[Survey on the prevalence of goiter in France].
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Demography↗
Biomedical subjects
R Mornex
Publications and source records attributed to R Mornex.
Determination of steady state and nonsteady-state glycerol kinetics in humans using deuterium-labeled tracer.
Using deuterium-labeled glycerol as tracer and gas-liquid chromatography-mass spectrometry techniques for the determination of isotopic enrichment, we have developed a simple and ethically acceptable method of determining glycerol appearance rate in humans under steady-state and nonsteady-state conditions. In normal subjects, the appearance rate of glycerol in the post-absorptive state was 2.22 +/- 0.20 mumol X kg-1 X min-1, a value in agreement with those reported in studies with radioactively labeled tracers. The ratio nonesterified fatty acid (NEFA) appearance rate/glycerol appearance rate ranged from 1.95 to 3.40. In insulin-dependent diabetic patients with a mild degree of metabolic control, the appearance rate of glycerol was 2.48 +/- 0.29 mumol X kg-1 X min-1. The volume of distribution of glycerol, determined by the bolus injection technique, was (mean) 0.306 l X kg-1 in normal subjects and 0.308 l X kg-1 in insulin-independent diabetic patients. To evaluate the usefulness of the method for determination of glycerol kinetics in nonsteady-state conditions, we infused six normal subjects with natural glycerol and calculated the isotopically determined glycerol appearance rate using a single compartment model (volume of distribution 0.31 l X kg-1). During these tests, the expected glycerol appearance rates were successively 5.03 +/- 0.33, 7.48 +/- 0.39, 9.94 +/- 0.34, 7.48 +/- 0.39, and 5.03 +/- 0.33 mumol +/- kg-1 X min-1, whereas the corresponding isotopically determined appearance rates were 4.62 +/- 0.45, 6.95 +/- 0.56, 10.85 +/- 0.51, 7.35 +/- 0.34, and 5.28 +/- 0.12 mumol X kg-1 X min-1.(ABSTRACT TRUNCATED AT 250 WORDS)
Adult↗
TRH and LH-RH distribution in discrete nuclei of the human hypothalamus: evidence for a left prominence of TRH.
Thyrotropin-releasing hormone (TRH) and luteinizing hormone-releasing hormone (LH-RH) have been measured by radioimmunoassay in individual human hypothalamic nuclei. A significant lateralization has been found for TRH in the ventromedial, dorsal and paraventricular nuclei, with higher concentration in the left side. In contrast LH-RH values did not differ between the left and the right side. This finding represents an additional example of cerebral specialization and the first report of lateralized peptide distribution in the human hypothalamus.
Adult↗
In vitro effects of endogenous opiate peptides on thyrotropin function: inhibition of thyrotropin-releasing hormone release and absence of effect on thyrotropin release.
Thyrotropin-releasing hormone (TRH) or thyroid-stimulating hormone (TSH) was measured by radioimmunoassay in the incubation medium of rat hypothalami or anterior pituitary halves, respectively. We studied the effect of opioid peptide addition (10(-8) to 10(-6) M) on TRH or TSH release. alpha- or beta-Endorphin decreased TRH release in a dose-dependent manner while only 10(-6) M Leu- or Met-enkephalin decreased TRH release. These inhibitory effects were prevented by addition of naloxone (10(-5) M). In the dose range used none of the opioid peptides modified TSH release. These results indicate that opioid peptides may play a role in the regulation of thyrotropin secretion via a hypothalamic action on TRH release.
Animals↗
[Comparison between the value of urinary free cortisol and 17-hydroxycorticosteroids for the diagnosis of Cushing's syndrome].
The usefulness for the diagnosis of Cushing's syndrome of urinary free cortisol and urinary 17-hydroxycorticosteroid (17-OHCS) determination was compared by measuring these substances in 17 normal and 28 obese subjects and in 19 patients with established Cushing's syndrome. These measurements were repeated in 16 obese subjects and 11 Cushing's syndrome patients after oral administration of dexamethasone (2 mg/day for 2 days, then 8 mg/day for 2 days). As a group, the patients with Cushing's syndrome had higher (p less than 0.001) excretion rate of both free cortisol and 17-OHCS, but the values observed in this group overlapped with those of normal and obese subjects. The overlap was not significantly different for free cortisol and 17-OHCS excretion. In each obese subject, oral dexamethasone decreased the urinary excretion rate of both free cortisol and 17-OHCS. Seven out of the eleven patients with Cushing's syndrome had no decrease of urinary free cortisol or 17-OHCS, whereas both values were slightly lower in one and decreased to levels similar to those obtained in obese subjects in the three remaining patients. It is concluded that there is no advantage in measuring free cortisol excretion instead of 17-OHCS excretion, either before of after a pituitary-adrenal suppression test, for the diagnosis of Cushing's syndrome.
17-Hydroxycorticosteroids↗
Determination of human ketone body kinetics using stable-isotope labelled tracers.
In order to avoid the use of radioactive tracers for the determination of human ketone body turnover, we have developed a method using a primed-continuous infusion of 13C-labelled acetoacetate or D-beta-hydroxybutyrate. Determination of the mole percent enrichment of blood acetoacetate and D-beta-hydroxybutyrate was performed by gas chromatography/mass spectrometry. In the post-absorptive state, the mean total ketone body appearance rate, determined in four subjects, was 3.74 mumol X kg-1 X min-1 using [3,4-13C2] acetoacetate and 2.76 mumol X kg-1 X min-1 using [3-13C]D-beta-hydroxybutyrate, values in agreement with those reported in studies with 14C-labelled tracers. In order to evaluate the usefulness of the method for determination of ketone body kinetics in non steady-state conditions, we infused four subjects with natural sodium acetoacetate and calculated the isotopically determined total ketone body appearance rate using a single compartment model (volume of distribution 0.20 l/kg; functional pool fraction: 1). During the tests with [3,4-13C2]-acetoacetate, the actual infusion rates of natural acetoacetate were 7.3 +/- 0.3, 14.6 +/- 0.8, 21.9 +/- 1.2 and 10.9 +/- 0.6 mumol X kg-1 X min-1 whereas the corresponding isotopically determined total ketone body appearance rates were respectively 9.2 +/- 1.0, 16.3 +/- 0.7, 23.1 +/- 1.1 and 10.7 +/- 0.8 mumol X kg-1 X min-1. During the tests with [3-13C]D-beta-hydroxybutyrate, the actual infusion rates were 8.4 +/- 0.5, 16.8 +/- 0.9, 25.2 +/- 1.4 and 12.6 +/- 0.8 mumol X kg-1 X min-1, and the isotopically determined appearance rates respectively 11.1 +/- 0.7, 16.7 +/- 0.7, 25.0 +/- 1.1 and 11.1 +/- 0.7 mumol X kg-1 X min-1.(ABSTRACT TRUNCATED AT 250 WORDS)
3-Hydroxybutyric Acid↗
Antiketogenic effect of glucose per se in vivo in man and in vitro in isolated rat liver cells.
The in vivo effect of glucose per se on blood ketone bodies, glycerol, and nonesterified fatty acids (NEFA) has been investigated in five normal (60 hours fasted) men receiving a somatostatin (SRIF) infusion (500 micrograms/h-1). When glycemia was raised over 10 mmol/L for 180 minutes by exogenous IV glucose infusion, neither insulin nor C peptide increase. NEFA and glycerol returned to fasting value in 40 minutes and remained stable. Ketone bodies decreased continuously and were significantly below the fasting values at the end of the study (1.3 +/- 0.3 mmol/L v 2.2 +/- 0.4 mmol/L, P less than 0.05). In order to ascertain whether glucose has been acting only on lipolysis or also on the liver ketogenic capacity, its effect was studied in vitro on isolated liver cells from 24-hour starved rats incubated with various amounts of palmitate. Glucose (30 mmol/L) did not affect the maximal ketogenic capacity (80 mumol/g (w/w)/h) measured with 1.6 mmol/L palmitate but increased the apparent palmitate K 0.5 for ketogenesis from 0.16 to 0.3 mmol/L. At physiologic free fatty acids concentration (0.22 mmol/L), glucose decreased ketogenesis by 90%. The effect was time-dependent, maximum after 30 minutes of incubation. Half-maximum inhibition by glucose was obtained at 6 mmol/L, a concentration at which lactate production was unaffected. These results suggest that glucose per se inhibits ketogenesis in vivo by acting probably both on lipolysis and on liver ketogenic capacity.
Animals↗
[Pheochromocytoma or the need for a diagnostic strategy].
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Adrenal Gland Neoplasms↗
Effects of ketone bodies on basal and insulin-stimulated glucose utilization in man.
Using the euglycemic clamp technique, we investigated the effects of high ketone body levels on basal and insulin-stimulated glucose utilization in normal subjects. Infusion of sodium acetoacetate in the postabsorptive state raised ketone body levels from 150 +/- 20 (+/- SE) mumol/liter to more than 1 mmol/liter. Endogenous glucose production declined from 2.71 +/- 0.20 mg kg-1 min-1 to 1.75 + 0.26 (P less than 0.01) and glucose utilization from 2.71 +/- 0.20 to 1.98 +/- 0.17 mg kg-1 min-1 (P less than 0.01), while blood glucose was maintained at the initial level by the infusion of glucose. There were no changes in plasma glucagon, insulin, or C-peptide. Plasma nonesterified fatty acids (P less than 0.01) and blood glycerol (P less than 0.01) and alanine (P less than 0.05) decreased, while blood lactate increased (P less than 0.01). Infusion of sodium bicarbonate had no effect on glucose kinetics. The decreases in glucose utilization and endogenous glucose production during the infusion of acetoacetate were not modified when the fall of plasma nonesterified fatty acids was prevented by iv heparin injection. During control euglycemic hyperinsulinemic clamps (1 and 10 mU kg-1 min-1 insulin infusion), endogenous glucose production was suppressed at the lowest insulin infusion rate; glucose utilization increased first to 7.32 +/- 0.96 mg kg-1 min-1 and then to 16.5 +/- 1.27 mg kg-1 min-1. During euglycemic hyperinsulinemic clamps with simultaneous sodium acetoacetate infusion, similar insulin levels were attained; endogenous glucose production was also suppressed at the lowest insulin infusion rate, and insulin-stimulated glucose utilization rates (7.93 +/- 1.70 and 15.80 +/- 1.30 mg kg-1 min-1) were not modified. In conclusion, acetoacetate infusion decreased basal, but not insulin-stimulated, glucose utilization. The increase in lactate during acetoacetate infusion in the postabsorptive state suggests that ketone body acted by decreasing pyruvate oxidation.
Acetoacetates↗
Regulation of peripheral plasma somatostatin like immunoreactivity in type I diabetes: role of the degree of metabolic control.
We have determined peripheral venous somatostatin like immunoreactivity (SLI) levels in 11 normal subjects (blood glucose--BG--: 4.4 +/- 0.1 mM; ketone bodies--KB--: 90 +/- 12 microM; plasma free fatty acids--FFA --: 340 +/- 42 microM), 4 Biostator controlled insulin dependent diabetics (BG: 5.4 +/- 0.2 mM; FFA: 418 +/- 38 microM; KB: 226 +/- 41 microM) and 7 poorly controlled ketotic diabetics (BG: 10.8 +/- 1.3 mM; FFA: 915 +/- 19 microM; KB: 2490 +/- 576 microM). SLI was determined again after 48 to 96 hours of intravenous insulin infusion for the 7 ketotic diabetics and after transient interruption of insulin infusion for the Biostator controlled diabetics. Relative to normal subjects ketotic diabetics had elevated SLI levels (29.7 +/- 5.9 vs 13.5 +/- 1.8 ng/L, p less than 0.01) whereas biostator-controlled patient had near to normal values (20.4 +/- 6.4 ng/L, p greater than 0.30). Transient arrest of insulin infusion in the Biostator controlled diabetics resulted only in a mild metabolic deterioration (BG: 12.8 +/- 2.1 mM; FFA: 640 +/- 146 microM; KB: 950 +/- 163 microM) without a significant rise of SLI. Intravenous insulin infusion in the initially ketotic patients decreased BG and KB in each subject (p less than 0.01) but decreased FFA (1097 +/- 170 to 453 +/- 74 microM, p less than 0.05) and SLI (34.0 +/- 12.0 to 9.8 +/- 2.4 ng/L, p less than 0.05) only in 4 patients whereas both FFA (737 +/- 107 to 725 +/- 25 microM) and SLI (27.6 +/- 4.7 to 20.3 +/- 4.7 ng/L) levels remained stable in the other 3. These results suggest that SLI levels in type I diabetics are dependent the degree of metabolic control and could be related to the variations of FFA concentrations.
Adolescent↗
Dephosphorylation of L-pyruvate kinase during rat liver hepatocyte isolation.
In isolated rat liver cells, the inhibition of L-pyruvate kinase (L-PK) by a cyclic AMP-dependent phosphorylation mechanism is involved in the hormonal control of glycolysis and gluconeogenesis. The aim of this study was to ascertain whether or not the in vivo phosphorylation state of the enzyme was maintained during the liver perfusion used to prepare isolated liver cells. When the L-PK phosphorylation state was studied indirectly in liver extracts by kinetic measurement, it was found that, during the perfusion, the S0.5 of phosphoenol pyruvate (PEP) for L-PK was decreased in a time-dependent manner from 1 +/- 0.08 to 0.64 +/- 0.1 mM (P less than 0.01) and 0.58 +/- 0.06 mM in liver cells. This shift was prevented only by the addition of glucagon to the perfusion medium. The extent of phosphorylation of L-PK was also estimated by incubation of the liver extract with [gamma-32P]ATP, protein kinase, and cyclic AMP, and measurement of 32Pi incorporated in L-PK by specific immunoprecipitation. In liver extracts removed at the beginning of the perfusion, 0.4 mol Pi/mol L-PK was incorporated and there was no stimulation by cyclic AMP. In contrast, in the liver extracts removed after 30 min of perfusion, cyclic AMP stimulated 32P incorporation two to threefold, and 1.6 mol Pi/mol L-PK was incorporated. These data suggest that L-PK was activated by a dephosphorylation mechanism during rat liver perfusion. This phenomenon could be involved in the classical inactivation of gluconeogenesis observed in the perfused rat liver model.
Animals↗
Lack of beta-adrenergic role for catecholamines in the development of hyperglycemia and ketonaemia following acute insulin withdrawal in type I diabetic patients.
In order to evaluate the role of beta-receptor mediated effects of catecholamines in the metabolic deterioration following insulin withdrawal in insulin-dependent diabetic patients we have measured in 5 patients metabolic substrate and hormone concentrations during a 6 hours arrest of insulin infusion, without or with a simultaneous infusion of propranolol. During insulin deprivation plasma epinephrine and norepinephrine increased slightly (from 107 +/- 10 ng/L to 173 +/- 6 ng/L and from 307 +/- 37 ng/L to 518 +/- 77/ng/L respectively (p less than 0.05), cortisol decreased physiologically, but growth hormone and glucagon were not significantly modified. Free insulin decreased progressively from 12.2 +/- 2.5 mU/L to 5.4 +/- 1.1 mU/L (p less than 0.01). Blood glucose and ketone bodies rose sharply before any significant change in catecholamine levels. Plasma free fatty acids and blood glycerol increased progressively and their rise appeared somewhat temporally related to the variations of catecholamine levels. The addition of propranolol to insulin deprivation did not modify the changes in hormone concentrations in spite of a slightly greater rise of epinephrine (from 78 +/- 4 ng/L to 179 +/- 7 ng/L, p less than 0.05) and norepinephrine (from 395 +/- 80 ng/L to 679 +/- 153 ng/L, p less than 0.05). The rises of glucose and ketone bodies were unaffected whereas the increases of free fatty acids and glycerol were slightly blunted. In conclusion, we have no evidence for a beta-adrenergic mediated role for catecholamines in the development of hyperglycaemia and ketonaemia in non-stressed insulin deprived diabetic patients, and only small evidence for a permissive effect on lipolysis.
Adult↗
[Physiopathology of the menopause].
The ageing of the ovary is marked by a diminution of the number of follicles and often of a decrease of the secretion of inhibine which entails the augmentation of the pituitary secretion. Although the menopausal ovary may not be absolutely inactive, its suddenly diminished secretory capacity then leads to a considerable fall of oestrogenic secretion. The author explains all the phenomena which allow the physiopathology of hot flushes to be assessed, and states the principal hypotheses which claim to explain them.
Adult↗
[Basedow's ophthalmopathy. Failure of treatment with plasma exchange and azathioprine].
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Azathioprine↗
Anti-tubulin antibodies in recent onset type 1 (insulin-dependent) diabetes mellitus: comparison with islet cell antibodies.
Antibodies to tubulin, the fundamental protein of microtubules, were studied by radioimmunoassay in patients with Type 1 (insulin-dependent) diabetes of varying duration and in healthy control subjects. Elevated levels of anti-tubulin antibodies were found in 46% of 28 patients with Type 1 diabetes of recent onset (less than or equal to 6 months) and in only 6.2% of 64 patients with long-standing Type 1 diabetes (duration 6-43 years). None of 34 DR3-positive normal subjects and none of 20 Type 2 (non-insulin-dependent) diabetic patients were positive for anti-tubulin antibodies. Anti-tubulin antibody levels were elevated in two out of 26 first-degree relatives of Type 1 diabetic patients. The specificity of the detection of anti-tubulin antibodies was demonstrated by dilution of the sera, competitive binding experiments between labelled and unlabelled tubulin, immunoblotting. Antibodies to tubulin were elevated in 60% of patients with islet cell surface antibodies and there was a significant association between anti-tubulin antibodies and islet-cell surface antibodies. These antibodies, however, recognize different specificities, since adsorption of islet cell surface antibody by rat islets did not alter the anti-tubulin antibody activity. Elevated anti-actin antibody responses were found in two out of 17 and one out of 26 patients with recent onset and long-standing Type 1 diabetes, respectively. In conclusion, anti-tubulin antibodies are detected in a high proportion of patients with diabetes of recent onset, are associated with islet cell surface antibodies and like islet cell surface antibodies decrease or disappear during the course of the disease.(ABSTRACT TRUNCATED AT 250 WORDS)
Actins↗
Metabolic alterations induced by chronic heat exposure in the rat: the involvement of thyroid function.
The effects of chronic exposure to high environmental temperature (34 degrees C) on T4 production rate, food-intake, growth-rate and resting metabolic rate were investigated in adult male rats. This study was designed to examine the extent of variations and possible relationships between these parameters. As compared to control rats of the same body weight kept at 25 degrees C, rats exposed to 34 degrees C for 3-4 weeks exhibited a retarded growth-rate: 2.3 vs 4.0 g/day, a reduced food-intake: 15.2 vs 23.2 g/day, a decreased T4 production-rate: 1.8 vs 2.7 micrograms/day and a decreased oxygen consumption: 4.0 vs 5.4 ml/min. Heat-exposure altered the 4 parameters to a similar extent. T4 supplementation (3 micrograms/day) which induced a decrease in plasma TSH concentration, did not restore a normal growth-rate in heat-exposed rats. The decreased food-intake of the heat-exposed rats was not associated with any significant changes in the daily pattern of variations of liver glycogen content, or in the mean daily levels of blood glucose or insulin. The ratio T3 to rT3 in plasma was not altered by chronic heat exposure. When rats which had been chronically exposed to heat (25 days at 34 degrees C) were exposed to 25 degrees C, growth-rate, food-intake and oxygen consumption rapidly increased to control values whereas the rate of T4 production remained low. It is concluded that (1) a decrease in thyroid hormone economy is not directly involved in the alterations of growth and energy expenditure in rats chronically exposed to heat, (2) heat exposure does not lead to the establishment of a fasted state resulting from a large reduction in voluntary food intake, (3) metabolic alterations induced by heat exposure are rapidly and completely reversible upon decreasing the environmental temperature.
Animals↗
Reduction of increased levels of blood glycerol and ketone bodies by propranolol in human hyperthyroidism: role of the fall of the triiodothyronine level.
Hyperthyroid patients in the postabsorptive state have elevated levels of blood glycerol and ketone bodies (KB): this is believed to be due to increased lipolysis and ketogenesis. These increased glycerol and KB levels return toward normal after oral propranolol administration. In order to investigate the mechanism of action of propranolol in hyperthyroid patients, we compared the effects of the oral administration of propranolol with those of timolol, propylthiouracil (PTU), and a placebo. The placebo had no effect. The free thyroxine index, immunoreactive insulin level and glucagon level were not modified by propranolol, timolol, or PTU. Propranolol decreased the pulse rate (P less than 0.01) and the levels of serum triiodothyronine (T3; P less than 0.05), blood glycerol (P less than 0.01), and KB (P less than 0.01). Like propranolol, timolol decreased the pulse rate (P less than 0.01) but had no effect on the T3, glycerol, or KB levels. Propylthiouracil did not modify the pulse rate, but like propranolol, it decreased the T3 (P less than 0.05), glycerol (P less than 0.01) and KB (P less than 0.01) levels. These results suggest that the metabolic actions of propranolol are not caused by its hemodynamic effects nor its beta-blocking properties but are mediated by the decrease of the T3 level.
Adolescent↗
Reduction by propranolol of urinary hydroxyproline excretion in human hyperthyroidism: a beta-receptor blockade effect or a membrane stabilizing mechanism?
In order to investigate the mechanism whereby oral propranolol administration reduces the increased rate of urinary hydroxyproline excretion (UHxE) of patients with hyperthyroidism, a comparison was made of the effects of the oral administration of propranolol-timolol, propylthiouracil (PTU), and a placebo to patients with hyperthyroidism and to normal controls. Propranolol decreased the pulse rate (P less than 0.01), serum triiodothyronine (T3) level (P less than 0.05), and UHxE (P less than 0.01) without modifying the serum free thyroxine index (FT4I) or parathormone (PTH) level. Timolol decreased the pulse rate (P less than 0.01) to the same extent as propranolol, had no effect on T3, FT4I, or PTH, and failed to decrease UHxE. Administration of PTU decreased the T3 level (P less than 0.05) to a similar extent as propranolol without modifying the FT4I or PTH level and had no effect on UHxE. Placebo administration had no effect. These results suggest that the reduction of UHxE by propranolol is not due to the beta-receptor-blocking properties of propranolol nor mediated by the propranolol-induced decrease in the level of T3 but is probably due to the membrane-stabilizing properties of propranolol.
Adult↗