The reported studies were designed to examine relationships between central nervous system histamine, histaminergic receptors (H1) and food intake in rats. The hypothesis being tested was as follows: "One component of the neuroregulation of food intake involves histaminergic activity in the hypothalamus as influenced by variation of histamine levels and/or H1 receptor concentrations." We performed combinations of dietary, surgical and pharmacological treatments on male or female rats. We fed groups of male or female rats diets containing either 4 g casein/100 g diet (low protein diet) or 25 q casein/100 g diet (normal protein). Rats with surgical ablation of the paraventricular nucleus did not decrease food intake when fed the low protein diet, whereas adrenalectomized rats did. Increasing central histamine levels decreased food intake, whereas decreasing central histamine increased food intake. Rats injected with histaminergic (H1) antagonists lost the ability to detect low protein diet in short-term experiments and had improved efficiency of weight gain. Rats that were fed the low protein diet or pair-fed the normal protein diet had greater H1 receptor concentrations in whole brain preparations when compared with rats fed the normal protein diet. No differences were noted due to gender. Thus, manipulation of histamine levels affected food intake as hypothesized, i.e., increasing central histamine decreased food in rats fed the normal protein diet, whereas decreasing central histamine or blockade of H1 receptors increased food intake in rats fed the low protein diet.
The Saturation Kinetics Model (SKM) is useful in describing many physiological responses as functions of a limiting dietary nutrient. However, as nutrients are fed at higher dietary concentrations, responses become inhibited and diminish from their usual plateaus. By adding an inhibition constant (Ks) to the SKM in a manner consistent with substrate inhibition (based on enzyme kinetics), it becomes possible to predict the inhibited portions of the nutrient-response curve. To test this, rats were fed diets of graded levels of casein (0-75%) or lysine (0-6.2%), and weight gains and food intakes were measured daily for up to 2 wk. The inhibition form of the SKM was able to predict the complete response range of each experiment, producing a Ks (weight gain) at a dietary level of 50.60% for casein and 7.56% for lysine. It was also possible to set up an upper and lower dietary nutrient concentration that encompassed the 100% response range for each response, thereby giving an inhibition or toxicity index of 2.02 for casein and 4.98 for lysine. This index allows one to set nutritional requirement levels precisely, optimizing responses without moving into inhibiting or toxic ranges of nutrients. Based on growth response curves, requirements were 25.61% for casein and 1.97% for lysine.
The reported studies were designed to examine relationships between whole-brain histamine receptors (H1) and food intake in male Sprague-Dawley rats. Three different experiments were conducted. In each experiment, control rats were fed normal protein (25 g casein/100 g food) and normal metabolizable energy (16.21 kJ/100 g food) diets. Feeding low protein diets (1 g casein/100 g food) elevated central H1 receptor concentrations (P < 0.0027) and reduced voluntary food intake (P < 0.007) compared with normal diets. Feeding low energy diets lowered H1 receptor concentrations (P < 0.0089) and increased voluntary food intake (P < 0.0012). Low quality protein diets also affected the central nervous histaminergic system. Whole-brain H1 receptor concentrations were significantly higher for rats fed low quality protein (25 g gelatin/100 g food) compared with rats fed casein (P < 0.0001). Rats fed medium quality protein (25 g wheat gluten/100 g food) or low quality protein ate significantly less food (P < 0.0001). In all experiments, dietary manipulation affected central histamine receptors. Elevated concentrations of H1 receptors were associated with a decrease in food intake whereas lowered concentrations of H1 receptors were associated with an increase in food intake (P < 0.001). The results of these experiments support the hypothesis that central histamine H1 receptor concentrations in male rats are inversely correlated with voluntary food intake and affected by dietary composition.
The objective of this study is to propose new methods for the determination of biological efficiency (the ability of a nutrient to produce a response) and for comparison of the efficiencies of alternate nutrient sources. The proposed methods are based on a four-parameter kinetic model which describes response as a function of intake. The comparison of the abilities of two proteins (casein and soybean protein concentrate) to promote weight gain in weanling rats is presented as an example; however, the model is also useful for other nutrients (proteins, amino acids, vitamins, minerals, etc.) and other responses (blood enzyme or protein levels, tissue enzyme levels, etc.). Application of the method leads to useful comparisons of nutrient sources as well as information concerning the maximum efficiencies and rates of nutrient utilization from different sources.
Male, weanling Sprague-Dawley rats were fed isocaloric diets containing graded levels of protein or amino acid mixtures. Food intakes and weight gains were recorded daily or every other day. Both short-term and long-term (64 days) experiments were carried out. Linear regressions of food intake versus time and weight gain versus time were used to establish daily weight gains and food intakes. The four-parameter mathematical model for physiological responses was used to predict daily food intake, daily weight gain, daily food intake per 100 g weight and efficiency of food conversion (daily weight gain/daily food intake) as functions of dietary protein concentration. The changes in the four parameters generated from the four-parameter model were examined as a function of time. Several aspects of food intake, weight gain and efficiency were shown to be functions of concentration of dietary protein.
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