title: Fructose-induced metabolic syndrome is associated with glomerular hypertension and renal microvascular damage in rats.
abstract: Fructose intake has been recently linked to the epidemic of metabolic syndrome and, in turn, the metabolic syndrome has been epidemiologically linked with renal progression. The renal hemodynamic effects of fructose intake are unknown, as well as the effects of different routes of administration. Metabolic syndrome was induced in rats over 8 wk by either a high-fructose diet (60%, F60, n = 7) or by adding fructose to drinking water (10%, F10, n = 7). Body weight and food and fluid intake of each rat were measured weekly during the follow-up. At baseline and at the end of wk 8, systolic blood pressure, plasma uric acid, and triglycerides were measured. At the end of week 8 glomerular hemodynamics was evaluated by micropuncture techniques. Wall thickening in outer cortical and juxtamedullary afferent arterioles was assessed by immunohistochemistry and computer image analysis. Fructose administration either in diet or drinking water induced hypertension, hyperuricemia, and hypertriglyceridemia; however, there was a progressive increment in these parameters with higher fructose intake (C<F10<F60). In addition, the F60 rats developed kidney hypertrophy, glomerular hypertension, cortical vasoconstriction, and arteriolopathy of preglomerular vessels. In conclusion, fructose-induced metabolic syndrome is associated with renal disturbances characterized by renal hypertrophy, arteriolopathy, glomerular hypertension, and cortical vasoconstriction. These changes are best observed in rats administered high doses (60% diet) of fructose.
authors.affiliation: Dept. of Nephrology, Instituto Nacional de Cardiología Ignacio Chávez, Juan Badiano 1. 14080, Mexico City, Mexico. lgsanchezlozada@hotmail.com
authors.forename: Laura G
authors.initials: LG
authors.lastname: Sánchez-Lozada
authors.forename: Edilia
authors.initials: E
authors.lastname: Tapia
authors.forename: Adriana
authors.initials: A
authors.lastname: Jiménez
authors.forename: Pablo
authors.initials: P
authors.lastname: Bautista
authors.forename: Magdalena
authors.initials: M
authors.lastname: Cristóbal
authors.forename: Tomás
authors.initials: T
authors.lastname: Nepomuceno
authors.forename: Virgilia
authors.initials: V
authors.lastname: Soto
authors.forename: Carmen
authors.initials: C
authors.lastname: Avila-Casado
authors.forename: Takahiko
authors.initials: T
authors.lastname: Nakagawa
authors.forename: Richard J
authors.initials: RJ
authors.lastname: Johnson
authors.forename: Jaime
authors.initials: J
authors.lastname: Herrera-Acosta
authors.forename: Martha
authors.initials: M
authors.lastname: Franco
mesh_terms: D000818:Animals; D001835:Body Weight / Q000187:drug effects / Q000502:physiology; D002196:Capillaries / Q000473:pathology; D004326:Drinking / Q000502:physiology; D004435:Eating / Q000502:physiology; D005632:Fructose / Q000494:pharmacology*; D006977:Hypertension, Renal / Q000503:physiopathology*; D007668:Kidney / Q000473:pathology; D007678:Kidney Glomerulus / Q000503:physiopathology*; D008297:Male; D024821:Metabolic Syndrome / Q000139:chemically induced* / Q000473:pathology* / Q000503:physiopathology; D009399:Nephrons / Q000473:pathology; D009929:Organ Size / Q000187:drug effects; D051381:Rats; D017207:Rats, Sprague-Dawley; D012079:Renal Circulation / Q000502:physiology*; D014280:Triglycerides / Q000097:blood; D014527:Uric Acid / Q000378:metabolism
chemical_list: D014280:Triglycerides; D014527:Uric Acid; D005632:Fructose