesis and therapeutics. Kidney Int. 69:213-217. Luis-Lima, S., C. García-Contreras, M. Vázquez-Gómez, S. Astiz, F. Carrara, F. Gaspari, N. Negrín-Mena, A. Jiménez-Sosa, H. Jiménez-Hernández, A. González-Bulnes, and E. Porrini. 2018a. A Simple Method to Measure Renal Function in Swine by the Plasma Clearance of Iohexol. Int J Mol Sci. 19:232. Lynch, M. R., M. T. Tran, and S. M. Parikh. 2018. PGC1alpha in the kidney. Am J Physiol Renal Physiol. 314:F1-8. Ma, S., X. Y. Zhu, A. Eirin, J. R. Woollard, K. L. Jordan, H. Tang, A. Lerman, and L. O. Lerman. 2016. Perirenal fat promotes renal arterial endothelial dysfunction in obese swine through tumor necrosis factor-α. J Urol. 195:1152-1159. Mandal, R., A. G. Loeffler, S. Salamat, and M. K. Fritsch. 2012. Organ weight changes associated with body mass index determined from a medical autopsy population. Am J Forensic Med Pathol. 33:382-389. Mandarim-de-Lacerda, S. B.-d.-S. I. B. S. T. C. L. B. V. S.-M. M. B. A. C. A. 2014. Animal models of nutritional induction of type 2 diabetes mellitus. Int J Morphol.32: 279-293 . Markoska, K., J. Masin-Spasovska, M. Polenakovic, and G. Spasovski. 2015. Urinary protein biomarkers in chronic kidney disease.BANTAO.13:1-3. Mentoor, I., M. Kruger, and T. Nell. 2018. Metabolic syndrome and body shape predict differences in health parameters in farm working women BMC Public Health. 18:453. Michels, W. M., D. C. Grootendorst, M. Verduijn, E. G. Elliott, F. W. Dekker, and R. T. Krediet. 2010. Performance of the Cockcroft-Gault, MDRD, and new CKD-EPI formulas in relation to GFR, age, and body size. Clin J Am Soc Nephrol. 5:1003-1009. Mishra, P., and D. C. Chan. 2014. Mitochondrial dynamics and inheritance during cell division, development and disease. Nat Rev Mol Cell Biol.15:634-646. Moreno-Fernandez, S., M. Garces-Rimon, G. Vera, J. Astier, J. F. Landrier, and M. Miguel. 2018. High Fat/High glucose diet induces metabolic syndrome in an experimental rat model. Nutrients 10:E1502. Mount, P., M. Davies, S. W. Choy, N. Cook, and D. Power. 2015. Obesity-related chronic kidney disease-the role of lipid metabolism. Metabolites 5:720-732. Munusamy, S., J. M. do Carmo, J. P. Hosler, and J. E. Hall. 2015. Obesity-induced changes in kidney mitochondria and endoplasmic reticulum in the presence or absence of leptin. American journal of physiology. Renal physiology Am J Physiol Renal Physiol. 309:F731-743. Myles, I. A. 2014. Fast food fever: reviewing the impacts of the western diet on immunity. Nutr J. 13:61. Nakayama, T., T. Kosugi, M. Gersch, T. Connor, L. G. Sanchez-Lozada, M. A. Lanaspa, C. Roncal, S. E. Perez-Pozo, R. J. Johnson, and T. Nakagawa. 2010. Dietary fructose causes tubulointerstitial injury in the normal rat kidney. Am J Physiol Renal Physiol. 298:F712-720. Nakhoul, N., and V. Batuman. 2011. Role of proximal tubules in the pathogenesis of kidney disease. Contrib Nephrol. 169:37-50. Okreglicka, K. 2015. Health effects of changes in the structure of dietary macronutrients intake in western societies. Rocz Panstw Zakl Hig. 66:97-105. Paley, C. A., and M. I. Johnson. 2018. Abdominal obesity and metabolic syndrome: exercise as medicine? BMC Sports Sci Med Rehabil. 10:7. Parikh, R. M., and V. Mohan. 2012. Changing definitions of metabolic syndrome. Indian J Endocrinol Metab. 16:7-12. Park, Y. W., S. Zhu, L. Palaniappan, S. Heshka, M. R. Carnethon, and S. B. Heymsfield. 2003. The metabolic syndrome: prevalence and associated risk factor findings in the US population from the Third National Health and Nutrition Examination Survey, 1988-1994. Arch Intern Med. 163:427-436. Pereira, R. M., J. D. Botezelli, K. C. da Cruz Rodrigues, R. A. Mekary, D. E. Cintra, J. R. Pauli, A. S. R. da Silva, E. R. Ropelle, and L. P. de Moura. 2017. Fructose consumption in the development of obesity and the effects of different protocols of physical exercise on the hepatic metabolism. Nutrients. 9: E405. Perlman, R. L. 2016. Mouse models of human disease: An evolutionary perspective. Evol Med Public Health. 2016:170-176. Pinto-Sietsma, S.-J., G. Navis, W. M. T. Janssen, D. de Zeeuw, R. O. B. Gans, and P. E. de Jong. 2003. A central body fat distribution is related to renal function impairment, even in lean subjects. Am J Kidney Dis. 41:733-741. Puelles, V. G., M. A. Zimanyi, T. Samuel, M. D. Hughson, R. N. Douglas-Denton, J. F. Bertram, and J. A. Armitage. 2012. Estimating individual glomerular volume in the human kidney: clinical perspectives. Nephrol Dial Transplant.27:1880-1888. Qin, N., T. Cai, Q. Ke, Q. Yuan, J. Luo, X. Mao, L. Jiang, H. Cao, P. Wen, K. Zen, Y. Zhou, and J. Yang. 2018. UCP2-dependent improvement of mitochondrial dynamics protects against acute kidney injury. J Pathol. 247:392-405. Rabe, M., and F. Schaefer. 2016. Non-transgenic mouse models of kidney disease. Nephron. 133:53-61. Reaven, G. M. 1988. Banting lecture 1988. Role of insulin resistance in human disease. Diabetes. 37:1595-1607. Reaven, G. M., C. Hollenbeck, C. Y. Jeng, M. S. Wu, and Y. D. Chen. 1988. Measurement of plasma glucose, free fatty acid, lactate, and insulin for 24 h in patients with NIDDM. Diabetes. 37:1020-1024. Ruggiero, C., M. Ehrenshaft, E. Cleland, and K. Stadler. 2011. High-fat diet induces an initial adaptation of mitochondrial bioenergetics in the kidney despite evident oxidative stress and mitochondrial ROS production. Am J Physiol Endocrinol Metab. 300:E1047-1058. Rysz, J., A. Gluba-Brzozka, B. Franczyk, Z. Jablonowski, and A. Cialkowska-Rysz. 2017. Novel biomarkers in the diagnosis of chronic kidney disease and the prediction of Its outcome. Int J Mol Sci. 18: E1702. Sachs, D. H. 1994. The pig as a potential xenograft donor. Vet Immunol Immunopathol. 43:185-191. Sandilands, E. A., N. Dhaun, J. W. Dear, and D. J. Webb. 2013. Measurement of renal function in patients with chronic kidney disease. Br J Clin Pharmacol. 76:504-515. Scarpulla, R. C., R. B. Vega, and D. P. Kelly. 2012. Transcriptional integration of mitochondrial biogenesis. Trends Endocrinol Metab. 23:459-466. Sharma, K., B. Karl, A. V. Mathew, J. A. Gangoiti, C. L. Wassel, R. Saito, M. Pu, S. Sharma, Y. H. You, L. Wang, M. Diamond-Stanic, M. T. Lindenmeyer, C. Forsblom, W. Wu, J. H. Ix, T. Ideker, J. B. Kopp, S. K. Nigam, C. D. Cohen, P. H. Groop, B. A. Barshop, L. Natarajan, W. L. Nyhan, and R. K. Naviaux. 2013. Metabolomics reveals signature of mitochondrial dysfunction in diabetic kidney disease. J Am Soc Nephrol. 24:1901-1912. Shulman, G. I. 2000. Cellular mechanisms of insulin resistance. J Clin Invest. 106:171-176. Simopoulos, A. P. 2016. An Increase in the Omega-6/Omega-3 fatty acid ratio increases the risk for obesity. Nutrients. 8:128. Skovsø, S. 2014. Modeling type 2 diabetes in rats using high fat diet and streptozotocin. J Diabetes Investig. 5:349-358. Smith, U. 2015. Abdominal obesity: a marker of ectopic fat accumulation. J Clin Invest. 125:1790-1792. Spurlock, M. E., and N. K. Gabler. 2008. The development of porcine models of obesity and the metabolic syndrome. J Nutr. 138:397-402. Statovci, D., M. Aguilera, J. MacSharry, and S. Melgar. 2017. The impact of western diet and nutrients on the microbiota and immune response at mucosal interfaces. Front Immunol. 8:838. Sumiyoshi, M., M. Sakanaka, and Y. Kimura. 2006. Chronic intake of high-fat and high-sucrose diets differentially affects glucose intolerance in mice. J Nutr. 136:582-587. Suárez-Rivero, J. M., M. Villanueva-Paz, P. de la Cruz-Ojeda, M. de la Mata, D. Cotán, M. Oropesa-Ávila, I. de Lavera, M. Álvarez-Córdoba, R. Luzón-Hidalgo, and J. A. Sánchez-Alcázar. 2017. Mitochondrial dynamics in mitochondrial diseases. Diseases. 5. Surwit, R. S., C. M. Kuhn, C. Cochrane, J. A. McCubbin, and M. N. Feinglos. 1988. Diet-induced type II diabetes in C57BL/6J mice. Diabetes 37:1163-1167. swamy, B. K. C. 2015. Streptozotocin - a diabetogenic agent in animal models. Human Journals. 3:253-269. Szeto, H. H., S. Liu, Y. Soong, N. Alam, G. T. Prusky, and S. V. Seshan. 2016. Protection of mitochondria prevents high-fat diet-induced glomerulopathy and proximal tubular injury. Kidney Int. 90:997-1011. Tang, C., J. Cai, and Z. Dong. 2016. Mitochondrial dysfunction in obesity-related kidney disease: a novel therapeutic target. Kidney Int. 90:930-933. Tang, C., L. He, J. Liu, and Z. Dong. 2015. Mitophagy: Basic mechanism and potential role in kidney diseases. Kidney Dis (Basel).1:71-79. Tobar, A., Y. Ori, S. Benchetrit, G. Milo, M. Herman-Edelstein, B. Zingerman, N. Lev, U. Gafter, and A. Chagnac. 2013. Proximal tubular hypertrophy and enlarged glomerular and proximal tubular urinary space in obese subjects with proteinuria. PloS one. 8:e75547. Tong, Y., J. Chuan, L. Bai, J. Shi, L. Zhong, X. Duan, and Y. Zhu. 2018. The protective effect of shikonin on renal tubular epithelial cell injury induced by high glucose. Biomed Pharmacother. 98:701-708. Toto, R. D., T. Greene, L. A. Hebert, L. Hiremath, J. P. Lea, J. B. Lewis, V. Pogue, M. Sika, and X. Wang. 2010. Relationship between body mass index and proteinuria in hypertensive nephrosclerosis: results from the African American Study of Kidney Disease and Hypertension (AASK) cohort. Am J Kidney Dis. 56: 896-906. Tran, M., D. Tam, A. Bardia, M. Bhasin, G. C. Rowe, A. Kher, Z. K. Zsengeller, M. R. Akhavan-Sharif, E. V. Khankin, M. Saintgeniez, S. David, D. Burstein, S. A. Karumanchi, I. E. Stillman, Z. Arany, and S. M. Parikh. 2011. PGC-1alpha promotes recovery after acute kidney injury during systemic inflammation in mice. J Clin Invest. 121:4003-4014. Tsuboi, N., Y. Okabayashi, A. Shimizu, and T. Yokoo. 2017. The renal pathology of obesity. Kidney Int Rep. 2:251-260. van der Heijden, R. A., J. Bijzet, W. C. Meijers, G. K. Yakala, R. Kleemann, T. Q. Nguyen, R. A. de Boer, C. G. Schalkwijk, B. P. Hazenberg, U. J. Tietge, and P. Heeringa. 2015. Obesity-induced chronic inflammation in high fat diet challenged C57BL/6J mice is associated with acceleration of age-dependent renal amyloidosis. Sci Rep. 5:16474. Van Laar, V. S., and S. B. Berman. 2009. Mitochondrial dynamics in Parkinson's disease. Exp Neurol. 218:247-256. Vatandoust, N., F. Rami, A. R. Salehi, S. Khosravi, G. Dashti, G. Eslami, S. Momenzadeh, and R. Salehi. 2018. Novel high-fat diet formulation and streptozotocin treatment for induction of prediabetes and type 2 diabetes in rats. Adv Biomed Res. 7:107. Wang, H., Y. Guan, M. A. Karamercan, L. Ye, T. Bhatti, L. B. Becker, J. A. Baur, and C. A. Sims. 2015. Resveratrol rescues kidney mitochondrial function following hemorrhagic shock. Shock. 44:173-180. Wang, H., P. Song, L. Du, W. Tian, W. Yue, M. Liu, D. Li, B. Wang, Y. Zhu, C. Cao, J. Zhou, and Q. Chen. 2011. Parkin ubiquitinates Drp1 for proteasome-dependent degradation: implication of dysregulated mitochondrial dynamics in Parkinson disease. J Biol Chem. 286:11649-11658. Wasung, M. E., L. S. Chawla, and M. Madero. 2015. Biomarkers of renal function, which and when? Clin Chim Acta. 438:350-357. Weinberg, J. M., M. A. Venkatachalam, N. F. Roeser, P. Saikumar, Z. Dong, R. A. Senter, and I. Nissim. 2000. Anaerobic and aerobic pathways for salvage of proximal tubules from hypoxia-induced mitochondrial injury. Am J Physiol Renal Physiol. 279:F927-943. Wicks, S. E., T. T. Nguyen, C. Breaux, C. Kruger, and K. Stadler. 2016. Diet-induced obesity and kidney disease - in search of a susceptible mouse model. Biochimie. 124:65-73. Wilcox, G. 2005. Insulin and insulin resistance. Clin Biochem Rev. 26:19-39. Wilson, C. R., M. K. Tran, K. L. Salazar, M. E. Young, and H. Taegtmeyer. 2007. Western diet, but not high fat diet, causes derangements of fatty acid metabolism and contractile dysfunction in the heart of Wistar rats. Biochem J. 406 :457-467. Wirthensohn, G., and W. G. Guder. 1986. Renal substrate metabolism. Physiol Rev. 66:469-497. Wong, S. K., K. Y. Chin, F. H. Suhaimi, A. Fairus, and S. Ima-Nirwana. 2016. Animal models of metabolic syndrome: a review. Nutr Metab (Lond). 13:65. Worachartcheewan, A., N. Schaduangrat, V. Prachayasittikul, and C. Nantasenamat. 2018. Data mining for the identification of metabolic syndrome status EXCLI J.17:72-88. Wu, J., and L. J. Yan. 2015. Streptozotocin-induced type 1 diabetes in rodents as a model for studying mitochondrial mechanisms of diabetic β cell glucotoxicity. Diabetes Metab Syndr Obes. 8:181-188. Xu, Q., P. Xia, X. Li, W. Wang, Z. Liu, and X. Gao. 2014. Tetramethylpyrazine ameliorates high glucose-induced endothelial dysfunction by increasing mitochondrial biogenesis. PloS one. 9:e88243. Yacoub, R., K. Lee, and J. C. He. 2014. The role of SIRT1 in diabetic kidney disease. Front Endocrinol (Lausanne). 5:166. Yang, H. C., Y. Zuo, and A. B. Fogo. 2010. Models of chronic kidney disease. Drug Discov Today Dis Models. 7 :13-19. Youle, R. J., and D. P. Narendra. 2011. Mechanisms of mitophagy. Nat Rev Mol Cell Biol. 12:9-14. Yuan, Y., S. Huang, W. Wang, Y. Wang, P. Zhang, C. Zhu, G. Ding, B. Liu, T. Yang, and A. Zhang. 2012. Activation of peroxisome proliferator-activated receptor-γ coactivator 1α ameliorates mitochondrial dysfunction and protects podocytes from aldosterone-induced injury. Kidney Int. 82 :771-789. Zhan, M., C. Brooks, F. Liu, L. Sun, and Z. Dong. 2013. Mitochondrial dynamics: regulatory mechanisms and emerging role in renal pathophysiology. Kidney Int. 83:568-581. Zhan, M., I. M. Usman, L. Sun, and Y. S. Kanwar. 2015. Disruption of renal tubular mitochondrial quality control by Myo-inositol oxygenase in diabetic kidney disease. J Am Soc Nephrol. 26:1304-1321. Zhang, M., X. Y. Lv, J. Li, Z. G. Xu, and L. Chen. 2008. The characterization of high-fat diet and multiple low-dose streptozotocin induced type 2 diabetes rat model. Exp Diabetes Res. 2008:704045. Zhou, Y., T. Cai, J. Xu, L. Jiang, J. Wu, Q. Sun, K. Zen, and J. Yang. 2017. UCP2 attenuates apoptosis of tubular epithelial cells in renal ischemia-reperfusion injury. Am J Physiol Renal Physiol. 313:F926-937. | |
dc.identifier.uri | http://tdr.lib.ntu.edu.tw/jspui/handle/123456789/72495 | - |
dc.description.abstract | 肥胖是近年來急遽增加的健康問題,且被認為是慢性腎臟疾病 (Chronic kidney disease, CKD) 的重要危險因素。腎臟是人體中高能量需求的器官之一,其粒線體含量和耗氧量僅次於心臟。近期研究指出,腎臟粒線體功能異常,可能加速其相關病程的進展。故本研究以高脂飲食誘導肥胖之李宋小型豬隻為模式探討粒線體功能與CKD之間的關係。
本研究共分三部分,第一部分使用5月齡之李宋豬 (10頭閹公豬和10頭母豬),起始體重為22.6±5.9公斤,並隨機分為兩組:對照飼糧 (Control, C) 組和高脂飼糧 (High fat diet, HFD) 組。餵飼六個月後,收集腎臟皮質進行分析。結果顯示,相較於C組,HFD組具有較重之體重和較厚的背部脂肪,且於腹部及頸部具有較多的油脂堆積。此外,血液生化值也指出HFD組別有較高的血糖、三酸甘油酯、總膽固醇以及游離脂肪酸和葡萄糖不耐之情況。HFD組中具有較重之腎臟重量以及較低之腎臟/體重比。HFD組之血液和尿液的肌酸酐、尿素及尿蛋白濃度亦高於C組。HFD組之腎絲球結構混亂、環間膜基質擴張、腎小管基底膜增厚和腎絲球纖維化的比例增加。此外, HFD豬隻腎臟皮質中發現三酸甘油酯累積、脂質過氧化增加以及腎臟抗氧化能力下降,推測其氧化壓力的發生。據此判定長期餵飼HFD確實可誘導李宋豬之腎皮質損傷。 為了觀察肥胖導致腎損傷之豬隻是否造成粒線體失常,所以第二部分為檢測肥胖豬隻其腎臟皮質粒線體功能表現,結果發現HFD組之ATP產量低於C組。於mRNA基因表現方面,HFD組之粒線體抗氧化能力指標 (UCP2) 表現量增加;粒線體生合成基因 (SIRT1和PGC-1α) 表現量下降;粒線體動態平衡上,HFD抑制粒線體分裂基因 (FIS1) 的表現量;蛋白質表現量則發現,HFD組別中分裂之DRP1、FIS1和融合之MFN2顯著增加,此結果顯示HFD可能造成腎臟粒線體功能異常的現象。 第三部分進一步透過體外實驗探討HFD誘發腎損傷的相關機制。利用棕櫚酸酯處理大鼠腎臟近端小管上皮細胞NRK-52E細胞株誘發脂毒性。結果發現,當棕櫚酸酯濃度增高,細胞存活率則會隨之降低、細胞凋亡現象也更為嚴重,且細胞的ATP產量也伴隨棕櫚酸酯濃度增加而下降,而在蛋白質表現量中也發現FIS1隨濃度增加而降低。 綜上所述,李宋小型豬隻經長期HFD餵飼會導致肥胖、血脂異常和腎臟損傷,同時伴隨著腎臟粒線體功能異常之現象,顯示出肥胖與腎臟疾病之關聯性。體外實驗發現,經棕櫚酸酯處理後即會造成細胞ATP產量降低,同時也顯示其對粒線體功能相關蛋白質有一定影響。因此,本研究推測粒線體功能對於肥胖導致腎損傷中扮演著重要角色。 | zh_TW |
dc.description.abstract | Obesity is a common and complex health problem which has dramatically increased in the recent decades. It is also considered as an independent risk factor for chronic kidney disease. Kidney is one of the most energy-demanding organs in the body, which exhibits a high mitochondrial content and oxygen consumption only next to the heart. Recent studies suggested that mitochondrial dysfunctions in kidney would accelerate the progression of renal diseases. The purpose of this study was to investigate the nexus between mitochondrial function and kidney injury using diet-induced obesity minipigs model.
This study was divided into three parts. The first part: five-month-old Lee-Sung minipigs (10 castrated male and 10 female pigs) with an initial weight of 22.6 ± 5.9 kg were randomly assigned into two groups; fed either a control diet (C) or a high-fat diet (HFD) for six months. The kidney cortex was collected for analysis. Compared with C group, HFD group had a heavier body weight, thicker back fat, higher plasma levels of glucose, triacylglycerol, total cholesterol, free fatty acid and glucose intolerance. A heavier kidney was observed in HFD pigs; whereas a smaller ratio of kidney weight to body weight was found in HFD group. Furthermore, the biomarkers of kidney injury, including blood creatinine, urine creatinine, urine urea, and urine protein were higher in HFD group. In histologic section of kidney cortex, glomerular disarranged structure, mesangial matrix dilatation, tubular basement membrane thickening and more glomerular fibrosis were observed in the HFD pigs. Moreover, greater triacylglycerol accumulation, increased lipid peroxidation, and decreased antioxidant capacity were found in the kidney cortex of HFD pigs. The results showed that long-term HFD feeding induced kidney injury in Lee-Sung minipigs. In order to observe whether HFD caused the renal injury through mitochondrial mechanisms. We next analyzed the function of the mitochondrial of renal cortex in obese pigs. The result showed that HFD pigs displayed a lower ATP production in the kidney than C group did. The expression of mitochondrial antioxidant capacity index (UCP2) was increased in the HFD group, whereas mitochondrial biogenesis genes (SIRT1 and PGC-1α) was downregulated by HFD, and mitochondrial dynamics gene (FIS1) was suppressed by HFD. The protein expressions of DRP1, FIS1, and MFN2 was upregulated in the HFD group, suggesting a mitochondrial dysfunction in the kidney. Finally, we explored the mechanism of HFD-induced renal injury through the in vitro model. Lipotoxicity was induced by palmitate treatment in NRK-52E cells (rat kidney proximal tubule epithelial cells). Palmitate treatment resulted in cell death in a dose dependent manner. In addition, ATP production was decreased with increasing palmitate concentration, and the protein expression of FIS1 was also decreased with increasing concentration. In conclusion, long-term feeding of HFD in Lee-Sung minipigs induced obesity, dyslipidemia and renal injury, in accompany with abnormal mitochondrial function in the kidney, suggesting an interrelationship with renal disease progression. Meanwhile, the in vitro study showed that palmitate treatment impaired ATP production, and it also showed an effect on mitochondrial function-related protein. Therefore, it is speculated that mitochondrial function plays an important role in obesity-induced kidney injury. | en |
dc.description.provenance | Made available in DSpace on 2021-06-17T06:59:54Z (GMT). No. of bitstreams: 1 ntu-108-R06626008-1.pdf: 4200882 bytes, checksum: 67ade80382eb71a723d9649b3e332dc1 (MD5) Previous issue date: 2019 | en |
dc.description.tableofcontents | 謝誌 I
中文摘要 II Abstract IV 圖目錄 IX 表目錄 X 第壹章、文獻回顧 1 一、代謝症候群 1 二、異常肥胖 3 1. 肥胖現況 3 2. 腹部肥胖 3 3. 胰島素阻抗 4 三、肥胖相關之慢性腎臟疾病 6 1. 慢性腎臟疾病 6 2. 肥胖相關之慢性腎臟疾病 7 四、腎臟中粒線體的平衡 11 1. 腎臟之粒線體 11 2. 肥胖相關的慢性腎臟疾病與粒線體功能異常之關係 15 五、高能量飲食 16 1.醣類 17 2.脂肪類 17 六、實驗動物 18 1. 囓齒動物 18 2. 迷你豬 19 3. 誘導肥胖的相關慢性腎臟疾病對動物模型之影響 21 第貳章、材料與方法 23 一、試驗設計 23 二、實驗飼糧 23 三、樣品採集 25 四、血液生化值、尿液檢測分析 26 1. 血液採集 26 2. 尿液採集 26 3. 血糖 (Plasma glucose) 26 4. 三酸甘油酯 (Triacylglycerol) 26 5. 總膽固醇 (Total cholesterol) 27 6. 靜脈葡萄糖耐受性測試 (Intravenous glucose tolerance test, IVGTT) 27 7. 游離脂肪酸 (Free fatty acid, FFA) 27 8. 肌酸酐 (Creatinine)測定 28 9. 尿素 (Urea)測定 28 10. 尿蛋白 (Total urine protein,UP)測定 28 五、蛋白質濃度測定 29 六、組織三酸甘油酯測定 29 七、抗氧化能力檢測 (Oxygen Radical Absorbance Capacity, ORAC) 29 1. 藥品配置 29 2. 試劑反應 30 八、脂質過氧化 (Thiobarbituric acid reactive substances, TBARS) 31 1. 藥品配置 31 2. 試劑反應 31 九、腎臟組織ATP測定 32 十、切片定量 33 十一、基因表現分析 33 1.抽取組織RNA及cDNA合成 33 2. Real-time PCR 34 十二、西方墨點法 (Western blot) 37 十三、細胞培養 38 十四、細胞存活率試驗 (MTT assay) 38 十五、細胞ATP測量 38 十六、細胞凋亡之測定 39 十七、統計分析 39 第參章、試驗結果 40 一、高油脂飼糧誘導李宋豬肥胖和血液生化值異常 40 二、高油脂飼糧誘導肥胖腎損傷 45 三、腎損傷導致粒線體功能異常 56 四、高油脂處理誘導腎小管細胞損傷 61 第肆章、問題與討論 65 一、高脂飼糧誘發肥胖李宋豬隻腎臟異常 65 1.腎臟損傷之生物標誌診斷 65 2.迷你豬隻模型模擬腎臟損傷之應用 68 二、肥胖誘發腎損傷豬隻粒線體功能表現 72 第伍章、結論 75 第陸章、參考文獻 76 | |
dc.language.iso | zh-TW | |
dc.title | 藉由飲食誘導肥胖豬隻探討粒線體功能在慢性腎臟
疾病扮演的角色 | zh_TW |
dc.title | The role of mitochondrial function in chronic kidney
disease in diet induced obese minipigs | en |
dc.type | Thesis | |
dc.date.schoolyear | 107-2 | |
dc.description.degree | 碩士 | |
dc.contributor.oralexamcommittee | 林原佑(Yuan-Yu Lin),張育嘉(Yu-Jia Chang),陳洵一(Shuen-Ei Chen) | |
dc.subject.keyword | 李宋豬,高脂飲食,腎損傷,粒線體功能, | zh_TW |
dc.subject.keyword | Lee Sung minipig,High fat diet,Renal damage,Mitochondria function., | en |
dc.relation.page | 85 | |
dc.identifier.doi | 10.6342/NTU201902206 | |
dc.rights.note | 有償授權 | |
dc.date.accepted | 2019-08-05 | |
dc.contributor.author-college | 生物資源暨農學院 | zh_TW |
dc.contributor.author-dept | 動物科學技術學研究所 | zh_TW |
顯示於系所單位: | 動物科學技術學系 |
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