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Protein-Energy Malnutrition Causes Deficits in Motor Function in Adult Male Rats
Mariam Alaverdashvili1, Xue Li2, Phyllis G Paterson2
1Neuroscience Research Group and College of Pharmacy and Nutrition, University of Saskatchewan, Saskatoon, Saskatchewan, Canada mariam.alaverdashvili@usask.ca.
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.
