Prolonged winter undernutrition and the interpretation of urinary allantoin:creatinine ratios in white-tailed deer

Abstract

The urinary allantoin:creatinine (A:C) ratio (expressed in micromoles of allantoin to micromoles of creatinine) has shown potential as an index of recent winter energy intake in preliminary controlled studies of elk ( Cervus elaphus ) involving mild condition deterioration (up to 11% loss of body mass). To ensure reliable nutritional assessments of free-ranging cervids by measuring A:C ratios of urine in snow, it is essential to extend this work. We assessed the effect of moderate and severe winter nutritional restriction on urinary A:C ratios of captive white-tailed deer ( Odocoileus virginianus ) that lost up to 32% body mass and related these ratios to metabolizable energy intake (MEI), body-mass loss, and other reported nutritional indicators. Deer in the control group were fed a low-protein, low-energy diet ad libitum, whereas deer in the treatment group were fed restricted amounts of the same diet. MEI was below the winter maintenance requirement for all deer, but was lower ( P = 0.029) in treatment deer than in control deer. Percent body-mass loss differed between the two groups as the study progressed, and represented the full range of physiological tolerance (0-32% loss). Mean A:C ratios of control deer, which lost up to 17.4% body mass, showed a slight increasing ( P = 0.086) trend, whereas initially similar A:C ratios of severely restricted deer increased ( P = 0.0002) markedly by the eighth week (0.52 vs. 0.09 µmol:µmol). The urinary A:C ratio was not related ( P = 0.839) to recent (2 days prior to urine sampling) MEI, but there was a marginally significant relation ( r 2 = 0.42, P = 0.110) between the A:C ratio and cumulative percent mass loss. The urinary A:C ratio was directly related to urinary urea nitrogen:creatinine ( r 2 = 0.59, P < 0.0001) and 3-methylhistidine:creatinine ( r 2 = 0.43, P < 0.0001) ratios. This study confirms that elevated and increasing A:C ratios may be due either to increasing energy intake or to accelerated tissue catabolism and increased endogenous contributions to urinary allantoin excretion.