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Food is of great role in human health. The best goal in this concept is variety in the diet and moderation. This hypothesis has been observed on bases of nutritional biochemistry. A single food, i.e., Phaseolus bean, was used at rates of 30, 50, and 100% replacements of the basal diet for aged rats. It was clear that the higher rate of morbidity and mortality due to this sort of malnutrition, or semistarvation, has been associated with some biological changes. Although beans are rich in containing proteins, the partial replacement of this plant food origin at 30% has shown to be a good help in keeping an optimal body weight (BW) of those aged animals, but any more degree of replacement has seen to be vital in affecting the animal health, hence 50% or over might resulted in animal death. It seemed that 25% may be useful in maintaining BW, meanwhile, a further rate of this plant origin replacement up to a specific level should be an effective way in treating obesity if used in a proper dietary system. In more details, organ morphologies and histopathological examination of some of which as spleen, brain, and liver are greatly affected by imbalanced diets. In another word, the metabolic differences rolled up by this sort of feeding negatively affected liver and brain expectancy or longevity. A number of tissues up normality, such as liver tissues dilatation and congestion of hepatoportal vessels, hepatocytes karyomegaly nuclei, congestion of central vein, and granular degeneration of hepatocytes with both most higher rates of replacement groups. Moreover, there were focal gliosis, pyknosis of neurons, brain edema, and hemorrhage in cerebrum and cerebellum in brain of the same groups. It is obvious that all these organ dysfunctions are frequently occurred as a response to these and similar kind of malnutrition, other than energy one, that has been existed for a long enough time. This weak homeostatic system has been shown as less control on the metabolic constants such as blood glucose (G), triglycerides (TG) and total cholesterol (TC). All those are most likely correlated with the organs subclinical defects mentioned before. It seems that this biological control that actually supported in the presence of balanced diet can be a biological up regulatory mechanisms, and the death eventually occurs due to a protein catabolic pathway due to a protein, the quality but not only quantity, malnutrition. It is an emergence metabolic system (EMS) that runs for longer time caused by a strengthen need for some micronutrients as well as high rate of nitrogenous metabolite accumulation. This protein turnover in such high rates beyond the biological capacity of both intracellular and extracellular compartments negatively affect the whole biological system including cells, tissues, organs, and eventually the blood chemistry as well. Refeeding with a proper system of animal high quality protein and some micronutrients might be vital. INTRODUCTION Food is of greatest role on human health. Food shouldn’t be judged in isolation, but in relation to the total diet and the individual’s needs (Guthre, 1993(1)). In selecting food moderation is a virtue. Moderate of calories and balanced 905 Bull High Inst Public Health Vol.37 No.4 [2007] nutrients are neckties to provide essential requirements. A 10 to 15% RDA calories from food of limited nutritional value is reasonable, more can lead to nutritional problems (Guthre, 1993)(1). Although the food production has markedly increased according to the world total production, several areas in this earth are suffering from food shortage. Understanding the biology of hunger might be one great step to rescue those people wherever they are. Biologically, however, with starvation progress and lean body (LB) mass decrease, both BMR and protein oxidation decrease. It has been very early to state that one of the most consistent autopsy findings of animal and human who died of pure starvation is the virtual absence of depot fat, both subcutancously and inernally (Keys et al., 1950)(2). In subjects ingesting hypocaloric diets, the effect of initial adiposity on protein turn over (PTO) and composition of N loss in relation to other confounding variables, e.g., composition of dieting, exercise, etc. is not fully understood. However, brain, gonads and skeleton appeared to be preferentially preserved (Elia, 1991, Forbes and Drenick 1979)(3,4). The biology of starvation stress has been explored at level of enzymes, hormones and genetics most recently (Harbison, et al., 2005(5); Mackay, 2005(6); Lee et al., 1999(7), Lee et al., 2000(8); Schadt et al., 2003(9); Teichert et al., 1989(10); Zinke et al., 2002(11); Nelson et al., 1995(12); and Seglen and Bohley 1992)(13). These studies involved man, animals, insects, and microorganisms. Moreover, relation between diet and hormonal balance was observed (Ahmed et al., 2003(14)). In this concern, Svanberg et al., (2000)(15) evaluated the effect of insulin like growth factor-I (rhIGF-I) in complex with binding protein 3 (IGFBP-3) compared to the effect of free IGF-I on muscle protein biosynthesis in undernourished animals. The female Sprague–Dawley rats (200 g) El-Dakak et al., 906 were initially semistarved in order to carry out this investigation. The rhIGFI/rhIGFBP-3 (SomatoKine) was a significant stimulator of muscle protein synthesis in chronically semistarved animals whereas IGF-I alone failed to increase protein synthesis during the same experimental conditions. This stimulation was because of increased initiation of translation, likely induced by more physiologic concentrations/kinetics of plasma IGF-I and amino acids following rhIGF-I/rhIGFBP-3 treatment, compared to IGF-I in its free form (Svanberg et al., 2000)(15). Likewise, the effects of dietary restriction on the kinetics of absorption in vivo of glucose, galactose and alphamethyl glucoside were assessed by electrical and chemical methods in the rat jejunum. Fasting for 3 days greatly decreased the apparent Kms obtained from electrical or chemical data for all the sugars but had no effect on those for Lvaline or L-methionine. Semistarvation caused a less pronounced reduction of the apparent Kms for the sugars. The dietaryinduced change in apparent Km for glucose was also observed in the fasted hamster. One interpretation of these changes is that the affinity of the carriers for sugars increases during dietary restriction, the greater the level of restriction the greater the increase . A standard diet obtained from two commercial sources was found to differ greatly in its effect on the electrogenic transfer system for alpha-methyl glucoside but had no effect on those for galactose and glucose (Debnam and Levin, 1975(16). From a metabolic point of view, previous work in humans and rats has revealed a link between perinatal growth retardation and glucose intolerance in adulthood. Both maternal semistarvation and severe diabetes are accompanied by 907 Bull High Inst Public Health Vol.37 No.4 [2007] perinatal growth retardation in rats. This study compared the effect of these conditions on tissue glucose uptake in their female offspring. Glucose uptake was measured as glucose metabolic index (GMI), using 2-deoxy[1-3H]-glucose, in the postabsorptive state and during euglycemic hyperinsulinemia (Holemans, et al., 1997)(17). The GMI was measured in insulin-sensitive tissues, e.g., skeletal muscles, diaphragm and white adipose tissue and in two noninsulin-sensitive tissues such as duodenum and brain of adult offspring of normal dames. Dames rendered diabetic with streptozotocin on d 11 of pregnancy, and dames fed halfnormal rations from d 11 of pregnancy. Whole-body insulin resistance, measured by decreased glucose infusion rate during hyperinsulinemia was milder in offspring of semistarved rats (O-SR) than in offspring of diabetic rats (O-DR) (Holemans, et al, 1997(17)). The basal GMI did not differ among the three groups in any tissue except tibialis anterior; during hyperinsulinemia, GMI was significantly greater in the insulin-sensitive tissues of all three groups. GMI of skeletal muscles and adipose tissue during hyperinsulinemia did not differ between control rats and O-SR; in contrast, the GMI was 25-50% lower in skeletal muscles of O-DR during hyperinsulinemia than in those of control rats or O-SR. Thus, maternal semistarvation and diabetes have dissimilar effects on peripheral insulin sensitivity of the adult female offspring. Because both conditions are associated with perinatal growth retardation and fetal hypoinsulinemia, other mechanisms must be identified to explain impaired glucose uptake by skeletal muscles in the offspring of diabetic rats (Holemans, et al., 1997)(17). The other mechanisms must be identified to explain impaired glucose, or any other nutrient, uptake by skeletal muscle upon semistarvation or some sort of diabetes is what so called the El-Dakak et al., 908 emergence metabolic system of a protein catabolic status (EMS). To put it more clear, some biological factors other than loosing weight or factor other than the shift in base metabolic ratio (BMR) may posses the main reason to death. The other metabolites that deviated with sever reduction in energy were the elevation of some blood parameters (Ahmed et al., 2006)(18). More accurate investigation is conducted to biologically explore this metabolic conjugation. It is clear that this emergence catabolic status of proteins ECS saves the animals, but its existence for longer time may posses a reverse effect. In another word, this ECS is a sort of hormonal oxidative imbalance, which abuses the biological system at the long run(18). Here, Attkin’s diet, as a reverse condition to starvation, may be used as a suitable answer for such scientific confusion. Here, we are observing the metabolic changes in conjugation with consuming imbalanced diet for longer run in order to figure out the real metabolic complication that lead to death. One m

Nutritional Biochemistry of Imbalanced Dietary Systems in Rats