Prevention of hyperphagia delays onset of renal degeneration in female obese zucker tfalfa rats

M. D. Gades, P. R. Johnson, G. A. Kavsen, B. A. Horwilz, Judith S Stern

Research output: Contribution to journalArticlepeer-review

2 Scopus citations


In humans, end stage renal disease is a major complication in diabetes and hypertension, and it is the primary cause of death in obese Zucker rats. Hyperlipidemia is thought to be causative. We tested the hypothesis that prevention of hyperphagia would modify the course of renal disease in female obese (falfa) Zucker rats. Ten obese female Zucker rats were studied: 5 were pair fed (PF) (restriction -28%) to lean controls from 7 to 20 wies of age, the period of maximal hyperphagia relative to leans; 5 were fed ad libitum (AL). All rats were fed AL from 20 to 33 wks of age. Urinary albumin excretion (UAE) A plasma triglycéride (TO) follow. PF reduced UAE at all rimes. Age (wks) 10 20 25 29 33 UAE (mg/24 hr) PF 0475 0.608 4.28 766 144 AL 20.1 216 338 371 311 Plasma TG (mg/dl) PF 124 397 - 1279 - AL 362 3233 - 4923 - UAE reached nephrotic range by 25 wks in AL. Hypertriglyceridemia preceded the onset of significant UAE. Plasma cholesterol was unaffected by PF and therefore not responsible for renal damage (data not shown). Food restriction in obese female Zucker rats for the 13 wks of maximal hyperphagia reduces TO levels, and both delays the onset and reduces the magnitude of UAE by 16 wks. Hypertriglyceridemia may play a role but cholesterolemia does not. (AG/DK 09945, DK 35747, T32 DK 07355).

Original languageEnglish (US)
JournalFASEB Journal
Issue number3
StatePublished - 1996
Externally publishedYes

ASJC Scopus subject areas

  • Agricultural and Biological Sciences (miscellaneous)
  • Biochemistry, Genetics and Molecular Biology(all)
  • Biochemistry
  • Cell Biology


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