title: Fructose induces tubulointerstitial injury in the kidney of mice.
abstract: Fructose induces several kinds of human metabolic disorders; however, information regarding fructose-induced kidney injury is still limited. This study examined fructose-induced kidney injury in mice and clarified the differential susceptibility of three mouse strains: C57Bl/6J, CBA/JN and DBA/2N. In this study all mice were fed with an equal calorie count for sixteen weeks to remove the influence of total energy intake from metabolic effects by fructose-feeding. Only DBA/2N mice, but not C57Bl/6J and CBA/JN mice, fed with fructose displayed tubulointerstitial fibrosis localized on the outer cortex of the kidney together with the increase of mRNA expression of Kim1 and Ngal in the absence of distinct glomerular lesions and albuminuria - decidedly different from diabetic nephropathy. In time-course study of DBA/2N mice fed with fructose diet, the inflammation and fibrosis in the outer cortex of the kidney were enhancing after eight weeks, in parallel with the accumulation of oxidative stress. This progression of renal damage in DBA/2N mice was accompanied with increasing mRNA expression of GLUT5. These results suggest that the responsiveness of GLUT5 expression to fructose at the kidney is one of pivotal roles for the progression of fructose-induced kidney injury.
authors.affiliation: Department of Medicine, Shiga University of Medical Science, Otsu, Shiga, Japan.
authors.forename: Masahiro
authors.initials: M
authors.lastname: Aoyama
authors.forename: Keiji
authors.initials: K
authors.lastname: Isshiki
authors.forename: Shinji
authors.initials: S
authors.lastname: Kume
authors.forename: Masami
authors.initials: M
authors.lastname: Chin-Kanasaki
authors.forename: Hisazumi
authors.initials: H
authors.lastname: Araki
authors.forename: Shin-Ichi
authors.initials: S
authors.lastname: Araki
authors.forename: Daisuke
authors.initials: D
authors.lastname: Koya
authors.forename: Masakazu
authors.initials: M
authors.lastname: Haneda
authors.forename: Atsunori
authors.initials: A
authors.lastname: Kashiwagi
authors.forename: Hiroshi
authors.initials: H
authors.lastname: Maegawa
authors.forename: Takashi
authors.initials: T
authors.lastname: Uzu
mesh_terms: D000209:Acute-Phase Proteins / Q000235:genetics; D000818:Animals; D024042:Collagen Type I / Q000235:genetics; D004040:Dietary Carbohydrates / Q000008:administration & dosage / Q000009:adverse effects*; D005353:Fibronectins / Q000235:genetics; D005632:Fructose / Q000008:administration & dosage / Q000009:adverse effects* / Q000378:metabolism; D015870:Gene Expression / Q000187:drug effects; D051246:Glucose Transport Proteins, Facilitative / Q000235:genetics / Q000378:metabolism; D051273:Glucose Transporter Type 2 / Q000235:genetics; D051296:Glucose Transporter Type 5; D000072596:Hepatitis A Virus Cellular Receptor 1; D007674:Kidney Diseases / Q000139:chemically induced* / Q000235:genetics / Q000473:pathology; D007684:Kidney Tubules / Q000187:drug effects* / Q000378:metabolism / Q000473:pathology; D000071068:Lipocalin-2; D054834:Lipocalins / Q000235:genetics; D008099:Liver / Q000378:metabolism; D008297:Male; D008565:Membrane Proteins / Q000235:genetics; D051379:Mice; D008810:Mice, Inbred C57BL; D008808:Mice, Inbred CBA; D008811:Mice, Inbred DBA; D015513:Oncogene Proteins / Q000235:genetics; D012333:RNA, Messenger / Q000096:biosynthesis; D054390:Receptors, CCR2 / Q000235:genetics
chemical_list: D000209:Acute-Phase Proteins; D024042:Collagen Type I; D004040:Dietary Carbohydrates; D005353:Fibronectins; D051246:Glucose Transport Proteins, Facilitative; D051273:Glucose Transporter Type 2; D051296:Glucose Transporter Type 5; C442240:Havcr1 protein, mouse; D000072596:Hepatitis A Virus Cellular Receptor 1; D000071068:Lipocalin-2; D054834:Lipocalins; D008565:Membrane Proteins; D015513:Oncogene Proteins; D012333:RNA, Messenger; D054390:Receptors, CCR2; C495682:Slc2a2 protein, mouse; C465351:Slc2a5 protein, mouse; C071332:Lcn2 protein, mouse; D005632:Fructose