Generation of Na+-Coupled Dicarboxylate Cotransporter (Nadc-1) Deficient Mice for the Study of Nadc-1's Role in Caloric Restriction and Renal Ischemia/Reperfusion Injury
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Home > Medicine & Health Science textbooks > Pre-clinical medicine: basic sciences > Physiology > Generation of Na+-Coupled Dicarboxylate Cotransporter (Nadc-1) Deficient Mice for the Study of Nadc-1's Role in Caloric Restriction and Renal Ischemia/Reperfusion Injury
Generation of Na+-Coupled Dicarboxylate Cotransporter (Nadc-1) Deficient Mice for the Study of Nadc-1's Role in Caloric Restriction and Renal Ischemia/Reperfusion Injury

Generation of Na+-Coupled Dicarboxylate Cotransporter (Nadc-1) Deficient Mice for the Study of Nadc-1's Role in Caloric Restriction and Renal Ischemia/Reperfusion Injury


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This dissertation, "Generation of Na+-coupled dicarboxylate cotransporter (NaDC-1) deficient mice for the study of NaDC-1's role in caloric restriction and renal ischemia/reperfusion injury" by Tsun-bond, Horace, Ho, 何存邦, was obtained from The University of Hong Kong (Pokfulam, Hong Kong) and is being sold pursuant to Creative Commons: Attribution 3.0 Hong Kong License. The content of this dissertation has not been altered in any way. We have altered the formatting in order to facilitate the ease of printing and reading of the dissertation. All rights not granted by the above license are retained by the author. Abstract: Abstract of the thesis entitled Generation of Na -Coupled Dicarboxylate Cotransporter (NaDC-1) Deficient Mice for The Study of NaDC-1's Role in Caloric Restriction and Renal Ischemia/Reperfusion Injury Submitted by Ho, Horace Tsun-Bond For the degree of Doctor of Philosophy at The University of Hong Kong January, 2007 The gene of interest in my PhD research is called NaDC-1 (Na -coupled dicarboxylate co-transporter). NaDC-1 is a sodium-dependent co-transporter that absorbs/reabsorbs Krebs cycle intermediates across the cell membrane and is expressed mainly in the epithelial cells of the intestine and kidney. NaDC-1 is thought to be involved in the uptake of various Krebs cycle intermediates from digested food in the intestine and re-absorption of these organic acids from the tubular filtrate in the kidney. NaDC-1 has been cloned from various mammalian species including rabbit, rat, human and mouse. Amino acid sequences between these orthologs show at least 75% or higher identity. The reason for our interest in NaDC-1 is based on a finding that several Drosophila mutants selected independently for longevity all have a mutated Drosophila homologue of NaDC-1 named Indy. It was postulated that a reduction of expression and activity in Indy led to a sub-optimal absorption of nutrients and recycling of metabolic by-products into cells for energy production, creating a situation similar to caloric restriction, which is the only effective means of prolonging life-span in mammals. It is thus of interest to better understand the physiological function of NaDC-1 and to determine whether it plays a role in caloric restriction/aging in mammals. In addition, availability of intracellular Krebs cycle intermediates has been suggested by in vitro studies to affect renal cell survival/recovery after hypoxia/reoxygenation. We therefore also looked at the possible involvement of NaDC-1 in ischemia/reperfusion injury in vivo. NaDC-1 deficient mice have been generated as the model for our studies. NaDC-1 deficient mice were found to have significantly higher urine excretion level of various Krebs cycle intermediates, confirming for the first time in vivo NaDC-1's proposed endogenous function of reabsorbing these intermediates from the tubular filtrate into renal cells in the kidney. However, no other phenotypes have been identified with this mouse model so far. NaDC-1 deficiency did not lead to spontaneous and short-term caloric restriction effects, nor did it seem to affect the severity of renal damage after ischemia/reperfusion injury. Nevertheless, this is the first and only known study of NaDC-1 in a mammalian system to date, and the availability of this mouse model should aide future studies in the attempt to elucidate the physiological function of NaDC-1. DOI: 10.5353/th_b3857523 Subjects: Carrier proteins - Physiology Ischemia Reperfusion injury Kidneys - Diseases - Animal models Mice - Physiology


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Product Details
  • ISBN-13: 9781374667631
  • Publisher: Open Dissertation Press
  • Publisher Imprint: Open Dissertation Press
  • Height: 279 mm
  • No of Pages: 172
  • Weight: 689 gr
  • ISBN-10: 1374667633
  • Publisher Date: 27 Jan 2017
  • Binding: Hardback
  • Language: English
  • Spine Width: 11 mm
  • Width: 216 mm


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Generation of Na+-Coupled Dicarboxylate Cotransporter (Nadc-1) Deficient Mice for the Study of Nadc-1's Role in Caloric Restriction and Renal Ischemia/Reperfusion Injury
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Generation of Na+-Coupled Dicarboxylate Cotransporter (Nadc-1) Deficient Mice for the Study of Nadc-1's Role in Caloric Restriction and Renal Ischemia/Reperfusion Injury
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