mortality when gerbils were restricted for long periods to dry-type diets without water or succulent feeds such as carrots or lettuce. Thus free access to water and/or succulent feeds should be provided when dry diets are used (Marston and Chang, 1965; Rich, 1968; McManus, 1971; Mele, 1972; Norris and Adams, 1972). Gerbils will voluntarily consume 4 to 10 mL water/100 g BW/day (Winkelman and Getz, 1962; Harriman, 1969; McManus, 1972). Total daily water intake (including free water in food and metabolic water) has been estimated as 8 to 13 percent of body weight (McManus, 1972; Holleman and Dieterich, 1973).
Purified diets fed to gerbils have contained 2 to 20 percent fat (Zeman, 1967; Arrington, 1968; Harriman, 1969; Arrington et al., 1973; Hegsted et al., 1973; Kroes et al., 1973; Hegsted et al., 1974), but the growth response to variation in dietary fat per se has not been quantitated. No minimum requirements for fat and essential fatty acids have yet been determined, although gerbils have been maintained for prolonged periods on purified diets containing as little as 1 to 2 percent of metabolizable energy from 18:2 [Pronczuk et al., 1994 (in press)].
Although the gerbil can convert linoleic acid to arachidonic acid, arachidonic acid is minimally present in plasma cholesterol esters and comparatively low in the body fat of the gerbil. The body fat of gerbils is higher in oleic and palmitic acid than is the body fat of rats (Gordon and Mead, 1964).
The gerbil responds to high-fat, high-cholesterol diets with increased HDL- and LDL-cholesterol concentrations, especially when diets contain casein, and may prove to be a useful model for the study of cholesterol metabolism (Nicolosi et al., 1976; Forsythe, 1986; DiFrancesco and Mercer, 1990). High dietary cholesterol leads to excess deposits in several body organs but not in arteries. However, older breeder animals fed natural-ingredient diets show spontaneous arteriosclerosis (Gordon and Cekleniak, 1961; Wexler et al., 1971; D'Elia et al., 1972).
Weight gains of 1 g/day were obtained when weanling gerbils (18 g) were fed purified diets containing 16 percent or more protein, but weight gains were lower (0.6 to 0.8 g/day) when the gerbils received diets containing 12 to 14 percent protein (Arrington et al., 1973). Young gerbils (38 g) fed purified diets with 13 percent protein as casein gained only 0.69 g/day as compared to gains of 0.81 to 0.88 g/day when fed 17 to 25 percent protein (Hall and Zeman, 1968). Based on these studies, the protein requirement of growing gerbils seems to be about 16 percent when dietary fat is 2 to 5 percent.
Little specific information is available on amino acid requirements of gerbils. However, purified diets based on amino acids have been fed to gerbils with mixed success (Otken and Garza, 1983). Gerbils fed an amino acid-based purified diet had greatly improved growth when taurine was added to the diet at a concentration of 4.5 g/kg (36 mmol/kg) (Otken et al., 1985). Taurine added at concentrations of 7 g/kg diet (60 mmol/kg diet) resulted in lower growth rates.
The amounts of minerals in natural-ingredient rodent diets commonly fed to gerbils (e.g., Table 2-3) are apparently sufficient to meet the needs of gerbils. In the absence of specific data on the requirements of gerbils, the recommended dietary concentrations of calcium (5.0 g Ca/kg diet) and phosphorus (3.0 g P/kg diet) are the same as for the rat (Table 2-2).
A low incidence (≤2 percent) of convulsive seizures, especially in response to handling, environmental change, or other stimulation, has been noted in many gerbil colonies (Marston and Chang, 1965; Zeman, 1967; Thiessen et al., 1968; Harriman, 1974; Loskota et al., 1974; McCarty, 1975). Gerbils fed a low-magnesium, purified diet had an elevated susceptibility to seizure in a novel environment; the seizures were eliminated when magnesium was added to the diet at 1.39 g/kg (Harriman, 1974). Gerbils fed purified diets low in calcium, sodium, or vitamin B6 did not have seizures. Gerbils develop some degree of alopecia when fed purified diets containing ≤1.0 g Mg/kg, with the severity related to the extent of magnesium deprivation. Alopecia became noticeable after 14 days when dietary magnesium was less than 0.12 g/kg, and a mortality rate of 70 to 83 percent occurred within 40 days when magnesium was 0.06 to 0.12 g/kg diet. A dietary concentration of 0.25 g Mg/kg prevented weight loss and death (A. E. Harriman, 1976, Oklahoma State University, personal communication). These results indicate a dietary magnesium requirement of ≥1.0 g/kg diet. A dietary concentration of 1.5 g/kg is recommended. This is higher than the requirement of the rat.