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 47,337 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

To study whether hyperthermia reproduces hormonal and metabolic responses seen in stress states such as mild infections, six normal male subjects underwent (i) a 3-h hot bath and (ii) a 3-h thermoneutral control period. During the hot bath body temperature rose by 1.2 +/- 0.03 degrees C (mean +/- SEM) and significant peaks of circulating growth hormone (56 +/- 9 vs 7 +/- 4 mU/l), adrenaline (310 +/- 34 vs 152 +/- 39 pmol/l), glucagon (19.2 +/- 4.3 vs 11.8 +/- 2.3 pmol/l) and cortisol were recorded together with slight hyperinsulinaemia (6.5 +/- 1.3 vs 5.3 +/- 1.0 mU/l, P less than 0.05). Hyperthermia was also accompanied by significant increases in circulating levels of free fatty acids (0.93 +/- 0.1 vs 0.46 +/- 0.1 mmol/l), 3-hydroxybutyrate (196 +/- 67 vs 50 +/- 18 mumol/l), glycerol (102 +/- 10 vs 48 +/- 5 mumol/l) and lactate. Blood alanine decreased and blood glucose remained constant. When an intravenous glucose tolerance test was performed during the last hour of hyperthermia signs of impaired first phase and enhanced second phase insulin responses were recorded. Calculated values for glucose disappearance also deteriorated (1.34 +/- 0.19 vs 2.04 +/- 0.50 %/min, P less than 0.05). We conclude that hyperthermia mimics most major metabolic and hormonal changes observed during mild infection and could provide a model to study these conditions.
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PMID:Metabolic and hormonal responses to exogenous hyperthermia in man. 268 66

The effect of insulin induced hypoglycemia on glucoregulatory hormones and intermediary substrates was studied in four infants (three boys and one girl, ages 12-89 days) with persistent hyperinsulinism secondary to nesidioblastosis (two) or microadenoma of the pancreas (two). During the "fasting test" the following data expressed as mean basal plasma values +/- SEM vs. mean hypoglycemic values +/- SEM were obtained: insulin (57.3 +/- 17.9 vs. 27.5 +/- 10.6 microU/ml), C-peptide (4.9 +/- 1.1 vs. 3.5 +/- 0.9 ng/ml), free fatty acids (0.30 +/- 0.01 vs. 0.32 +/- 0.02 mmol/l), beta-hydroxybutyrate (less than 0.03 vs. 0.05 +/- 0.02 mmol/l), alanine (204.0 +/- 67.5 vs. 228.3 +/- 64.9 mumol/l), lactate (5.3 +/- 0.7 vs. 5.4 +/- 1.1 mg/dl), pyruvate (41.3 +/- 4.8 vs. 19.7 +/- 4.2 mg/dl). These data suggest "inappropriate" elevation of insulin and C-peptide levels, inhibition of lipolysis and lack of gluconeogenic substrates secondary to endogenous HI. An increase of cortisol (6.5 +/- 4.1 vs. 16.3 +/- 5.7 micrograms/dl), adrenaline (0.015 +/- 0.05 vs. 0.25 +/- 0.24 ng/ml) (3 out of 4) and noradrenaline (0.28 +/- 0.06 vs. 0.64 +/- 0.14 ng/ml) was noted, whereas only minute increase was found for glucagon (134.3 +/- 51.7 vs. 177.0 +/- 76.2 pg/ml) and HGH (5.7 +/- 1.1 vs. 7.1 +/- 1.1 ng/ml). Although some stimulation of neonatal glucoregulatory hormones was evident, this was not strong enough for counteracting endogenous HI.
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PMID:[Diagnostic evaluation of persistent neonatal hypoglycemia using the fasting test: behavior of glucoregulatory hormones and intermediary metabolites (1)]. 282 19

Subjective feeling of fatigue was quantified before and 20 days after elective uncomplicated abdominal surgery in 16 otherwise-healthy patients and compared with changes in heart rate and various hormonal and substrate responses to a 10-minute bicycle exercise (65% of preoperative maximal work capacity) preoperatively and postoperatively. Postoperatively, fatigue increased (p less than 0.001) from 3.0 +/- 0.5 to 5.3 +/- 0.5 arbitrary units (mean +/- SEM). Heart rate, plasma catecholamines, and serum growth hormone, lactate, alanine, and glycerol values always increased, whereas serum insulin values decreased in response to exercise (p less than 0.01). During exercise, only heart rate (p less than 0.01) and lactate (p less than 0.05) values were higher postoperatively compared with preoperatively. Increase in fatigue postoperatively correlated significantly to increase in heart rate (p less than 0.01) and correlated positively, but not significantly, to increase in plasma levels of noradrenaline (p = 0.08), growth hormone (p = 0.09), and alanine (p = 0.08) during exercise, but not to increase in serum lactate values (p greater than 0.8). Thus, after uncomplicated surgery, there was increased fatigue and amplified metabolic and cardiovascular response to a given absolute work load. These findings are similar to those observed during detraining and suggest a therapeutic role of exercise in the treatment of postoperative fatigue.
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PMID:Fatigue and cardiac and endocrine metabolic response to exercise after abdominal surgery. 291 3

We evaluated a GnRH agonist (GnRHa) as a potential single stimulus to both pituitary and ovarian secretion in 13 girls with true precocious puberty. We compared the GnRH agonist [6-D-(2-naphthyl)alanine]GnRH acetate (nafarelin, Syntex) administered as a single sc injection of 0.2 microgram/kg to GnRH infused iv in a dose of 2 micrograms/kg X h for 3 h and assessed the response of plasma steroid intermediates in estradiol (E2) biosynthesis. Although serum LH and FSH levels increased to similar peaks 3 h after commencing GnRH and nafarelin testing, they rose faster (P less than 0.01 at 1 h) and remained elevated longer (P less than 0.05 at 24 h) after nafarelin administration. At the third hour of testing with either agent, LH and FSH rose 8.8- and 3.4-fold, respectively (P less than 0.001 vs. baseline), whereas the rise in E2 was inconsistent and averaged only one third (P less than 0.02). However, plasma E2 increased later after nafarelin, but not after GnRH, rising from a baseline level of 30 +/- 6 (+/- SEM) to 115 +/- 13 pg/ml at 24 h (P less than 0.001). The least E2 response to nafarelin at this time was 150%. This rise is probably an underestimate of the maximum E2 rise, since a 6-fold response to nafarelin was found at 12 h in patients sampled then. Measurement of steroid intermediates from progesterone and 17 alpha-hydroxypregnenolone to E2 indicated that the response to nafarelin was typical of normal ovarian follicular secretion. That is, plasma levels of the intermediates in E2 biosynthesis rose less than 2-fold, and only the elevations in androstenedione, from 58 +/- 10 to 78 +/- 16 ng/dl (P less than 0.05), and estrone, from 14 +/- 3 to 38 +/- 7 pg/ml (P less than 0.02), at 24 h were significant. The greater effectiveness of nafarelin than GnRH in stimulating E2 secretion appears to be related to the more prolonged gonadotropin response. The magnitude, consistency, specificity, and rapidity of the gonadotropin and E2 responses to nafarelin indicate that this is a promising agent for rapidly testing pituitary and ovarian function simultaneously.
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PMID:The rapid ovarian secretory response to pituitary stimulation by the gonadotropin-releasing hormone agonist nafarelin in sexual precocity. 294 12

Rats of 230 g were treated with 0.1 mg of dexamethasone twice daily for 2 days (n = 5) and 14 days (n = 9). Controls received isotonic saline. During the first week of dexamethasone treatment the rats lost weight rapidly (up to 9 g/day). The weight loss diminished during the second week of treatment. The fasting blood insulin concentration increased sevenfold in the dexamethasone-treated rats. Fasting blood glucagon and glucose concentrations were not different from controls. In the dexamethasone-treated rats the fasting alpha-amino-N concentrations were lower: 4.0 +/- 0.3 mmol/l (mean +/- SEM) versus 6.8 +/- 0.3 mmol/l in controls. The capacity of Urea-N Synthesis, determined during alanine loading was: after 2 days of treatment 14.7 +/- 1.7 mumol/(min 100 g), after 14 days of treatment 7.9 +/- 0.8 mumol/(min 100 g), and in controls 7.5 +/- 1.0 mumol/(min 100 g) (mean +/- SEM). In conclusion, glucocorticoid treatment leads to a transient change in the liver function as to hepatic amino-N conversion, implying that more amino-N than normal is eliminated as urea-N after 2 days of treatment. This may contribute to the early, but not the late body weight loss.
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PMID:Dexamethasone increases the capacity of urea synthesis time dependently and reduces the body weight of rats. 304 15

In order to study the effect of hyperglucagonaemia on nitrogen metabolism in diabetes, zinc protamine glucagon 60 micrograms was injected subcutaneously 3 times daily for 4 weeks into streptozotocin diabetic rats (n = 5), adequately treated with long acting insulin. This raised the plasma concentration of glucagon to 725 +/- 125 (mean +/- SEM), which is not different from that found in portal blood of uncontrolled diabetic rats: 400 +/- 75 ng/l. The controls were 5 diabetic rats treated with insulin alone and 5 non-diabetic rats. Compared with control rats the nitrogen balance was reduced (p less than 0.05) and the nitrogen contents of carcass, heart, intestines, and kidneys were reduced by 15-30% (p less than 0.05) in the glucagon treated rats. The hepatic capacity of urea synthesis and the alanine elimination rate were determined in the 3 above-mentioned groups, and confirmed in 3 identical groups followed for only 2 weeks; and in addition in a group of glucagon treated diabetic rats, where the long acting glucagon was substituted by neutral insulin the last two days before investigation.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Exogenous hyperglucagonaemia in insulin controlled diabetic rats increases urea excretion and nitrogen loss from organs. 306 29

Brief starvation is accompanied by decreased circulating levels of most amino acids, which has been attributed to an increased splanchnic uptake of amino acids, primarily alanine, for gluconeogenesis. However, quantitative data on splanchnic exchange of amino acids and gluconeogenic precursors is lacking. Consequently, arterial concentrations and splanchnic exchange of whole blood amino acids, ketone bodies, glucose, and gluconeogenic precursors were measured in 16 prolonged fasted (60 to 64 hours) and 15 overnight fasted (12 to 14 hours) healthy, nonobese subjects. After the 60-hour fast net splanchnic glucose production decreased by 41% to 0.31 +/- 0.02 mumol/L (P less than .001), whereas the splanchnic uptake of gluconeogenic precursors increased and could account for the total glucose output. Net splanchnic uptake of taurine, threonine, serine, glycine, lysine, histidine, and arginine rose significantly in response to fasting (P less than .05 to .01) due to increased splanchnic fractional extraction. Although the splanchnic fractional extraction of alanine was augmented by 40% (P less than .001), net splanchnic uptake was not influenced by fasting. Total net splanchnic uptake of amino acids increased by 68%, from 231 +/- 44 mumol/min in the postabsorptive state to 388 +/- 63 mumol/min (mean +/- SEM) (P less than .05) in the 60-hour fasted state. However, only one half of this rise was accounted for by gluconeogenic amino acids.
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PMID:Splanchnic metabolism of amino acids in healthy subjects: effect of 60 hours of fasting. 319 1

1. The present study examined the effect of an infusion of the dipeptide alanylglutamine or of the corresponding amino acids alanine and glutamine in equimolar amounts (10 mumol min-1 kg-1) on the canine hindlimb exchange of alanine and glutamine in the post-operative anaesthetized dog. In contrast to glutamine, the dipeptide alanylglutamine is stable in aqueous solution and therefore would be a suitable substrate for parenteral nutrition. 2. The infusion of alanylglutamine increased (a) the arterial concentration of alanylglutamine to a plateau level (120 +/- 9.5 mumol/l, mean +/- SEM) 20 min after start of the infusion, (b) the mean arterial alanine concentration from 761 +/- 42 to a plateau of 1500-1700 mumol/l (P greater than 0.01) and (c) the arterial glutamine concentration from 407 +/- 51 to a plateau of 1050-1500 mumol/l (P greater than 0.01). Alanine and glutamine levels were slightly higher (14% and 26%, respectively, NS) in the group receiving the equimolar amount of alanine and glutamine. 3. Infusion of alanylglutamine for 1 h abolished the net efflux of glutamine (from -0.80 +/- 0.1 to -0.03 +/- 0.2 mumol min-1 kg-1; P greater than 0.05) and invoked a net influx of alanine (from -0.50 +/- 0.19 to +0.27 +/- 0.14 mumol min-1 kg-1; P greater than 0.01). These changes were similar to those achieved when the two amino acids were infused. 4. This study demonstrates that during short-term administration of alanylglutamine or of the corresponding amino acids the nitrogen release from the hindlimb of the anaesthetized post-operative dog via alanine and glutamine is reduced.
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PMID:Alanylglutamine reduces muscle loss of alanine and glutamine in post-operative anaesthetized dogs. 320 96

Cerebrospinal fluid (CSF) histidine concentration was significantly elevated in seven patients early in the alcohol withdrawal syndrome (206.3 +/- 74.4 (SEM) nanomols/ml CSF). When these same patients were restudied an average of six days later when alcohol withdrawal was clinically resolved, their mean CSF histidine concentration continued to be significantly elevated (164.7 +/- 24.7) when compared to normal (12.0 +/- 0.5 nanomols/ml CSF). Other amino acids (aspartic acid, serine, alanine, methionine, leucine, tyrosine, phenylalanine, lysine and arginine) showed no definite changes from normal, and no change during the course of alcohol withdrawal. Possible reasons for these high concentrations and the extreme variability (especially early in alcohol withdrawal) are discussed.
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PMID:Elevated cerebrospinal fluid histidine in alcohol withdrawal. 322 84

These studies were designed to further test the hypothesis that corticotropin-releasing hormone (CRH) is released from axons innervating the noradrenergic neurons of the locus coeruleus (LC) and serves to activate these neurons during stress responses. Specifically, the effects of exogenous CRH on the electrophysiological activity of LC neurons in unanesthetized rats were characterized. Intracerebroventricular (I.C.V.) injection of CRH (0.3-3.0 micrograms) caused a dose-dependent increase in LC spontaneous discharge rates that became statistically significant 6-9 min after injection and was still evident 30-40 min later. A 1.0 and 3.0 micrograms amount of CRH caused peak increases of 86 +/- 32% and 184 +/- 29% (SEM), respectively. In contrast, neither the lowest dose of CRH (0.3 microgram) nor a high dose of Ala 14CRH (3.0 micrograms), an inactive analog of CRH, altered LC spontaneous activity. The effects of CRH administration on sensory-evoked activity of LC neurons were also determined. As previously reported (Foote et al., 1980; Aston-Jones and Bloom, 1981b), the repeated presentation of auditory tone stimuli resulted in a brief enhancement of LC discharge, which was usually followed by a period of relatively decreased activity. Administration of 1.0 or 3.0 micrograms CRH enhanced basal discharge during sensory testing, but discharge rates during the excitatory component of the sensory response were not altered. Quantitative analyses revealed that these doses of CRH produced a statistically significant decrease in the ratio of sensory-evoked to basal discharge rates. Additional analyses of the temporal distribution of discharge activity for individual recording sites during sensory testing demonstrated that 1.0 and 3.0 micrograms CRH altered relative response magnitudes to a statistically significant extent in 7 of 10 and 5 of 7 cases, respectively, while 0.3 microgram CRH and 3.0 micrograms Ala 14CRH were without effect. The present results are consistent with previous studies of CRH effects on LC activity in anesthetized rats (Valentino et al., 1983; Valentino and Foote, 1987). However, in unanesthetized animals, CRH is more potent in increasing tonic activity and does not decrease the absolute magnitude of sensory-evoked activity. The present results support the hypothesis that CRH released from fibers innervating the LC may affect the tonic activity of these cells and the relationship between tonic discharge and phasic, sensory-evoked activity.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Corticotropin-releasing hormone increases tonic but not sensory-evoked activity of noradrenergic locus coeruleus neurons in unanesthetized rats. 325 21


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