title: Protein-Energy Malnutrition Causes Deficits in Motor Function in Adult Male Rats.
abstract: BACKGROUND
  Adult protein-energy malnutrition (PEM) often occurs in combination with neurological disorders affecting hand use and walking ability. The independent effects of PEM on motor function are not well characterized and may be obscured by these comorbidities.
  
  
  OBJECTIVE
  Our goal was to undertake a comprehensive evaluation of sensorimotor function with the onset and progression of PEM in an adult male rat model.
  
  
  METHODS
  In Expt. 1 and Expt. 2, male Sprague-Dawley rats (14-15 wk old) were assigned ad libitum access for 4 wk to normal-protein (NP) or low-protein (LP) diets containing 12.5% and 0.5% protein, respectively. Expt. 1 assessed muscle strength, balance, and skilled walking ability on days 2, 8, and 27 by bar-holding, cylinder, and horizontal ladder walking tasks, respectively. In addition to food intake and body weight, nutritional status was determined on days 3, 9, and 28 by serum acute-phase reactant and corticosterone concentrations and liver lipids. Expt. 2 addressed the effect of an LP diet on hindlimb muscle size.
  
  
  RESULTS
  PEM evolved over time in rats consuming the LP diet. Total food intake decreased by 24% compared with the NP group. On day 28, body weight and serum albumin decreased by 31% and 26%, respectively, and serum α2-macroglobulin increased by 445% (P < 0.05) in the LP group compared with the NP group. Forelimb dysfunction (173% increase in adaptive flexed-arm-hang score) developed on day 2 in rats fed the LP diet (P < 0.001), whereas abnormal walking (34% decreased incidence of correct hindlimb placement) developed by day 27 (P < 0.05). Relative to the NP diet, the LP diet reduced the cross-sectional area of gastrocnemius medialis (P < 0.05).
  
  
  CONCLUSIONS
  PEM in adult male rats causes a variety of sensorimotor abnormalities that develop at different stages of malnutrition. This model can be used in combination with disease models of sensorimotor deficits to examine the interactions between nutritional status, other treatments, and disease progression.
authors.affiliation: Neuroscience Research Group and College of Pharmacy and Nutrition, University of Saskatchewan, Saskatoon, Saskatchewan, Canada mariam.alaverdashvili@usask.ca.
authors.forename: Mariam
authors.initials: M
authors.lastname: Alaverdashvili
authors.affiliation: Neuroscience Research Group and College of Pharmacy and Nutrition, University of Saskatchewan, Saskatoon, Saskatchewan, Canada.
authors.forename: Xue
authors.initials: X
authors.lastname: Li
authors.affiliation: Neuroscience Research Group and College of Pharmacy and Nutrition, University of Saskatchewan, Saskatoon, Saskatchewan, Canada.
authors.forename: Phyllis G
authors.initials: PG
authors.lastname: Paterson
mesh_terms: D000818:Animals; D001835:Body Weight; D003345:Corticosterone / Q000097:blood; D018753:Diet, Protein-Restricted; D004044:Dietary Proteins / Q000008:administration & dosage; D005552:Forelimb / Q000503:physiopathology; D008297:Male; D009043:Motor Activity; D018482:Muscle, Skeletal / Q000503:physiopathology; D011502:Protein-Energy Malnutrition / Q000503:physiopathology*; D051381:Rats; D017207:Rats, Sprague-Dawley; D012709:Serum Albumin / Q000378:metabolism; D000511:alpha-Macroglobulins / Q000378:metabolism
chemical_list: D004044:Dietary Proteins; D012709:Serum Albumin; D000511:alpha-Macroglobulins; D003345:Corticosterone
keywords: acute-phase reactants; motor function; performance-based measures; protein-energy malnutrition; rat model