Showing papers in "American Journal of Physiology-endocrinology and Metabolism in 1980"
TL;DR: The rate constants of FDG in man were found to be comparable to those of deoxyglucose in rat and in rhesus monkey and the subject-to-subject variation of LCMRGlc as measured by the present method was comparable to that of other methods that measure whole-brain CMRglc.
Abstract: A method for the determination of local cerebral metabolic rates of glucose (LCMRGlc) in normal man is described. The method employs [18F]2-fluoro-2-deoxy-D-glucose (FDG) and emission-computed tomography (ECT). FDG was injected intravenously as a bolus. Radioactivities in separate brain regions were measured with ECT. Plasma FDG concentration following injection was measured from blood samples. A mathematical model that describes the kinetics of FDG transports was employed to determine the transport rate constants of FDG and to convert the radioactivity measurements to metabolic rates. The model has taken into account the possible dephosphorylation reaction from FDG-6-PO4 (FDG-6-P) to free FDG in brain tissues. Experiments were performed in 13 normal volunteers. The rate constants of FDG in man were found to be comparable to those of deoxyglucose in rat and in rhesus monkey. The average LCMRGlc in gray and in white matter were found to be 7.30 +/- 1.18 (SD) and 3.41 +/- 0.64 mg/min per 100 g brain tissue, respectively. The subject-to-subject variation of LCMRGlc as measured by the present method was comparable to those of other methods that measure whole-brain CMRGlc.
999 citations
TL;DR: Leucine metabolism in vivo can be determined from a primed, continuous infusion by measuring, at isotopic steady state, plasm [-13C]leucine enrichment, expired 13CO2 enrichment, and CO2 production rate.
Abstract: Leucine metabolism in vivo can be determined from a primed, continuous infusion of L-[1-13C]leucine by measuring, at isotopic steady state, plasm [-13C]leucine enrichment, expired 13CO2 enrichment, and CO2 production rate. With an appropriate priming dose of L-[1-13C]leucine and NaH13CO3, isotopic steady state is reached in less than 2 h, and the infusion is completed in 4 h. The method can determine rates of leucine turnover, oxidation, and incorporation into protein with typical relative uncertainties of 2, 10, and 4%, respectively. The method requires no more than 1 ml of blood and uses stable isotope rather than radioisotope techniques. Thus, the method is applicable to studies of human beings of all ages. L-[1-13C]leucine may be infused with a second amino acid labeled with 15N for simultaneous determination of the kinetics of two amino acids.
496 citations
TL;DR: The loss of muscle mass and its protein content contrasts with the relative constancy of the nonmuscle lean tissue and suggests that skeletal muscle is particularly vulnerable to the aging process.
Abstract: The techniques of prompt gamma neutron-activation analysis for the measurement of total-body nitrogen and whole-body counting for the measurement of total-body potassium were used to determine the mass of muscle and nonmuscle lean tissue and their protein content in 135 normal male and female subjects, 20–80 yr of age. Age-related changes in the size of the muscle and nonmuscle compartments and their protein content provide basic data for the investigation of protein metabolism in aging subjects and in individuals with various metabolic disorders, particularly wasting diseases such as cancer. Significant age-related changes in the size of various body compartments were noted. The loss of muscle mass and its protein content contrasts with the relative constancy of the nonmuscle lean tissue and suggests that skeletal muscle is particularly vulnerable to the aging process.
325 citations
TL;DR: Calcium transport in the intestine increases late in pregnancy, peaks during lactation, and then falls to control values by 3 wk postweaning in both vitamin D-replete and D-deficient animals, suggesting that some factor(s) independent of vitamin D is stimulating intestinal calcium transport during the reproductive cycle.
Abstract: The factors involved in calcium homeostasis during the mammalian reproductive cycle and specifically in the control of active calcium transport in the intestine have not been thoroughly investigate...
142 citations
TL;DR: It is suggested that skeletal muscle, and not liver, is the organ primarily responsible for the increased sensitivity to insulin-induced glucose uptake with exercise training and that this response is enhanced after overnight fasting.
Abstract: Spontaneously exercised rats show at rest enhanced responsiveness to exogenous insulin and lower plasma insulin levels after oral glucose than sedentary control rats. To assess insulin sensitivity of specific organs, glucose uptake by perfused hindlimb muscle and liver from resting exercise-trained rats was compared with perfused organs from control rats. Glucose uptake, assessed by metabolic clearance formulas, was 17% faster in hindlimbs from exercise-trained rats when perfused without added insulin and 43% faster at perfusate insulin levels of 40 microU/ml. After an overnight fast, glucose clearance in exercise-trained hindlimbs increased over controls by 57% in the basal state and by 97% at low perfusate levels. In contrast, glucose clearance by livers from both fed and fasted exercise-trained rats was less than one-half that of livers from control rats. These results suggest that skeletal muscle, and not liver, is the organ primarily responsible for the increased sensitivity to insulin-induced glucose uptake with exercise training and that this response is enhanced after overnight fasting.
134 citations
TL;DR: decreased in vivo endochondral bone growth and development during diabetes is the result of 1) inhibition of insulin-dependent mesenchymal cell proliferation, 2) decreased and delayed cartilage formation due to impairment, and 3) reduced insulin- dependent calcification and ossification.
Abstract: The influence of streptozotocin-induced diabetes on discrete stages of matrix-induced endochondral bone formation has been investigated. Mesenchymal cell proliferation was inhibited in diabetic rats as evidenced by a 65% reduction of ornithine decarboxylase (ODC) activity and a 56% reduction of [3H]thymidine incorporation per microgram DNA compared to nondiabetic controls; the inhibition was prevented by insulin treatment. In diabetic animals, chondrogenesis on day 7 was reduced by 49% compared to control animals as assessed by 35SO4 incorporation. Exogenous insulin was stimulatory to cartilage development when present during days 0 through 4 (mesenchymal cell proliferation). Calcification of cartilage and osteogenesis were reduced by more than 50% in diabetic rats and corrected by insulin as measured by alkaline phosphatase activity and 45Ca incorporation. Decreased in vivo endochondral bone growth and development during diabetes is the result of 1) inhibition of insulin-dependent mesenchymal cell proliferation, 2) decreased and delayed cartilage formation due to impaired mesenchymal cell proliferation, 3) decreased and delayed vascular invasion prior to chondrolysis and osteogenesis, and 4) reduced insulin-dependent calcification and ossification.
125 citations
TL;DR: Results indicate that physiological perturbations of VLDL TG production need not be accompanied by an alteration inVLDL apoB production, and the regulation of apoprotein B (apoB) secretion in man is understood.
Abstract: As a first step toward understanding the regulation of apoprotein B (apoB) secretion in man, we have simultaneously studied the production of very-low-density lipoprotein (VLDL) apoB and VLDL trigl...
122 citations
TL;DR: Normal and adrenalectomized rats treated with cortisone lost 2% of their initial body weight per day, whereas controls gained weight at a rate of 2%/day, suggesting that loss of muscle weight and protein content as well as increased amino acid release resulted from the reduction in protein synthesis.
Abstract: Normal and adrenalectomized rats treated with cortisone lost 2% of their initial body weight per day, whereas controls gained weight at a rate of 2%/day. Five days of treatment resulted in a 25% reduction in the weights of a number of mixed fiber type muscles, but did not affect the weights of heart or soleus, a muscle consisting of slow-twitch red fibers. Reductions in muscle weights were accompanied by a loss of protein and RNA. Perfused hemicorpus preparations from rats receiving 5 days of treatment released several amino acids in greater amounts than the controls. Protein synthesis in perfused gastrocnemius was reduced 50-60% after 3 or 5 days of steroid treatment. This reduction was due to a loss of RNA and to an inhibition of translation resulting from an impairment in peptide-chain initiation. In contrast, RNA content and initiation were not altered in heart and soleus. Protein degradation in perfused hemicorpus and cathepsin D activity in gastrocnemius were unaffected by cortisone treatment, suggesting that loss of muscle weight and protein content as well as increased amino acid release resulted from the reduction in protein synthesis.
122 citations
TL;DR: In streptozotocin diabetic rats bearing intrahepatic, presumably denervated islet isografts, these rapid insulin responses to oral saccharin and tap water stimulation were completely abolished, whereas the early insulin response to intravenous glucose was decreased by only about 30%.
Abstract: The ability of saccharin, in comparison with glucose and tap water, to elicit glycemia-independent neurally mediated insulin secretion was investigated in chronically catheterized, freely moving rats. Plasma glucose and insulin concentrations were measured continuously from venous blood with a sampling resolution of one per minute. In normal rats, 1 ml of 0.15% saccharin caused a significant rapid rise in peripheral plasma insulin levels lasting up to 5 min, without significant changes in glycemia. Tap water alone also induced a transient elevation in insulinemia but was much smaller than the saccharin-induced response. In streptozotocin diabetic rats bearing intrahepatic, presumably denervated islet isografts, these rapid insulin responses to oral saccharin and tap water stimulation were completely abolished, whereas the early insulin response to intravenous glucose was decreased by only about 30%. These results are consistent with the concept of gustatory and other oral sensory signals acting as triggers for neurally mediated insulin release.
122 citations
TL;DR: Obese subjects also developed hyperketonemia significantly more slowly than did normal-weight subjects, yet demonstrated substantially the same changes in magnitude and direction in carnitine and its metabolites.
Abstract: Carnitine metabolism was studied in normal-weight and obese subjects by measurement of carnitine and its acyl derivatives in plasma and urine. When first fed an isocaloric, low-carnitine diet, both groups showed a decrease in plasma total carnitine, primarily due to a decrease in the free carnitine fraction. Urinary free carnitine excretion also fell significantly. When fasting was instituted, plasma total carnitine concentration increased. This was the net result of a rapid increase in short-chain and long-chain acylcarnitine and a delayed decrease in free carnitine. Urinary excretion of short-chain acylcarnitines increased parallel to rising plasma concentrations, whereas free carnitine excretion first decreased and then tended to increase slightly. Both plasma and urinary short-chain acylcarnitine correlated with beta-hydroxybutyrate. All of these changes were reversed by refeeding, in the obese even with a low-carnitine hypocaloric intake. Obese subjects also developed hyperketonemia significantly more slowly than did normal-weight subjects, yet demonstrated substantially the same changes in magnitude and direction in carnitine and its metabolites.
108 citations
TL;DR: The experiments demonstrate that, when fafa rats are prevented from expressing hyperphagia throughout life, the complete obese "syndrome" still develops and support the concept that a peripheral metabolic adaptation results in preferential shunting of dietary substrate in the restricted obese rats to adipose tissue with concomitant decreases in other tissues.
Abstract: The free-feeding, genetically obese rat is hyperphagic, hyperinsulinemic, and hypertriglyceridemic and has increased fat cell size and number compared to its lean littermate. These experiments demonstrate that, when fafa rats are prevented from expressing hyperphagia throughout life, the complete obese "syndrome" still develops. Furthermore, life-long food restriction does not prevent increased lipoprotein lipase in the fafa rat. The data support the concept that a peripheral metabolic adaptation, probably in lipid metabolism, results in preferential shunting of dietary substrate in the restricted obese rats to adipose tissue with concomitant decreases in other tissues.
TL;DR: Maternal PTH was significantly related to the arteriovenous difference of 1,25(OH)2D levels (P < 0.01) in cord blood, and it possibly enhances the synthesis of 1-25( OH) 2D during the final stage of fetal development.
Abstract: Plasma levels of calcium and of parathyroid hormone (PTH) were comparable in the mothers at delivery and in nonpregnant controls; magnesium was decreased (P < 0.001) in maternal blood; and phosphate (P < 0.001), 1,25-dihydroxyvitamin D (1,25(OH)2D) (P < 0.001), and calcitonin (CT) (P < 0.01) were raised. Cord levels of calcium (P < 0.01), magnesium (P < 0.05), and CT (P < 0.01) were higher, and PTH (P < 0.01) was lower than in the maternal blood. Levels of 25(OH)D, 1,25(OH)2D, and 24,25(OH)2D lower in fetal than in maternal blood (P < 0.01) and significant linear correlations between the vitamin D metabolites examined in mothers and neonates (P < 0.001) are consistent with a diffusion barrier across the placenta and/or different affinities of binding proteins. Plasma levels of 25(OH)D and 24,25(OH)2D were significantly related (P < 0.01), suggesting precursor product type, relationships. Levels of 1,25(OH)2D higher in arterial than in venous umbilical blood (P = 0.06, sign test; P < 0.005, paired t test) suggest that the fetus participates in the synthesis of 1,25(OH)2D. Maternal PTH was significantly related to the arteriovenous difference of 1,25(OH)2D levels (P < 0.01) in cord blood, and it possibly enhances the synthesis of 1,25(OH)2D during the final stage of fetal development.
TL;DR: The effects of acute (2-day) and long-term diabetes on rates of protein synthesis, peptide-chain initiation, and levels of RNA were examined in rat skeletal muscles that are known to have differing proportions of the three fiber types: fast-twitch white, fast- twitch red, and slow-twitch red.
Abstract: The effects of acute (2-day) and long-term (7-day) diabetes on rates of protein synthesis, peptide-chain initiation, and levels of RNA were examined in rat skeletal muscles that are known to have d...
TL;DR: Evidence is presented in support of the hypothesis that the rise in cytosolic calcium ions resulting from changes in calcium and other aspects of cellular metabolism is responsible for many of the alpha-adrenergic actions of catecholamines.
Abstract: Epinephrine and norepinephrine binding sites with the physiological characteristics of alpha-adrenergic receptors have been identified in the plasma membranes of liver and other cells. Interaction of catecholamines with these receptors causes a mobilization of calcium ions from mitochondria and perhaps other intracellular stores in liver cells. In other cells, there may also be influx of extracellular calcium ions. Evidence is presented in support of the hypothesis that the rise in cytosolic calcium ions resulting from these changes is responsible for many of the alpha-adrenergic actions of catecholamines. Possible mechanisms by which activation of alpha-adrenergic receptors causes changes in calcium and other aspects of cellular metabolism are discussed.
TL;DR: It is concluded that the decrease in dietary energy from 8.0 to 2.1 MJ did not influence protein turnover, but that dietary protein was necessary if rates of whole-body protein synthesis and breakdown were to be maintained.
Abstract: Rates of whole-body protein synthesis and breakdown in obese subjects have been measured by three methods: constant intravenous infusion of [1-14C]leucine, repeated oral doses of [15N]glycine, and a single oral dose of [15N]glycine. The three techniques gave similar rates of synthesis and breakdown when the subjects received a normal diet containing 8.0 MJ and 70 g protein. After 3 wk on a low-energy diet (2.1 MJ), repeat measurements were made. When the low-energy diet contained protein (50 g), rates of protein synthesis and breakdown were little different from those with the normal diet. When the low-energy diet contained no protein, there was a 40% fall in whole-body protein synthesis and a smaller fall in breakdown. Excretion of 3-methylhistidine in the urine did not change with either low-energy diet. We conclude that the decrease in dietary energy from 8.0 to 2.1 MJ did not influence protein turnover, but that dietary protein was necessary if rates of whole-body protein synthesis and breakdown were to be maintained.
TL;DR: An in vitro rat muscle preparation that can contract at rates of 12-240 twitches/min maintained total adenine nucleotide content (ATP, ADP, AMP) at near resting levels and the preponderance of fast-twitch fibers correlated with the observed mechanical performance of the muscle.
Abstract: An in vitro rat muscle preparation is described that can contract at rates of 12–240 twitches/min. Maximum dF/dt paralleled maximum twitch tension, their ratio being constant at approximately 8 ms ...
TL;DR: Reults confirm that the thyroparathyroid glands influence plasma 1,25(OH)2D but they also provide evidence for a PTH-independent response of plasma 1-25-dihydroxyvitamin D to Ca restriction.
Abstract: The increase of plasma 1,25-dihydroxyvitamin D (1,25(OH)2D) in response to Ca restriction has been suggested to be essentially mediated by parathyroid hormone (PTH) In this study, we have assessed
TL;DR: Findings suggest that sleep might be related to both the nature and the degree of utilization of the circulating metabolites, and that rats that received the highly nutritive composite solution showed significant increase in both SWS and PS.
Abstract: Unrestrained food-deprived rats received their daily caloric needs through continuous or discontinuous intravenous infusions of specific nutritive substances over a period of 3 consecutive days each, and the effect on sleep monitored by electroencephalogram was examined. Continuous glucose or lipid infusions did not affect the daily sleep quotas. Amino-acid infusion brought about a significant increase in paradoxical sleep (PS), whereas slow-wave sleep (SWS) remained unchanged. Rats that received the highly nutritive composite solution showed significant increase in both SWS and PS. The same increase in SWS and PS was observed when exogenous insulin was coinfused with continuous infusion of glucose or when glucose infusions were discontinuous. These findings suggest that sleep might be related to both the nature and the degree of utilization of the circulating metabolites. A model for the action on sleep of nutrients at the systemic level was proposed; only when substances are metabolized is there a direct effect on sleep mechanisms.
TL;DR: In hearts supplied some, but not all, of the substrate mixtures, cardiac work maintained efficiently of protein synthesis and inhibited protein degradation, indicating that faster protein synthesis did not depend on increased amino acid availability.
Abstract: Cardiac work increased protein synthesis in hearts supplied glucose (mixture 1), glucose-insulin-glucagon-lactate-beta-hydroxybutyrate (mixture 2) or palmitate-beta-hydroxybutyrate-glucose (mixture...
TL;DR: The results suggest that the relation between sleep and feeding and their concomitant circadian fluctuation are possibly modulated by a common factor, namely the metabolic rate that is influenced by the lipogenesis/lipolysis rate.
Abstract: Sleep and feeding patterns were continuously recorded in rats under intravenous saline (control) and alternating insulin-epinephrine (experimental) infusions. The infusion of insulin (lipogenetic hormone) during the normally light period (0800-1600) replaced by epinephrine (lipolytic hormone) during the normally lipogenetic dark period (1600-0800) resulted in a complete inversion of the normal circadian distribution of sleep and feeding patterns and also of their correlation. Insulin infusion resulted in low blood glucose and glycerol levels whereas epinephrine increased these physiological parameters. Different control conditions showed that the fluctuations of sleep and feeding were dependent on the rate of utilization of the circulating metabolites at the cellular level. These results together with previous data suggest that the relation between sleep and feeding and their concomitant circadian fluctuation are possibly modulated by a common factor, namely the metabolic rate that is influenced by the lipogenesis/lipolysis rate.
TL;DR: The studies indicate that the undirectional clearance by brain of both testosterone and estradiol is inversely related to the SHBG level and the fraction of hormone transported into brain greatly exceeds the free (dialyzable) moiety and is essentially equal to the albumin-bound fraction of plasma testosterone or Estradiol.
Abstract: The effect in vivo of the plasma proteins in human serum on the transport of [3H]testosterone (T), [3H]-dihydrotestosterone (DHT), and [3H]estradiol (E2) through the brain capillary wall, i.e., the blood-brain barrier, was studied in anesthetized rats using a tissue-sampling-single-injection technique, In the absence of plasma proteins, approximately 90% of plasma T, DHT, or E2 was transported into brain on a single pass after a bolus carotid injection of labeled hormone. Serum was obtained from 57 patients in seven different clinical conditions: pregnancy, oral contraceptive use, thin and obese postmenopausal, follicular phase female, hirsutism, and normal male; the level (mean +/- SD) of sex hormone-binding globulin (SHBG) varied from 17 +/- 5 nM (hirsutism) to 323 +/- 83 nM (pregnancy). When the carotid injection solution was made 67% serum, the amount of T, DHT, or E2 transported into brain was inhibited in proportion to the concentration of SHBG. Among the patient groups, an overall linear inverse correlation between the mean SHBG level and the mean extraction of unidirectional influx of testosterone (r = 0.99) and estradiol (r = 0.98) was observed. These studies indicate that a) the undirectional clearance by brain of both testosterone and estradiol is inversely related to the SHBG level and b) the fraction of hormone transported into brain greatly exceeds the free (dialyzable) moiety and is essentially equal to the albumin-bound fraction of plasma testosterone or estradiol.
TL;DR: The results indicate that in man epinephrine can cause hyperglycemia via both alpha- and beta-adrenergic stimulation of glucose production and suppression of glucose clearance, either directly or indirectly.
Abstract: Epinephrine (50 ng . kg-1 . min-1) was infused for 120 min in seven normal volunteers alone (combined alpha- and beta-adrenergic stimulation), with propranolol (alpha-adrenergic stimulation), and with propranolol plus phentolamine (alpha-adrenergic blockade superimposed on alpha-adrenergic stimulation). During alpha-adrenergic stimulation, plasma glucose and glucose production increased 32 and 42% less, respectively, than during infusion of epinephrine alone, whereas glucose clearance was suppressed comparably. Plasma insulin decreased during alpha-adrenergic stimulation but increased during infusion of epinephrine alone. Plasma epinephrine was threefold greater during infusion of epinephrine plus propranolol than during infusion of epinephrine alone. When alpha-adrenergic blockade was superimposed on alpha-adrenergic stimulation, the increases in plasma glucose and glucose production as well as the decreases in plasma insulin and glucose clearance observed during alpha-adrenergic stimulation were virtually abolished, whereas plasma epinephrine levels were unaltered. These results indicate that in man epinephrine can cause hyperglycemia via both alpha- and beta-adrenergic stimulation of glucose production and suppression of glucose clearance, either directly or indirectly. alpha-Adrenergic effects on glucose production and clearance may be mediated by inhibition of insulin secretion.
TL;DR: The data reveal that circulating levels of alcohol that do not result in hepatic or testicular injury are toxic for bone, and alcohol treatment was associated with a significant decrease in urinary calcium excretion, but had no effect on phosphate excretion nor on its renal tubular re absorption.
Abstract: Chronic ethanol administration to growing rats for 56 days resulted in circulating levels of 140 mg/dl, approximating concentrations that characterize alcoholic intoxication in man. This degree of alcohol ingestion, although without gross or histological effect on the liver or testicles, was attended by decreased trabecular bone volume despite a normal rate of skeletal mineralization as measured by time-spaced tetracycline labeling. Concomitant serum levels of calcium, phosphate, magnesium, creatinine, glutamic oxalacetic transaminase, alkaline phosphatase, testosterone, and 25-hydroxyvitamin D were normal. Although alcohol treatment was associated with a significant decrease in urinary calcium excretion, it had no effect on phosphate excretion nor on its renal tubular reabsorption. The data reveal that circulating levels of alcohol that do not result in hepatic or testicular injury are toxic for bone.
TL;DR: Differences in reactivity and contractility of aorta and PV in progressive stages of experimental diabetes could be due to alterations in calcium handling and its metabolism in arterial and venous smooth muscle cells in the diabetic state.
Abstract: Responses of isolated aorta and portal vein (PV) to norepinephrine (NE), angiotensin II (AII), KCl, and CaCl2 were investigated in alloxan diabetic rats. Based on serum biochemical parameters (i.e., glucose, cholesterol, triglycerides, and creatinine) (alloxan, 150 mg/kg), diabetic rates were divided into three groups: 1) mildly diabetic at 1 week (only elevated glucose levels), 2) moderately diabetic at 4 wk (elevated glucose, triglycerides, and creatinine), and 3) severely diabetic at 8 wk (all serum biochemical parameters elevated). The sensitivity (i.e., ED50) of aortic smooth muscle from diabetic rats when compared to saline controls was 1) unchanged in mild diabetes; 2) decreased to KCl, AII, and CaCl2 in moderate diabetes; and 3) decreased to KCl, NE, and CaCl2 in severe diabetes. Ability of aortic smooth muscle to develop maximal contractions (i.e., contractility) to all these agonists was markedly diminished in severe diabetes. Spontaneous phasic contractions of PV from diabetic rats exhibited progressively greater tension as the disease advanced. Unlike aortas, contractility of PV to vasoactive agents was not affected at any stage of diabetes. PV sensitivity to AII in moderate diabetes and to Ca in severe diabetes was decreased when compared to saline controls. These differences in reactivity and contractility of aorta and PV in progressive stages of experimental diabetes could be due to alterations in calcium handling and its metabolism in arterial and venous smooth muscle cells in the diabetic state.
TL;DR: Regulation of respiration by catecholamines was studied in adipocytes isolated from interscapular brown adipose tissue of warm-acclimated rats by rapid digestion of collagenase to reveal that norepinephrine elicits thermogenesis at physiological concentrations (less than or equal to 1 microM) predominantely via beta 1-adrenergic pathways.
Abstract: Regulation of respiration by catecholamines was studied in adipocytes isolated from interscapular brown adipose tissue of warm-acclimated rats by rapid digestion of collagenase. (-)-Norepinephrine ...
TL;DR: The results obtained indicate that a number of physiological factors may affect plasma ADH levels during PEEP, including the carotid body and aortic arch baroreceptors as wells as sensors of intracranial pressure.
Abstract: In an attempt to define more precisely the various mechanisms involved in antidiuretic hormone (ADH) release during positive end-expiratory pressure ventilation (PEEP), experiments were performed o...
TL;DR: The relationship between plasma osmolality and plasma vasopressin is not stable during dehydration in the whole range and that hypovolemia probably can influence the secretion rate and/or metabolic clearance rate and thereby the relationship.
Abstract: The relationship between plasma osmolality (pOsm) and plasma vasopressin (pAVP) was studied in 13 human subjects during dehydration. The fit of linear, log-linear, parabolic, and exponential models was tested. For all of the data, the nonlinear models had the best fit. However, when individual differences in either gain or threshold were allowed for, the linear models were better than log-linear models. Finally, analyses were made with individual data points. Linear models had the best fit in half of the subjects, whereas for the others the parabolic model gave the best fit. For those subjects investigated in the low range of the osmoregulatory curve, a linear relationship was found, whereas, for those having the most pronounced increase in pOsm, the most significant improvement was found with the parabolic model. This finding indicates that the relationship is not stable during dehydration in the whole range and that hypovolemia probably can influence the secretion rate and/or metabolic clearance rate and thereby the relationship.
TL;DR: Cardiac hypertrophy as measured by the increase in cardiac mass was not prevented by such treatment with 1,3-diaminopropanol, showing that the increased content of polyamines was not essential for the hypertrophic response.
Abstract: Treatment with thyroxine for 7 days to produce myocardial hypertrophy led to an increase in the content of putrescine, spermidine, and spermine in the rat heart. The content of decarboxylated S-adenosylmethionine, the source of the aminopropyl groups needed for polyamine synthesis, was increased by the thyroxine treatment as were the activities of ornithine and S-adenosylmethionine decarboxylases. The enhanced S-adenosylmethionine decarboxylase activity measured in vitro was due to an increase in the amount of enzyme protein as measured by immunotitration with a specific antiserum. In vivo, decarboxylation of S-adenosylmethionine was, therefore, increased both by the increased amount of enzyme protein and by the elevated concentration of putrescine (which activates the enzyme) brought about by the enhanced ornithine carboxylase activity. Spermine synthase did not change significantly during the treatment and spermidine synthase increased only slightly. Therefore, the accumulation of polyamines was mediated predominantly via the increased availability of both putrescine and decarboxylated S-adenosylmethionine. Administration of 1,3-diamino-2-propanol led to a rapid reduction in the activity of ornithine decarboxylase in the heart, and continued exposure to this substance by its inclusion in the drinking water completely prevented the increase in concentration of putrescine and polyamines in response to thyroxine. However, cardiac hypertrophy as measured by the increase in cardiac mass was not prevented by such treatment with 1,3-diaminopropanol, showing that the increased content of polyamines was not essential for the hypertrophic response.