title: Severe dietary restriction initiated in aged rats: evidence for poor adaptation in terms of protein metabolism and intestinal functions.
abstract: BACKGROUND
  Protein energy malnutrition is a common finding in elderly people, increasing morbidity and mortality in aged inpatients. Investigations need to be developed to counteract malnutrition-induced alterations early and to avoid potential irreversible lesions. The aim of this experimental study was to evaluate time-response to severe dietary restriction (DR) initiated in aged rats in terms of protein metabolism and digestive trophicity.
  
  
  METHODS
  After the acclimatization period, 22-month-old male rats were randomized into six groups: three control groups, fed ad libitum for 3, 6 or 12 weeks with a standard diet and three corresponding dietary-restricted groups fed for the same periods with only 50% of the spontaneous intake. Intestinal mucosa, liver and skeletal muscles (soleus, extensor digitorum longus and tibialis anterior muscle) were removed when the rats were killed.
  
  
  RESULTS
  DR induced dramatic body weight loss (up to 50% of initial body weight after 12 weeks DR). Protein metabolism was affected in terms of nitrogen balance (P < 0.01) and protein content, in particular at the splanchnic level. Morphometrically, the intestine structure was altered after 12 weeks of DR (P < 0.01), and this atrophy was correlated with malabsorption of mannitol (P < 0. 01). Ileal hydrolase activities were decreased throughout the 12 weeks of DR.
  
  
  CONCLUSIONS
  Aged rats clearly exhibit a defect of adaptation to long-term DR initiated at an advanced age. Severe DR leads to malnutrition, which becomes of major importance after 12 weeks, in particular at the intestine level. Hence, application of these experimental results to elderly, malnourished people may contribute to a better knowledge of denutrition-induced disorders.
authors.affiliation: Laboratory of Biochemistry, Molecular Biology and Nutrition, Pharmacy School, CRNH, Clermont-Ferrand, France.
authors.forename: C
authors.initials: C
authors.lastname: Chambon-Savanovitch
authors.forename: C
authors.initials: C
authors.lastname: Felgines
authors.forename: M C
authors.initials: MC
authors.lastname: Farges
authors.forename: P
authors.initials: P
authors.lastname: Pernet
authors.forename: J
authors.initials: J
authors.lastname: Cézard
authors.forename: F
authors.initials: F
authors.lastname: Raul
authors.forename: L
authors.initials: L
authors.lastname: Cynober
authors.forename: M P
authors.initials: MP
authors.lastname: Vasson
mesh_terms: D000375:Aging / Q000502:physiology*; D000818:Animals; D001835:Body Weight; D004044:Dietary Proteins / Q000378:metabolism; D004063:Digestion; D002149:Energy Intake; D007413:Intestinal Mucosa / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology*; D043322:Lactase; D007792:Lactulose / Q000652:urine; D008099:Liver / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology*; D008297:Male; D008353:Mannitol / Q000652:urine; D008762:Methylhistidines / Q000652:urine; D018482:Muscle, Skeletal / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology*; D009748:Nutrition Disorders / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology*; D009929:Organ Size; D011506:Proteins / Q000378:metabolism*; D051381:Rats; D017207:Rats, Sprague-Dawley; D013393:Sucrase / Q000378:metabolism; D001616:beta-Galactosidase / Q000378:metabolism
chemical_list: D004044:Dietary Proteins; D008762:Methylhistidines; D011506:Proteins; D008353:Mannitol; D007792:Lactulose; D043322:Lactase; D001616:beta-Galactosidase; D013393:Sucrase; C028118:3-methylhistidine