Biochemical parameters in athletes before and after having run 160 kilometres

A number of biochemical and haematological parameters, including plasma electrolytes, parameters of hepatic and renal function, plasma enzymes and free fatty acids were measured in 13 athletes before and after a 160-km 24-hour race. The runners were divided into 2 groups: group A, who competed the 160 km within 24 hours and group B, who either ran for 24 hours, or who retired before completing the distance. Minimal changes were found in the plasma electrolyte patterns in either group, whereas blood urea and creatinine levels increased during the race. The plasma enzymes increased to varying extents, the greatest increases being in lactic dehydrogenase, aspartate aminotransferase and the skeletal muscle specific MM isoenzyme of creatinine phosphokinase. Total bilirubin also increased, but no conclusive evidence of hepatic decompensation was found. Plasma free fatty acids levels were very markedly raised in 12 of the runners, the highest increases occurring in group A. All runners ingested carbohydrate during the race and this probably explains why the blood glucose levels increased slightly but remained within normal limits in all the athletes at the end of the race.     

Serum leptin and IGF-I levels in cystic fibrosis

(3S,4R)-4-(4-Fluorophenyl)-3-[[3,4-(methylenedioxy)phenoxy]methyl] piperidine [(3S,9R)-3, paroxetine] is a selective serotonin reuptake inhibitor (SSRI) used as an antidepressant in humans. In previous studies, we reported that certain (1R)-3 beta-(substituted phenyl)nortropane-2 beta-carboxylic acid methyl esters (2a) exhibited high affinity and reasonable selectivity for the serotonin transporter (5-HTT). The major structural differences between 2a and (3S,4R)-3 are that 2a possesses a different absolute stereochemistry and has an ethylene bridge not present in 3. In addition, 2a possesses a carbomethoxy substituent adjacent to the aryl ring, whereas (3S,4R)-3 contains a [3,4-(methylenedioxy)phenoxy]methyl group. In this study, we present the synthesis and biological evaluations of six of the possible eight isomers of 3-(4-fluorophenyl)-2-[[3,4-(methylenedioxy)phenoxy]methyl]nortropane+ ++ (4). The data for inhibition of [3H]paroxetine binding show that (1R)-2 beta, 3 alpha-4c, which has the same stereochemistry as paroxetine, has the highest affinity at the 5-HTT. Strikingly, the most potent compounds for inhibition of [3H]WIN-35,428 binding were not the (1R)-2 beta, 3 beta-isomers but rather (1R)-2 beta, 3 alpha-4c and (1S)-2 beta, 3 alpha-4f. Conformational analyses show that these isomers exist in a flattened boat conformation with pseudoequatorial substituents. Thus, the binding data show that this conformation is recognized by the DAT-associated binding site and also suggest that this conformation of paroxetine is recognized by the 5-HTT-associated binding site.     

Serum progesterone levels in patients with gastric adenocarcinoma before and after gastrectomy

We experienced a case of a hepatic subcapsular hematoma after extracorporeal shock wave lithotripsy (ESWL) for a right renal stone. To our knowledge this presentation is the second case in the Japanese literature. A 63-year-old female with a right renal stone received 2,800 shots of 14.0 kilo-volts shockwave with Sonolith 3,000. Preoperative examination of the blood disclosed no abnormalities in the coagulating system except slight reduction of platelet count and slight impairment of liver function. Postoperative routine ultrasound echograms revealed a hepatic subcapsular hematoma although she had no symptom. The size of the hematoma measured 11.0 x 5.0 cm in computed tomograms (CT). She was carefully observed without any treatments because the hematoma did not increase in size. CT scans 6 months after the ESWL treatment demonstrated neither hematoma nor masses in the liver. As a complication of ESWL for urolithiasis a hepatic subcapsular hematoma is very rare. We herein presented the case and discussed the complications of ESWL briefly in the literature.     

Serum leptin levels in women with anorexia nervosa

Leptin is a protein encoded by the ob gene that is expressed in adipocytes and regulates eating behavior via central neuroendocrine mechanisms. Serum leptin levels have been shown to correlate with weight and percent body fat in normal and obese individuals; however, it is not known whether the regulation of leptin is normal below a critical threshold of body fat in chronic undernutrition. We investigated serum leptin levels in 22 women, aged 23 +/- 4 yr, with anorexia nervosa. Duration of disease, weight, BMI, percent body fat, and serum leptin levels were determined for each patient. Nutritional status was assessed further by caloric intake and measurement of insulin and insulin-like growth factor I (IGF-I) levels. Twenty-three healthy women, aged 23 +/- 4 yr, taking no medications, with normal menstrual function and body mass index (BMI) between 20-26 kg/m2 (mean, 23.7 +/- 1.7 kg/m2), served as a control population for comparison of leptin levels. Subjects with anorexia nervosa were low weight (BMI, 16.3 +/- 1.6 kg/m2; normal, 20-26 kg/m2) and exhibited a striking reduction in percent body fat (7 +/- 2%; normal, 20-30%). The mean serum leptin level was significantly decreased in subjects with anorexia nervosa compared with that in age- and sex-matched controls of normal body weight (5.6 +/- 3.7 vs. 19.1 +/- 8.1 ng/mL; P < 0.0001). Serum leptin levels were correlated highly with weight, as expressed either BMI (r = 0.66; P = 0.002) or percent ideal body weight (r = 0.68; P = 0.0005), body fat (r = 0.70; P = 0.0003), and IGF-I (r = 0.64; P = 0.001), but not with caloric intake or serum levels of estradiol or insulin in subjects with anorexia nervosa. The correlation between leptin and body fat was linear, with progressively lower, but detectable, leptin levels measured even in patients with less than 5% body fat, but was not significant when the effects of weight were taken into account. In contrast, the correlation between leptin and IGF-I remained significant when the effects of weight, body fat, and caloric intake were taken into account. In normal controls, leptin correlated with BMI (r = 0.55; P = 0.007) and IGF-I (r = 0.44; P < 0.05), but not with fat mass. These data demonstrate that serum leptin levels are reduced in association with low weight and percent body fat in subjects with anorexia nervosa compared to normal controls. Leptin levels correlate highly with weight, percent body fat, and IGF-I in subjects with anorexia nervosa, suggesting that the physiological regulation of leptin is maintained in relation to nutritional status even at an extreme of low weight and body fat.     

Immune parameters in athletes before and after strenuous exercise

Secretory IgA levels were studied in nationally ranked Nordic skiers before and after the national cross-country races held in February 1981. Comparing the skiers with age-matched controls, there was significantly lower level of salivary IgA before the race. Concentrations of IgA decreased further following the competition (50 kn for males; 20 km for females) to very low levels. There also were a significant increase in the percentage of B lymphocytes and a decrease in the null population (non-T, non-B) in the athletes after the race compared with the controls. The mechanism responsible for these changes is unknown, but the low salivary IgA levels may result from depletion of nasal fluid and/or malfunction of the mucosal plasma cells due to a decrease temperature in the mucous membranes. We speculated that a temporary antibody deficiency on the mucosal surface might lead to a susceptibility to acquiring viral and bacterial infections, especially during the interval immediately following strenuous exercise.     

Serum leptin levels do not rise during pregnancy in age-matched rats

The serum leptin profile and its production in adipose tissue during pregnancy and lactation were investigated along with changes in appetite and factors reflecting nutritional status in 11-week-old rats. Serum leptin levels in pregnant rats were stable except on day 20 of pregnancy and significantly reduced during lactation compared to nonpregnant rats (P < 0.001). Circulating leptin levels corresponded with changes in appetite during pregnancy and postparturition. Leptin mRNA in parametrial adipose tissue reflected the circulating levels, also being significantly reduced during late pregnancy and during lactation (P < 0.05). Leptin mRNA expression was observed in placenta, but the amount suggested little influence on circulating leptin levels. These results indicate that reduction in leptin mRNA in parametrial adipose tissue and circulating leptin levels may increase appetite during late pregnancy and lactation and may play a role in regulating metabolic homeostasis around parturition in rats.     

Serum prostate-specific antigen concentration before and after vasectomy

Recent epidemiologic studies have suggested that a risk factor for the development of carcinoma of the prostate may be previous vasectomy. As a majority of prostate cancer cases diagnosed in the U.S. are detected by an elevation in prostate-specific antigen (PSA), an elevation in PSA due to vasectomy may underpin this association. There have been no published reports on the relationship between PSA before and after vasectomy. To study this relationship, this study was undertaken to determine the effects of vasectomy on PSA. Twenty-five men undergoing vasectomy were studied with serial PSA determinations prior to and following vasectomy. Analysis of data suggests that PSA is not affected by previous vasectomy and that other causes for an increased detection in this cohort may be operational.     

Serum total homocysteine concentration before and after renal transplantation

BACKGROUND: Hyperhomocysteinemia is by now an established risk factor for the development of atherosclerosis. Total homocysteine concentration (tHcy) correlates inversely with glomerular filtration rate, and it is roughly three times as high in hemodialysis patients as in healthy individuals. Therefore, tHcy would be expected to fall markedly after successful renal transplantation. The aim of the present study was to assess the changes in tHcy associated with renal transplantation. METHODS: tHcy was analyzed in samples collected before renal transplantation and at six months after transplantation in 55 stable patients, all of whom were treated with cyclosporine (CS). tHcy was also analyzed in samples from 55 controls characterized by markers of renal function that matched those of the post-transplant state. RESULTS: At six months after transplantation, tHcy was significantly decreased as compared with pretransplant tHcy (27.7 +/- 14.8 vs. 36.9 +/- 21.3 micromol/liter, P < 0.001). Post-transplant tHcy was markedly higher than the tHcy of the control group (27.7 +/- 14.8 vs. 16.0 +/- 5.3 micromol/liter, P < 0.0001). The post-transplant change in tHcy ranged widely, the average change being a reduction of 14%. Sixteen patients (29%) actually manifested an increase in post-transplant tHcy. The post-transplant changes in tHcy correlated inversely with pretransplant tHcy (r = -0.66, P < 0.0001) and directly with the changes in serum albumin concentrations (r = 0.35, P < 0.05) and CS trough concentrations (r = 0.29, P < 0.05). A multivariate analysis, including the post-transplant changes in serum concentrations of folate and albumin as well as creatinine clearances explained 21% of the change in tHcy (P < 0.05). After inclusion of the CS concentration, an independent predictor, the model accounted for 28% of the post-transplant change in tHcy (P < 0.01). CONCLUSION: The post-transplant reduction in tHcy was far smaller than expected with respect to renal function, and the post-transplant changes in the major biochemical determinants of tHcy contributed relatively little to explain the change in tHcy. Thus, the results suggest the post-transplant introduction of one or more factors that induce an increase in tHcy. Treatment with CS appears to be such a factor.     

Adenohypophyseal-gonadal dysfunction in male haemodialyzed patients before and after subtotal parathyroidectomy

The function of the adenohypophyseal-gonadal axis in haemodialyzed male patients is modified: the serum testosterone level is low, and the gonadotropin levels are increased. The pathogenetic role of secondary hyperparathyroidism in this disorder has not previously been defined. The area under the curve (AUC) and the secretion kinetics of testosterone, luteinizing hormone (LH), and follicle-stimulating hormone after administration of LH-releasing hormone were examined in 7 dialyzed men with secondary hyperparathyroidism (mean age 36.2, range 20-47 years) before and 3 and 6 months after parathyroidectomy (PTX). The operation was successful in all 7 patients, as intact parathyroid hormone declined markedly during both postoperative periods as compared with the values before PTX: 81 +/- (SEM) 34 and 138 +/- 57 ng/1 versus 965 +/- 116 ng/l (p < 0.01 and p < 0.0l). The testosterone AUC prior to PTX (63 +/- 115 nmol/l x min) and 3 months (-4 +/- 36 nmol/l x min) and 6 months after PTX (-62 +/- 69) did not differ significantly, as was the case with LH AUC (1,110 +/- 223 and 1,214 +/- 331 and 1,020 +/- 314 U/l x min, respectively) and follicle-stimulating hormone AUC (525 +/- 334 and 634 +/- 347 and 533 +/- 264 U/l x min, respectively). The secretion kinetics of all three hormones was atypical as compared with healthy men of similar age, but it did not change after PTX. There were no correlations between the sexual indicators and parathyroid hormone, 1,25(OH)2D3, calcium, or phosphate during the individual periods. These findings indicate that secondary hyperparathyroidism is probably not involved in the dysfunction of the adenohypophyseal-gonadal axis in dialyzed men.     

Serum leptin and energy expenditure in children

Leptin has been hypothesized to play an important role in energy balance by affecting both energy intake and energy expenditure. The purpose of our study was to determine the relationship between fasting serum leptin concentrations and measures of energy expenditure in prepubertal children. We measured total energy expenditure (TEE; by the doubly labeled water technique), resting energy expenditure (REE; after an overnight fast), activity energy expenditure (AEE; TEE-REE), body composition (by dual energy x-ray absorptiometry), and fasting serum leptin concentration (by RIA) in 76 children. Simple correlations showed that all measures of energy expenditure (TEE, REE, and AEE) were positively related to the serum leptin concentration (r = 0.50, P < 0.001; r = 0.45, P < 0.001; and r = 0.30, P < 0.01, respectively). However, after adjusting for body composition (fat-free mass and fat mass), gender, and ethnicity, serum leptin concentrations were not related to any measure of energy expenditure (TEE, P = 0.61; REE, P = 0.97; AEE, P = 0.65). These latter findings were further confirmed using structural equation models with leptin and energy expenditure as dependent variables, and fat-free mass and fat mass as independent variables. Results from these models showed no direct effect of leptin and no indirect effect of fat mass (through leptin) on any measure of energy expenditure, when a path between fat mass and energy expenditure was present in the model. Thus, our data do not support the hypothesis that the serum leptin concentration (independent of fat mass) is related to measures of energy expenditure in children.     

Serum mineral changes in dithizone-induced diabetes before and after insulin treatment

In this study, diabetes was induced by intravenous injection of dithizone. In dithizonised diabetic animals, the levels of serum zinc, iron, and potassium were found to be higher than normal, while those of serum calcium and sodium were lower. Copper and magnesium levels were unchanged. After treatment with insulin, most of these serum levels approached the normal, except for serum potassium and magnesium.     

Serum leptin concentrations in Caucasian and African-American girls

Because African-American girls are heavier, taller, and mature earlier than Caucasian girls, we hypothesized that the serum leptin concentration differs between the two groups. Serum leptin concentrations were measured by immunoassay in 12-h fasted blood samples collected from 79 Caucasian and 57 African-American girls between 8 and 17 yr of age. Body composition was measured by dual-energy x-ray absorptiometry, sexual maturity by physical examination, and physical fitness by treadmill testing. Serum leptin concentrations were positively correlated (P < 0.01) with maturation, body fatness, and insulin and were higher (6.6 ng/mL, P < 0.01) in the African-American girls after adjusting for age. The difference remained significant (P < 0.01) but was reduced to 3.2 ng/mL after controlling for differences in maturation, fat mass, and physical fitness. The higher serum leptin levels might play an important role in the accelerated growth and sexual maturation of African-American girls.     

Serum levels of müllerian inhibiting substance in preterm and term male neonates

PURPOSE: Müllerian inhibiting substance, also called anti-müllerian hormone, is responsible in the embryo for the regression of the müllerian structures. During the second and third trimesters the physiological functions that müllerian inhibiting substance may have after the period of müllerian duct regression are poorly understood. We obtained information on müllerian inhibiting substance levels in the male newborn during this period of gestation. MATERIALS AND METHODS: Müllerian inhibiting substance was measured by an enzyme immunoassay in cord blood obtained at birth in 27 preterm (25 to 36 weeks of gestation) and 92 term (37 to 42 weeks) male neonates. RESULTS: Cord serum müllerian inhibiting substance concentrations were relatively high from 25 to 31 weeks (mean plus or minus standard deviation 86.4 +/- 36.1 ng./ml.) and then they decreased from 32 weeks to term (mean 24.2 +/- 14.0 ng./ml.). CONCLUSIONS: The decline early in the third trimester may be consistent with müllerian inhibiting substance having a function during the second but a diminished role in the third trimester.     

Variations in glucocorticoid levels within the physiological range affect plasma leptin levels

In March 1996, an epidemic of Shigella sonnei infection occurred in Ooamishira-sato Town, Chiba Prefecture. Colicine typing, antibiotic resistance patterns, plasmid profiles, pulsed-field gel electrophoresis (PFGE) and random amplified poly-morphic DNA (RAPD) were used for the investigation of the epidemic. Ninety-four isolates from patients exhibited three different colicine types and five different antibiotic resistance patterns. But the patterns of plasmid profile, PFGE and RAPD were uniform among the isolates with different colicine type and antibiotic resistance pattern. It is possible that these isolates belonged to a single bacterial clone and circulated through human to human.     

Effects of gonadotropin and testosterone treatments on plasma leptin levels in male patients with idiopathic hypogonadotropic hypogonadism and Klinefelter's syndrome

Since little is known about the effects of gonadotropin and testosterone treatment on leptin levels in male hypogonadism, we determined fasting plasma leptin levels before and 3 months after treatment in 21 patients with idiopathic hypogonadotropic hypogonadism (IHH), 16 patients with Klinefelter's syndrome and 20 male controls. Patients with IHH were treated with hCG/human menopausal gonadotropin, whereas patients with Klinefelter's syndrome received T treatment. Plasma leptin levels were measured by an RIA with a sensitivity of 0.5 microg/L. Mean leptin levels in patients with IHH before treatment (9.23+/-4.09 microg/L) were not significantly different from those in patients with Klinefelter's syndrome (7.29+/-5.05 microg/L; z=-1.41; P=0.15). Leptin levels in both IHH and Klinefelter's syndrome groups were, however, significantly higher than in the normal men (3.91+/-1.67 microg/L) (P<0.001 and P<0.01, respectively). Mean leptin levels did not change significantly 3 months after the initiation of gonadotropin (11.6+/-6.44 microg/L) or T (8.32+/-5.17 microg/L) treatment in either IHH or Klinefelter's syndrome. Our study demonstrated that mean plasma leptin levels are not influenced by short-term gonadotropin or T treatment in male hypogonadism.     

Increase in serum leptin and uterine leptin receptor messenger RNA levels during pregnancy in rats

Pregnancy is a physiological state associated with significant changes in appetite, thermogenesis, and lipid metabolism, functions which are regulated in part by a hormone, leptin, secreted by adipocytes. Leptin has also been shown to have a role in reproduction, promoting centrally-regulated maturation of the reproductive system and signaling the presence of adequate maternal energy stores for fertility. Here we demonstrate that serum leptin levels are modulated during normal rat pregnancy with a 1.8-fold increase during pregnancy followed by a decrease just before parturition. Leptin receptor mRNA levels in the uterus are also regulated with an increase about 2.7-fold during this same period, whereas there is no change in other tissues examined. The results suggest that leptin may play a role during pregnancy, perhaps regulating energy utilization.     

Plasma leptin levels and body fat distribution

The relation between body fat distribution and plasma leptin levels in the human was investigated in 51 obese and 41 non-obese subjects. Plasma levels of leptin showed a positive correlation with body mass index and subcutaneous fat area at the umbilicus level. However, a significant correlation between its plasma levels and visceral fat area was found in neither non-obese nor obese subjects. These results suggest that plasma leptin levels might be attributed mainly to the extent of subcutaneous adiposity in human obesity.     

beta-Endorphin and adrenocorticotrophin after incremental exercise and marathon running--female responses

Investigations of exercise-induced increases in beta-endorphin, adrenocorticotropic hormone (ACTH) and cortisol concentration have been carried out mainly in men. Data concerning the female reaction are sparse and less clear. In a comparison between incremental exercise and marathon running 14 experienced female marathon runners volunteered to run to exhaustion according to an incremental treadmill protocol. They ran a marathon 4 weeks later. Blood was analysed for beta-endorphin, ACTH and cortisol concentration immediately prior to the laboratory treadmill test, 3, 30 and 60 min later, as well as prior to the marathon, after 60 min and 120 min of running and 3, 30 min, and 24 h after completion of the run. At each blood collection, lactate concentration, heart frequency and perceived exertion were determined. The mean marathon running time was 3.22 h. Baseline concentrations for beta-endorphin of 22 pmol.l-1 before the marathon and 19 pmol.l-1 before the treadmill exercise increased 1.4-fold 30 min after the marathon and 1.9-fold after the treadmill exercise; for ACTH the baseline of 4.7 and 4.0 pmol.l-1 was increased by 8.3- and 10.3-fold, respectively. Cortisol concentration rose exponentially from a baseline 17 micrograms.dl-1 and peaked at 2.2-fold 30 min after the run, when the maximal concentration also had been reached after the treadmill test, increasing 1.3-fold from a baseline of 21 micrograms.dl-1. The maximal values for cortisol concentration after both exercises differed from each other, while the maxima of ACTH and beta-endorphin concentrations were similar. The ACTH and beta-endorphin concentration declined more slowly during the recovery after the marathon than after the treadmill. Cortisol concentration was below baseline 24 h later. In comparison with men studied earlier, female marathon runners showed higher baseline concentrations and lesser increases in beta-endorphin and lower baseline concentrations and larger increases in ACTH concentration after both types of exercise. The delayed decrease in concentration of the hormones after the marathon was similar in male and female runners.