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Influence of the Endocrine System on Growth and Development R 331. INFLUENCE OF THE ENDOCRINE SYSTEM ON GROWTH AND DEVELOPMENT R. J. GERRITS A. R. S., U. S. D. A. Introduction The field of endocrinology cannot be defined in a manner entirely acceptable to all biologists or animal scientists. This is understandable as there are many points of view and many voids in our knowledge in this area. It is very hard to give a precise definition for an endocrine gland because all cells possess some secretory capacity and therefore contribute to the internal environment of the organism. For the most part the term "hormone" is probably applied too loosely and to a great variety of unrelated substances. Hormones can be identified as chemical agents which are synthesized by circumscribed parts of the body, generally specialized ductless glands, and are carried by the circulatory system to another part of the body where they evoke systemic adjustments by acting on rather specific target tissues or organs (Turner, 1966). In general, hormones regulate many processes such as growth, regeneration, reproduction, blood chemistry, metabolic rate, etc. Hormones act on the organs and tissues of the body by regulating the rate of specific metabolic reactions without contributing much at all to the constituent cell. It can be said that ad- justments to hormone levels require duration rather than speed, as opposed to the rapid coordinations of the body that are controlled by the nervous system. These biochemical adjustments are accomplished at the cellular level by virtue of their power to augwnt or restrain special enzyme sys- tems. It is important that hormones be released at the right time and in the proper amounts of the normal organism if they are to accomplish their specific mission. Hormones are ineffective unless the target cells and tissues are capable of responding to them. While it is neaxly impossible to separate the neural and the hormonal components of regulatory processes, the complex system of endocrine glands in the vertebrates is quite clear. This system includes the pitui- tary, thyroid, parathyroid, adrends, gonads, pancreatic islets, and the hormone-producing part of the gastrointestinal tract. The material pre- sented in this paper will be limited to a very small segrnent of the endo- crine system and the effects on growth. More specifically, I will attempt to discuss in this paper some of the important influences that are exerted by the hormone somatotrophin (STH growth hormone). Also I will present some selected material on the effect of testosterone (as an endogenous hormone) and of melengestrol acetate (a synthetic hormone) on growth. Hormones of the adenohypophysis Seven hormones are known to have been released from the adeno- hypophysis, namely: somatotrophin ( STH or growth hormone) ; corticotrophin (ACTH) ; thyrotrophin (TSH) ; prolactin (lactogenic hormone or luteotrophin) ; follicle-stimulating hormone (FSH) ; luteinizing hormone (LH or interstitial cell-stimulating hormone) ; and melanophore-stimulating hormone (MSH) . All 332. of these hormones are proteins or peptides, and three of them (FSH, LH, and TSH) contain carbohydrate in addition to amino acids. Somatotrophin (STH) It has been well established that STH is secreted by the acidophil cells of the -pars distalis and that the principal action of growth hormone is on growth of bone and muscle. Growth hormones isolated from different species exhibit different physiochemical properties. The molecular weight of STH hormone ranges from 21,500 to 48,000 in man, pig, beef, and sheep. The growth hormones with lower molecular weights are more acidic thhn those with higher weights. Also, it is important to know that body growth response of STH hormone is different among the various vertebrates and that the rat responds to somatotrophin from numerous mammalian species. The most common test employed is the tibia test. After administration of the hor- mone, the increase in width of the proximal epiphyseal cartilage of the tibia of the hypophysectomized female rat or mouse is determined. STH pro- duces continuous growth and widens the cartilages in proportion to the amounts given. Mechanisms of hormone action There is a considerable amount of knowledge about the chemistry of hormones and their --in vivo and --in vitro effects. However, sufficient re- search, especially in vertebrates, has not been conducted to disclose fully how any hormone actually performs at the molecular level. Levine and Gold- stein (1955) and Smith --et al. (1961) have demonstrated that insulin promotes the transfer of glucose into the cells of certain tissues, such as muscle and fat. Three general points, each with varying modifications, have been proposed to explain the mechanisms of hormone action, namely: 1. Hormones exert a direct effect on intracellular enzyme systems. 2. Hormones act to control permeability relationships at the cell surface or elsewhere and hence indirectly control condition enzymic react ion. 3. Hormones may produce their effects directly by activating or suppressing particular genes. In our attempt to understand the mechanisms of hormone action we must refer to work that has been conducted with insects. Microscopic ex- amination of the giant chromosomes of chironomous larvae has shown that the administration of ecdysone causes a puffing of certain genes. The inference is that the activated genes (DNA) begin to synthesize specific RNA which is transferred to the cytoplasm where it acts as template for the synthesis of a particular protein, e.g., enzymes (Karlson, 1962). The work of Liao and Williams-Ashman (1962) suggests that certain vertebrate hormones may act in a similar manner. It will be most interesting to see how far this concept can be substantiated in processes other than development in mannals. 333. Biological action At one time it was assumed that STH had only an effect on general body growth, particularly the skeleton, and when extracts rich in STH pro- duced other action they were attributed to contaminating factors. There is now sufficient evidence to show that STH plays an important role in the metabolism of proteins, fats, and carbohydrates and also serves as a synergist to enhance the effects of other hormones. The effect of STH on protein metabolism Amino acids not utilized by animals are normally converted to urea and eliminated through the urine. It has been ably demonstrated that STH encourages the animal to retain amino acids which are the essential building blocks for protein and that the body weight increase normally observed after treatment with STH is an actual increase in tissue protein. Knobil (1961) states that one important aspect of STH action is to promote the transfer of extracellular amino acids across cell membranes, particularly into muscle cells. Milman and Russell (1950), Li --et al. (1949), and Luck --et al. (1954) have demonstrated that the administration of growth hormones lowers blood amino acid nitrogen. Swislocki and Szego (1965) also demonstrated this effect in hypophysectomized ad lib fed rats. In the later study blood-amino nitrogen (BAN) levels in the growth hormone treated rats were significantly lower than the controls at one and five hours after treatment with STH. In a recent study Beach and Kostyo (1968) showed that when rats were injected daily intraperitoneally with bovine growth hormone for seven days the amount of DNA in the muscles rectus femoris, gastrocnemius, pectoralis -'major and diaphragm was increased significantly. When STH was administered for one day it had no effect on the DNA of these muscles. However, following seven days of treatnmt, with the hormone, the amount of DNA in each of the muscles was markedly elevated. Since there was a con- comitant increase in muscle weight, the concentration of DNA in terms of micrograms per mg. of wet muscle was altered significantly. These data show that growth hormone can increase the amount of DNA in skeletal muscles of hypophysectomized rats. Thus, it seems reasonable to assume that the increase in muscle DNA which occurs during the normal course of growth in rats is dependent in some measure on pituitary growth hormone. Effect of STH on liDids metabolism The experiments of Welt and Wilhelmi (1950) suggested that growth hormone administration leads to a reduction of lipid synthesis. Their initial studies have subsequently been supported by several workers. Hypophysectomy retards the mobilization of depot fat and tends to ameliorate ketosis in the diabetic subject. STH encourages the movement of unesterified fatty acids from fat reserves, consequently decreasing body fat and increasing the lipid content of the blood plasma and live. In support of this, Swislocki and Szego (1965)showed that elevated levels of plasma nonesterified fatty acids occurred after the administration of growth hor- mones to hypophysectomized rats. 334. Effect of STH on carbohydrate metabolism The following general statements may be male regarding the action of STH on carbohydrate metabolism when administered to mammals (Turner, 1966) : 1. The hormone tends to produce hyperglycemia, thils aggravating diabetes. 2. It inhibits the action of insulin and insulin effect. 3. It increases muscle glycogen when given to hypophysec- tomized subjects. 4. It produces a permanent diabetes mellitis in certain species when given over prolonged periods. The latter effect probably results from the eventual destruction of the 8-cells of the pancreatic islets which secrete insulin. It has been shown that rats receiving excessive carbohydrates by tube feeding develop tem- porary diabetes when given STH. Studies on STH in meat animals Baird --et d. (1952) assayed the hypophysis of two strains of pigs selected for eight generations on the basis of rapid and slow rate of gain. The two strains reached ultimate size at significantly different ages. When the growth hormone content of the pituitary glands of the two strains was determined, it was found that at dl ages at which cornpaxisons were made the glands of the faster growing strain contained significantly more somatotro- phin per unit of gland tissue than did the glands of the slower growing strain.
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