Submitted to: Journal of Nutritional Biochemistry
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 12/29/2002
Publication Date: 4/1/2003
Citation: Reeves, P.G. 2003. Patterns of food intake and self-selection of macronutrients in rats during short-term deprivation of dietary zinc. Journal of Nutritional Biochemistry. 14:232-243. Interpretive Summary: Zinc deficiency tends to cause anorexia (reduction in food intake) in many species of animals, including humans. This phenomenon has been known for more than 50 years, but the biochemical mechanism that brings it about has eluded scientists. Numerous active peptides and other hormones involved in the regulation of food intake are known to be produced or destroyed by zinc-dependent enzymes. However, to date, there has been no clear evidence that zinc deficiency is affecting the activities of these enzymes to the point of affecting food intake. This study was designed to determine the food intake patterns and the selection patterns of dietary macronutrients (protein, carbohydrate, fat) in the early stages of zinc deficiency in hopes of shedding some light on the possible mechanism involved. In one experiment, minute-by-minute food intake was monitored during the development of zinc deficiency. The results showed that the intake patterns of the deficient rats did not differ from those of the control rats, only that the deficient rats ate less food than the controls. In another experiment, rats were offered a choice of three diets differing in contents of protein, fat, and carbohydrate during the development of zinc deficiency. This experiment showed that zinc deprived rats self-selected a diet that contained less protein and more carbohydrate than the zinc adequate rats. Based on studies by other scientists, these data suggest that an intestinal hormone called cholecystokinin that is regulated by dietary protein and degraded by a zinc-dependent enzyme might be involved.
Technical Abstract: Although it has been known for more than 50 years that zinc (Zn) deficiency regularly and consistently causes anorexia in many animal species, the basic mechanism(s) that causes this phenomenon still remains an enigma. The following studies describe feeding behavior in the early stages of zinc deficiency in the rat model. In one experiment, we used computerized feeding monitors that measured the intake of individual rats at 10-min intervals over each 24-hr period. Male rats were acclimated to the cages and fed a Zn-adequate egg-white-based diet, or a similar diet with <1.0 mg Zn/kg. Food intake was monitored for seven, consecutive 24-hr periods. The 24-hr food intake pattern of the Zn-deprived rats did not differ from the controls; they simply ate less food, mainly during the night hours, with no differences between groups during the day. Although Zn-deprived rats ate less food than controls, the percentage of total diet consumed during night and day did not differ between groups. In another experiment, we simultaneously offered male rats three isocaloric diets with different macronutrient compositions and with or without adequate Zn, and measured the amount of each diet selected during seven 24-hr periods. The three diets contained either 57% protein from egg white, 30% fat from soybean oil, or 80% carbohydrate from a combination of starch, hydrolyzed starch, and sucrose. For the first four days on experiment, rats selected similar amounts of each diet. Then the Zn-deprived rats began to select only 50% as much of the protein diet as the controls. Similar results were obtained when the data were expressed on the basis of each macronutrient as a percentage of the total diet selected. Zn-deprived rats selected a diet that contained 8% protein, 73% carbohydrate, and 6% fat while the Zn-adequate rats selected 12% protein, 69% carbohydrate, and 6% fat. Fat intake was not affected by Zn-deprivation. The results confirm our previous findings, and are discussed in terms of Zn-deprivation blunting the pathways of signal transduction that involve the peptide hormones known to affect food intake regulation.