Increase In Total Body Weight Research Articles

Serum prostate specific antigen, sex hormone binding globulin and free androgen index as markers of pubertal development in boys

Prostate specific antigen (PSA) expression in the prostate gland is regulated by androgens. Serum levels of PSA are undetectable by routine assays in normal boys. Measurable values could serve as a marker for pubertal development. In order to explore this question, we measured serum PSA levels in normal boys throughout puberty and examined the interrelationships with various hormonal and physical developmental changes. Sera from 77 normal boys in Tanner stages I to V (T-I to T-V) were analysed for PSA levels by a sensitive time-resolved fluoro-immunometric assay (sensitivity: 0.012 microgram/l). In addition, sex hormone binding globulin (SHBG), insulin like growth factor I (IGF-I), IGF binding protein 3(IGFBP-3) and testosterone were measured. PSA was detectable in 0% of Stage T-I (n = 16), 33% of T-II (n = 18), 65% of T-III (n = 17) and 100% of T-IV (n = 10) and T-V (n = 16) boys. PSA levels rose significantly according to stage (P < 0.05). Also, there were significant (P < 0.05) increments in serum testosterone, IGF-I and IGFBP-3 levels from stages T-I to T-IV. PSA showed a positive correlation with testosterone (r = 0.86, P < 0.001), IGF-I (r = 0.66, P < 0.001), and IGFBP-3 (r = 0.34, P = 0.004) levels. Both PSA and these analytes, however, showed significant overlap between stages T-I and T-II with only 6/18 (33%) and 12/18 (66%) of T-II subjects having PSA and testosterone levels, respectively, above the T-I range. In contrast, serum SHBG levels decreased markedly from stages I to II (P < 0.001). At the calculated best cut-off point for SHBG of 50 nmol/l, 16/18 T-II subjects had values below the T-I range (sensitivity = 89%). Because of this decrement of SHBG and the increasing testosterone secretion in early puberty, the Free Androgen Index (FAI = Testosterone/SHBG) could even better differentiate the onset of puberty with all except one of the T-II subjects having FAI levels above the T-I range (sensitivity = 94.4%). The decrease of SHBG in T-II subjects coincided with an increase in total body weight (P = 0.001) and body mass index (BMI, P = 0.0003). Despite the continuing pubertal rise in testosterone, SHBG levels showed a rebound increment from T-II-T-III subjects (P = 0.02) with a concomitant decrease in BMI (P = 0.0014). Prostate specific antigen closely reflects serum free androgen activity during puberty. However, it was unable to differentiate the earliest pubertal development. In comparison, SHBG levels and Free Androgen Index are more sensitive markers for the onset of puberty in boys. The inverse association between SHBG levels and BMI in pubertal stages Tanner stages, I to III suggests that body fatness, via its effect on insulin sensitivity, may play an important role in the regulation of SHBG production during early pubertal development.

Systemic treatment with epidermal growth factor causes organ growth concomitant with reduced circulating levels of IGF-I and IGFBP-3: time-dependent changes in female rats

Systemic treatment with epidermal growth factor (EGF) in neonatal rats reduces circulating levels of insulin-like growth factor I (IGF-I) and causes somatic growth retardation. In this study, we investigated the effects of EGF treatment on the IGF system and on visceral organ growth and longitudinal growth in mature rats. We treated female Wistar rats for 0 (n = 16), 1 (n = 8), 2 (n = 8), 3 (n = 8), or 4 (n = 8) weeks with subcutaneous EGF (150 microg/kg/day). The animals were weighed once a week. At sacrifice, various viscera were removed and weighed. Blood and serum samples obtained at sacrifice were analysed for growth hormone (GH), IGF-I, IGF binding proteins (IGFBPs) and various routine parameters. EGF treatment increased the total body weight. All parts of the gastrointestinal tract, the liver, the pancreas, the spleen, the bladder, the suprarenal glands and the ovaries increased proportionately more in weight than the increase in total body weight; the heart and the kidneys increased proportionately in weight whereas the weight of the perirenal fat was reduced. There were no changes in tail length but the mean length of the tibia was slightly increased in the group treated for 4 weeks with EGF. Circulating GH was unchanged but IGF-I and IGFBP-3 were reduced approximately 25 and 45%, respectively, in all EGF treated groups. There were no changes in the hepatic content of IGF-I and IGFBPs. In conclusion, systemic EGF treatment causes visceral growth concomitant with reduced circulating levels of IGF-I and IGFBP-3 in mature female rats.

Effects of orthotopic liver transplantation on body composition.

The effects of orthotopic liver transplantation on body composition are unclear. We aimed to assess changes in body composition after transplantation using dual energy x-ray absorptiometry and total body potassium. Dual energy x-ray absorptiometry and total body potassium counting to assess muscle mass were performed in 55 patients before and up to 24 months after liver transplantation and the results expressed as paired data before and at time intervals after transplantation. The results showed that total body weight fell by 3.6 +/- 1.3 kg (p < 0.02) at 1 month, with a maximal fall in lean tissue mass at 2-5 months of 4.8 +/- 1.2 kg (p < 0.003). Thereafter, no change in lean tissue mass was recorded, although there were increases at 12 and 24 months of total body weight (11.5 +/- 2.4 kg, 7.8 +/- 3.1 kg; p < 0.03, respectively) and fat mass (12.9 +/- 2.2 and 10.5 +/- 2.7 kg; p < 0.003). A fall in total body potassium was seen at 1 month (118 +/- 12 mmol; p < 0.003) and 2-5 months (176 +/- 9.9 mmol; p < 0.03), which mirrored the fall in lean mass. After liver transplantation there is an initial fall in body weight due to a loss of lean mass. Lean mass does not recover after transplantation, although there is an increase in fat mass that leads to the observed increase in total body weight.

Evidence for retarded kidney growth in sudden infant death syndrome.

The aim of the study was to compare the growth rate of the kidneys of infants who died of sudden infant death syndrome (SIDS) and control babies under 1 year; 227 infants who died in St. Petersburg from 1983 to 1990 and who met the criteria for SIDS were included in the study; 138 infants who died suddenly of respiratory infections within the same period constituted a control group. The infants did not have signs of dehydration, malformations, tumours or intrauterine infections. Morphologically the kidneys were intact. Factors which might influence the weight of the kidneys at the time of death were: the cause of death (whether SIDS or not), gender, gestational age, weight, length and ponderal index at birth, age, weight and length at death. Stepwise (forward) linear regression analysis identified three variables which in combination most accurately and independently influenced the predicted weight of the kidneys. These were the cause of death, gender and weight at the time of death. The weight of the kidneys increased by 6.0 g for each increase in total body weight of 1,000 g [95% confidence interval (CI) 5.0-7.0 g], in boys the kidney weight was 3.3 g (95% CI 1.6-5.0 g) higher than in girls and in the SIDS babies kidney weight was 2.5 g (95% CI 0.8-4.2 g) less than controls. Delayed kidney growth may be an indicator of increased risk of SIDS in infants under 1 year and may contribute in some cases.

Retarded heart growth in the victims of sudden infant death: possible implications for lethal mechanisms.

The study was aimed to compare the weight of the heart at death in infants who died of sudden infant death (SID) and in control infants under 1 year old. The study included 227 infants who died in St. Petersburg in 1983 to 1990 and who met the criteria of SID. One hundred and thirty-eight infants who died within 24 h out of hospital of defined respiratory infections within the same period of time constituted a control group. Infants with signs of malformations, tumours, and intrauterine infections were excluded from the study. A linear regression model was used in data analysis. No statistically significant association was found between the weight of the heart by the time of death and the following variables: gender, birth weight and length, ponderal index at birth, gestational age, calendar age at death, and length at death. Two variables which significantly influenced the heart weight and entered the linear regression model were infant's weight by the time of death and the cause of death (whether SID or not). No statistically significant interaction was found for these two parameters. It was found that each increase in total body weight by 1000 g brought with it an increase in the heart weight by 4 g (95% CI = 3.6-4.4); for the SID babies, the weight of the heart was less than for the control ones by 1.6 g (95% CI = 0.3-2.9 g). Retarded heart growth may lead to functional disturbances and may contribute to possible mechanisms in some SID cases.

Hypertension induced by high salt intake in absence of volume retention in reduced renal mass rats

Reduction of renal mass (RRM) combined with a high-salt diet results in volume retention, a rise of cardiac output, and hypertension. The present studies were designed to determine whether prevention of volume retention would alter the rise of mean arterial pressure (MAP) in RRM rats given high salt. Rats were studied in a modified metabolic cage to permit continuous determination of total body weight (TBW). In group 1, NaCl was increased from 1 to 14.5 meq/day and delivered isotonically. In group 2, NaCl was increased while TBW was servo-controlled to a constant level. Group 3 was also servo-controlled, but rats received an intravenous infusion of an arginine vasopressin V1 antagonist throughout the study. MAP in group 1 rose 24 mmHg by day 4 of high salt with a parallel increase of TBW of 26 g. In group 2, MAP rose 48 mmHg by day 4 of high salt, while TBW was controlled to within 0.6% of control body weight. With inhibition of vasopressin V1 receptors (group 3), MAP rose 39 mmHg. Nearly equivalent amounts of NaCl were retained in all groups, which was associated with no change of plasma Na in group 1 but an increase of nearly 7 meq/ml in groups 2 and 3. Hematocrit fell nearly 9% in groups 2 and 3 compared with a 4% reduction in group 1. The results suggest that under conditions where net retention cannot occur, high salt intake increases MAP by an osmotically driven fluid transfer from cells, which results in an even greater expansion of blood volume.(ABSTRACT TRUNCATED AT 250 WORDS)

Role of blood volume expansion in Dahl rat model of hypertension

Continuous measurement and servo control (SC) of total body weight of unrestrained rats were used to investigate the role of volume expansion in the development of hypertension in Dahl salt-resistant (SR) and Dahl salt-sensitive (SS) rats. A change in sodium intake from 1 to 20 meq/day was associated with an increase in total body weight of 7.2% in both SS and SR rats over 96 h. Plasma sodium (pNa) increased from 145.0 to 147.4 meq/l in both SS (n = 10) and SR (n = 10) rats. Only in the SS rats was the volume expansion associated with an increase in arterial pressure of 27 +/- 3 mmHg. Prevention of the volume expansion by SC blocked the rise in arterial pressure in the SS rats (n = 10) but increased pNa from 143.5 to 152.4 meq/l. Hematocrit fell from 36.6 to 27.5% in both non-SC groups but decreased less in SC groups (35.7 to 32.0%). Plasma volume expansion from 17.6 +/- 0.6 to 25.2 +/- 0.8 ml in non-SC rats was greatly blunted by SC. In non-SC rats, SS (n = 10) and SR (n = 9) rats an increase in salt intake was associated with a rise in cardiac output from 413 +/- 6 to 507 +/- 12 ml.min-1.kg-1 in both groups. These results indicate that fluid retention is required to trigger the rise of pressure in Dahl SS rats.

Verapamil ameliorates clinical, pathologic and biochemical manifestations of experimental chagasic cardiomyopathy in mice

The influence of long-term verapamil administration on the consequences of Trypanosoma crud infection in mice was studied with regard to animal mortality, morbidity, myocardial pathologic features and myocardial beta-adrenergic adenylate cyclase activity. Verapamil administration dramatically decreased the mortality rate from 60% to 6% during the 70 day period of infection. Three clinical stages of infection were evident. In the acute stage (17 days after infection with maximal parasitemia), verapamil treatment not only decreased the incidence of myocardial disease (fibrosis and inflammation), but also protected myocardial beta-adrenergic adenylate cyclase activity. In addition, there was no increase in total body weight, which was regarded as an index of right-sided heart failure. In the subacute stage (30 to 60 days after infection), administration of verapamil continued to decrease myocardial disease and preserve beta-adrenergic adenylate cyclase activity. In addition, verapamil ameliorated the morbidity and mortality associated with this stage of infection.The chronic stage of infection was characterized by a decrease in myocardial disease and in beta-adrenergic adenylate cyclase activity. Thus, independent of the state of infection, long-term verapamil treatment enhanced betaadrenergic adenylate cyclase activity. In addition, verapamil ameliorated the morbidity associated with infection. Although the relation among these various effects of verapamil in the setting of T. cruziinfection remains to be determined, collectively the results suggested that verapamil administration attenuated the consequences of T. cruziinfection.

Role of Vasopressin in Regulation of Sodium Excretion

It has been proposed that arginine vasopressin (AVP) contributes to the regulation of renal sodium excretion by direct intrarenal actions, by neural-hormonal interactions, and via secondary effects of fluid volume retention. The present studies were designed to determine the extent to which the natriuretic effects of AVP are secondary to volume expansion. Three groups of dogs were studied: the first was infused with AVP for 2 weeks in amounts that increased plasma levels from 3 to 15 pg/mL, while water intake was maintained constant by intravenous (iv) water infusion. The second group received the same amount of AVP and was permitted to drink ad libitum. The third group was infused with the same amount of AVP, while total body weight and volume were maintained at a constant level by use of an electronically servo-controlled water infusion system. The results showed a large increase in total body weight (+1.5 kg) and arterial pressure (mean arterial pressure (MAP); +40 mm Hg) in dogs receiving a fixed water intake. This was accompanied by a continuing natriuresis over a 2-week period and severe hyponatremia (115 mEq/L). Dogs allowed ad libitum drinking retained much less fluid (+0.5 kg). MAP was not significantly elevated, and natriuresis did not occur in this group, but hyponatremia was observed (130 mEq/L), and plasma renin activity (PRA) was suppressed. Servo-controlled dogs exhibited no change in MAP, plasma sodium, or PRA, and only a small (-15 mEq) natriuresis occurred on day 1 of AVP infusion.(ABSTRACT TRUNCATED AT 250 WORDS)

Decreased urea synthesis in cafeteria-diet-induced obesity in the rat.

Feeding rats with a cafeteria diet resulted in increases in total body weight and in epididymal-adipose-tissue weight. Those rats excreted significantly less N than did controls. The amount of N ingested by cafeteria-diet-fed rats was kept equal to that of controls. This decrease in N excretion is explained by a decrease in urinary excretion of urea. This may be due to the following facts. The rate of synthesis of urea from precursors by isolated hepatocytes from cafeteria-diet-fed rats was lower than in controls. In cafeteria-diet-fed rats the activities of all the enzymes of the urea cycle are decreased. The major percentage decreases are those of carbamoylphosphate synthetase (EC 6.3.4.16) and of argininosuccinate synthetase (EC 6.3.4.5), the enzymes probably involved in the regulation of the overall rate of the cycle. When rats are switched to normal chow diet, the enzyme activities return to normal values. The uptake of amino acids by liver of cafeteria-diet-fed rats is lower than in controls. These results contrast with those obtained previously by using other models of obesity in rat (i.e. genetic or hypothalamic), in which N excretion was increased.

The acute toxicity and teratogenicity of nickel in pregnant rats

The increased susceptibility of the pregnant rat to intraperitoneally administered nickel (Ni) is apparent at 12 and 19 days of pregnancy and cannot be due, therefore, to be increase in total body weight. Teratogenic malformations occur when Ni is administered during organogenesis and are maximal at dose levels that are toxic for the dam. The yolk was sac and chorioallantoic placentas accumulate Ni, but this does not prevent the transport of the metal to the embryo or foetus. The Ni concentrations in the comceptuses decrease more slowly with time than those in the maternal organs. In the foetuses, the decrease in concentration is due to the increase in weight, since the content of Ni increases between 4 h and 24 h. Foetal uptake of [ 14C]thymidine, [ 3H]leucine and 65Zn is unaffected at 3 h after the injection of the dam with 4 mg Ni/kg body wt. Incorporation of [ 3H]leucine into foetal protein, but not the incorporation of [ 3C]-thymidine into DNA, is decreased at this time. A major effect of treatment with this teratogenic dose is an increase in the maternal plasma glucose concentration which, in turn, alters the supply of the sugar to the foetus. The possible relevance of temporary foetal hyperglycaemia to teratogenesis is discussed.

Chronic Hyperinsulinemia in the Fetal Rhesus Monkey: Effects of Physiologic Hyperinsulinemia on Fetal Growth and Composition

One of the hallmarks of the hyperglycemic-hyperinsulinemic infant of the diabetic mother (IDM) is macrosomia and selective organomegaly. Primary hyperinsulinemia, with insulin levels similar to those observed in human IDMs at delivery, was produced in the fetal rhesus monkey during the last third of gestation. The effects of this physiologically relevant hyperinsulinemia, in the absence of hyperglycemia, on fetal growth were studied. Fetal macrosomia, with a 23% increase in total body weight, was observed in physiologically hyperinsulinemic fetuses. A similar 27% increase in weight was produced by fetal insulin levels that were 10 times higher. A logarithmic correlation was observed between fetal birth weight ratio and fetal plasma insulin concentration. In contrast to this increase in weight, skeletal growth, as measured by crown-heel length and head circumference, was not affected by hyperinsulinemia. Only cardiomegaly was found in the low-dose hyperinsulinemic fetuses, whereas cardiomegaly, hepatomegaly, and splenomegaly were produced by hyperinsulinemia in which insulin levels were in the highest range. Compositional analysis of heart and skeletal muscle indicated no differences in the protein, RNA and DNA concentration, or in the protein-to-DNA ratio in hyperinsulinemic fetuses. We interpret these data as indicating that fetal insulin plays the predominant role in controlling the normal, as well as the augmented, fetal weight characteristic of the human infant of the diabetic mother.

The Effects of Dietary Carbohydrate on Larval Development and Lipogenesis in the Parasite, Exeristes roborator (Fabricius) (Hymenoptera: Ichneumonidae)

Dietary carbohydrate was necessary for larval development of the parasitic wasp, Exeristes roborator, reared on fatty acid-free artificial media containing 6% free amino acids. Fifty percent mortality occurred when larvae were reared on carbohydrate-free diets but a level of 2% glucose, fructose, or sucrose resulted in over 80% of the insects completing larval development. Development time decreased with increasing dietary carbohydrate level. Accompanying these effects on development were increases in total body weight brought about by increased lipid and protein levels. The lipid concentration of larvae reared on carbohydrate-free diets was only one-quarter that of larvae reared on diets containing 8% carbohydrate, and the concentration in insects reared on 6% carbohydrate diets was not significantly different from that of host-reared larvae. The total lipids were composed largely of phospholipid, sterol, and triglyceride. The relative level of the latter increased from 10% in insects reared on diets lacking carbohydrate to 50% in those reared on diets containing 6% carbohydrate. The importance of dietary carbohydrate

Growth of crustacean muscles and muscle fibers

The superficial flexor (SF) muscle of the crayfish (Procambarus clarkii) abdomen increases in volume in direct proportion to increases in total body weight during ontogeny. This increase in SF muscle mass occurs solely (Figs. 1, 2) by an increase in the width and length of SF muscle fibers (i.e., the number of SF muscle fibers remains constant). Unlike vertebrate muscle fibers, these crustacean muscle fibers increase in length by increases in sarcomere length (Fig. 3). This increase in sarcomere length during ontogeny must occur via a continuous lengthening of actin and myosin filaments since the relative lengths of the A and I bands remain essentially unchanged as these fibers lengthen. Similar results are reported for the opener muscle of the cheliped (Figs. 5–7).

The effect of feeding frequency on the growth on composition of individual organs in the rat.

1. The effect of consuming the same total amount of food in either one large meal or several small meals per d was studied using weanling male rats. 2. The increase in total body-weight was the same in both instances, but the weights of the liver, kidneys, femur, small intestine and stomach were greater, and those of the spleen and residual carcass were smaller, in meal-eating rats than in continuously fed control animals. These differences persisted into the adult state. 3. No differences in gross chemical compositions were found between the corresponding organs of the two groups of rats, and the differences in weight appeared to be the result of changes in the general growth rate of individual organs. 4. The hypertrophy of the kidneys in meal-eaters was due to an increase in mean cell size, but the increased weight of the liver and reduced weight of the spleen appeared to be largely the result of changes in the number of cells present.

Relationship between body composition and insulin and growth hormone responses in obese adolescents.

The clinical characteristics and predicted body composition of ten obese nondiabetic and six normal adolescents were compared in regard to plasma insulin, growth hormone, glucose, free fatty acids and alpha-amino nitrogen in response to different stimuli. Analysis of the data suggested the presence of two groups of patients. In obese Group A there was no family history of obesity, the youngsters first became obese between seven to twelve years of age, had a normal height for age, moderate increase in body weight and estimated total body fat, and normal or less than normal fasting levels of insulin. In obese Group B there was a strongly positive family history of obesity, the subjects became obese in infancy or early childhood, they were tall for their age, had marked increase in total body weight and total body fat as well as significantly higher than normal fasting insulin levels. Hyperinsulinemia was present in Group A during the oral glucose tolerance test and protein glucose meal. Normal insulin responses were observed during the protein meal and the arginine tolerance test. On the other hand, Group B manifested hyperinsulinemia in response to all stimuli. Both obese groups had undetectable plasma growth hormone levels during both the protein and the protein-glucose meal, but normal growth hormone responses during the oral glucose and the arginine tolerance tests. The differences in plasma levels of glucose and free fatty acids were minimal. Significant differences in plasma alpha-amino nitrogen values were observed during the protein-glucose meal. Differences in the hormonal responses of obese adolescents and adults are discussed. Possible explanations for heterogeneous responses of obese adolescents are presented.

Suppression of thyroid function by pituitary tumor MtTW5.

A transplantable pituitary tumor, MtTW5, which secretes prolactin and growth hormone but no TSH or ACTH, causes a marked increase in total body weight and in the weight of most internal organs. However, the pituitary glands of tumor-bearing rats weighed significantly less in proportion to body weight than did pituitaries in control rats. Incorporation of 131I into the trichloroacetic acid-soluble and the protein fractions of the thyroid and serum was measured. Less 131I was incorporated into these fractions of the thyroid and into the protein fraction of serum of tumor-bearing rats than in control rats. These results were obtained in intact female, spayed female, nephrectomized female and male rats. After acute treatment with propylthiouracil, tumor-bearing rats incorporated less 131I into their thyroids than did controls similarly treated with propylthiouracil. Thus, the primary defect in the thyroid of tumorbearing rats is in its inability to concentrate iodine from the blood. Histological examination o...

EFFECT OF COLD ACCLIMATION ON ELECTROLYTE DISTRIBUTION IN RAINBOW TROUT (SALMO GAIRDNERII)

The effect of adaptation to constant low environmental temperature on water and electrolyte distribution in skeletal muscle and brain has been studied in 2-year-old rainbow trout. Following introduction to 6 °C of trout previously acclimated to 16 °C, measurements were made, at intervals, of plasma Na, K, Cl, Ca, Mg, and phosphate and of brain and muscle Na, K, and Cl. Plasma, muscle, and brain tissue showed a transient but significant drop in water content during the first days of cold exposure. A coincident paradoxical increase in total body weight suggests the possibility of an osmotic withdrawal of body water by the gut contents during this period. Cl space and Cl–K space estimates of muscle extracellular space were not significantly influenced during cold acclimation. Most of the plasma electrolytes measured showed significant transient alterations in concentration.Significant reciprocal changes in brain Na and K concentration were measured shortly after transfer to 6 °C and a large (61%) increase in brain Cl concentration occurred after 3 weeks of cold adaptation.Large, rapid but mostly transient shifts in muscle Na and K occurred. During the first 3 days of cold exposure muscle lost 61% of the Na and 30% of the K present before transfer. This loss is reflected in a rise in plasma Na and K. The possibility that the unusual efflux of intrafiber Na and K together might represent a forced extrusion of positive charge following a temperature-induced intrafiber loss of organic anions or gain of divalent cations is discussed.

Studies on the effect of hormone administration on body weight and on tibial epiphysial cartilage width in intact, hypophysectomized and adrenalectomized rats.

SUMMARY 1. The effects of feeding, hormone administration, unilateral nephrectomy and adrenalectomy on width of tibial cartilage and total body weight in intact and hypophysectomized young male rats were measured. 2. Unilateral nephrectomy and adrenalectomy have no effect on the cartilage width of both intact and hypophysectomized rats, although adrenalectomy causes a loss in weight in the intact rat. 3. Intact rats, both young and adult, fed enough to maintain but not to put on weight, show a reduction of cartilage width to hypophysectomized levels. 4. Growth hormone alone (1 mg. and 3 mg./day for 14 days) causes a marked increase in cartilage width but only a 50–60% increase in total body weight in the hypophysectomized rat. 5. Adrenocorticotrophin (ACTH: 2 i.u./day for 14 days) causes a significant reduction in both cartilage width and total body weight in the hypophysectomized rat. 6. Thyrotrophin (TSH: 1 i.u./day) and Prolactin (1 mg. and 2 mg./day) caused significant increases in both total body weight and cartilage width in the hypophysectomized rat. 7. Luteinizing hormone (LH: 0·01 mg./day) together with follicle stimulating hormone (FSH: 1·0 mg./day) caused a significant increase in body weight, but had no effect on cartilage width in the hypophysectomized rat. 8. Both doses of combined hormones (growth hormone, ACTH, TSH, prolactin, FSH and LH administered together) caused a marked increase in cartilage width and a smaller increase in total body weight in the hypophysectomized rat.

SIGNIFICANT CHANGES IN THE LIPID AND WATER CONTENT OF THE THYMUS GLAND IN ALBINO RATS BEARING WALKER CARCINOMA 256

The investigation was designed to measure hydrolipotropic variations in the thymus gland of albino rats bearing Walker carcinoma 256. This was done upon 27 pairs of littermate albino rats, one of each pair inoculated and one not inoculated with Walker carcinoma 256. The life history of the tumor was evenly represented in the series. Tumor growth was found to be accompanied by a statistically significant increase in total body weight, due to water retention, and decrease in the weight of the thymus gland. The total amount of water, dry weight, total lipid, neutral fat, total fatty acids, free cholesterol, and phospholipid were significantly less in the thymus gland of tumor-bearing albino rats. The concentrations, per unit dry weight, of total lipid, neutral fat, and total fatty acids in the thymus gland were not significantly affected by tumor growth. The similar concentrations of water, total cholesterol, free cholesterol, and phospholipid were significantly increased in the thymus gland of tumor-bearing albino rats. These changes indicated a hydrolipotropic effect of the tumor upon the thymus gland. A pyramidal, up-and-down, change in the concentrations of phospholipid and the three cholesterol fractions in the thymus gland at T/RC coefficients of 30 to 60, together with a marked loss of weight by the gland, suggested the effect upon the thymus gland of factor(s) other than the hydrolipotropic influence.