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Biomedical subjects

J Girard

Publications and source records attributed to J Girard.

At least 217 records · Page 12Linked to original sources
PubMed1988

Decreased hepatic fatty acid oxidation at weaning in the rat is not linked to a variation of malonyl-CoA concentration.

In rats weaned on a high-carbohydrate diet, hepatic fatty acid oxidation capacity is decreased when compared to suckling rats. Previous studies (Benito et al., 1979) suggested that a malonyl-CoA-dependent mechanism could be at the origin of this decrease. Studies on isolated hepatocytes show that despite, respectively, a low and a high lipogenic rate in suckling and weaned rats, malonyl-CoA concentrations are similar in the two groups. This might be due to the lower ratio fatty acid synthetase/acetyl-CoA carboxylase (EC 6.4.1.2) activities during suckling than after weaning. Different rates of hepatic fatty acid oxidation despite similar malonyl-CoA concentrations can be explained by the 2.5-fold higher carnitine palmitoyltransferase I (EC 2.3.1.21) activity in suckling rats together with a 7-fold higher Ki for malonyl-CoA. This precludes a tight control of fatty acid oxidation by [malonyl-CoA] in suckling rats. Weaning on a high-fat carbohydrate-free diet abolishes the changes previously described for the kinetic characteristics of carnitine palmitoyltransferase I suggesting that nutritional modifications rather than a developmental stage are involved. Thus, during the suckling-weaning transition, a variation of [malonyl-CoA] is not responsible for the decrease in hepatic fatty acid oxidation. It involves, in addition, a decrease in carnitine palmitoyltransferase I activity and an increase of the sensitivity of this enzyme to malonyl-CoA.

ATP Citrate (pro-S)-Lyase↗
PubMed1988

Human growth hormone in urine: development of an ultrasensitive radiometric assay.

An immunoradiometric assay for human growth hormone (HGH) has been developed which has a detection limit of 1 ng/l and can measure HGH in unextracted urine from normal children and adults. The assay is based on a two-step procedure, using a solid-phase goat-anti-HGH immunosorbent for immunoextraction and [125I]-labeled monoclonal HGH-antibody for detection and quantification. The assay is not affected by urea, NaCl or changes of pH from 5-8. The mean urine HGH concentration in normal children is 6.78 +/- 7.6 (SD) pg/ml, in patients with HGH-deficiency 1.3 +/- 0.9 pg/ml which increases to 11.7 +/- 13.4 pg/ml on the day of growth hormone injection.

Evaluation Studies as Topic↗
PubMed1988

Interaction of cortisol and epinephrine in the regulation of leucine kinetics in man.

To assess the interaction of the two major stress hormones epinephrine and cortisol in the regulation of leucine kinetics in man, epinephrine (50 ng/kg/min) was infused either alone or in combination with cortisol (2 micrograms/kg/min) into two groups of 6 postabsorptive normal male subjects during 180 min. Plasma leucine concentrations decreased by 28% (p less than 0.05) from baseline during epinephrine treatment (plasma levels 515 pg/ml); this was due to a decrease of leucine appearance (determined by 1-13C-leucine infusions) by 23% (p less than 0.025); leucine oxidation decreased by 29% (p less than 0.05). However, when plasma cortisol concentrations were elevated to supraphysiological levels (16.3 mumol/l) during epinephrine administration, the decreases of leucine plasma concentrations, appearance and oxidation were abolished. Plasma glucose and FFA concentrations were similarly elevated during both kinds of treatment. Since leucine appearance represents a measurement of total body protein breakdown and leucine disappearance into non-oxidative pathways reflects protein synthesis, the data indicate that plasma epinephrine concentrations during severe stress exert a protein anabolic effect in man which may counteract catabolic properties of elevated plasma cortisol.

Adult↗
PubMed1988

Fatty acid metabolism in hepatocytes isolated from rats adapted to high-fat diets containing long- or medium-chain triacylglycerols.

Fatty acid oxidation and synthesis were studied in isolated hepatocytes from adult rats adapted for 44 days on low-fat, high-carbohydrate (LF), diet or high-fat diets, composed of long-chain (LCT) or medium-chain (MCT) triacylglycerols. The rates of [1-14C]octanoate oxidation were almost similar in each group studied, whereas the oxidation of [1-14C]oleate was 50% lower in the LF group than in animals adapted to high-fat diets. The rates of oleate oxidation are inversely correlated with the rates of lipogenesis. However, it seems unlikely that [malonyl-CoA] itself represents the sole mechanism involved in the regulation of oleate oxidation during long-term LCT or MCT feeding, since: (1) despite a 3-fold higher concentration of malonyl-CoA in MCT-fed rats than in LCT-fed ones, the rates of oleate oxidation are similar; (2) when malonyl-CoA concentration is increased after stimulation of lipogenesis (by adding lactate + pyruvate) in MCT-fed rats, to a level comparable with that of the LF group, the rate of oleate oxidation remains 55% higher than that measured under similar conditions in the LF-fed rats; (3) in the LF group, the 90% decrease in malonyl-CoA concentration [by 5-(tetradecyloxy)-2-furoic acid] is not associated with a stimulation of oleate oxidation. By contrast, the sensitivity of carnitine palmitoyltransferase I (CPT I) to malonyl-CoA is markedly decreased in the LCT- and MCT-fed rats, by 90% and 70% respectively. The relevance of this decrease in the sensitivity of CPT I is discussed.

Animals↗
PubMed1988

Proton-proton correlations at small relative momentum in neon-nucleus collisions at E/A=400 and 800 MeV.

Proton-proton small angle correlations have been measured in neon-nucleus collisions, using the 4 pi detector Diogene, at 400 and 800 MeV per nucleon incident energies. Values of the size of the emitting region are obtained by comparison with the Koonin formula, taking into account the biases of the apparatus. The dependence of the density on target mass and incident energy is also analysed.

Carbon↗
PubMed1988

Long-term treatment of central precocious puberty with an intranasal LHRH analogue: control of pituitary function by urinary gonadotropins.

Daily subcutaneous doses of luteinizing hormone-releasing hormone (LHRH) analogues are a well-established therapy for gonadotropin-dependent precocious puberty. Reports on intranasally administered analogues, however, are controversial. We studied the effect of intranasal D-Ser(TBU)6-LHRH(BUS) on growth rate, skeletal maturation, and urinary gonadotropins in five girls and one boy with central precocious puberty (CPP) who had been treated for 1.4-2.3 years (mean 1.9). Because of the potential antifertility effects of LHRH analogues, testicular histology was analysed in the boy. In the five children with accelerated growth, the bone age-related velocity of height gain decreased from 10.58 +/- 2.77 to 5.82 +/- 1.8 cm/year (means +/- SD, P less than 0.01), and the ratio of change in bone age to change in chronological age fell below 1. Basal luteinizing hormone (LH), and LHRH-stimulated LH and follicle stimulating-hormone, at pubertal levels before treatment, decreased significantly in all children, normalizing in four (P less than 0.04). During therapy, pituitary function was best controlled by urinary LH, which correlated with clinical data. After 13 months of therapy, testicular histology showed degenerated Sertoli cells, and absence of B- and Ap-spermatogonia and of primary spermatocytes in the boy. We conclude that: (1) Efficient long-term suppression of central precocious puberty--including accelerated growth and skeletal maturation--can be maintained by intranasal dosage of BUS. (2) Urinary LH reflects pituitary function and proves to be a reliable guide to adjustment of the LHRH-analogue dose regimen.(ABSTRACT TRUNCATED AT 250 WORDS)

Administration, Intranasal↗
PubMed1988

Effects of pregnancy and fasting on muscle glucose utilization in the rabbit.

The effects of fasting on maternal glucose metabolism were investigated in nonpregnant and 29-day pregnant conscious rabbits. Pregnancy decreased the glucose metabolic index by 60% in maternal red postural muscles. Fasting induced similar modifications in nonpregnant rabbits and exaggerated the changes observed in fed pregnant animals. These data suggest that the decreased glucose utilization by maternal red muscles observed during pregnancy and fasting is related to the increase in circulating fat-derived substrates, because the fall in plasma insulin concentration is a specific adaptation to fasting.

Adipose Tissue↗
PubMed1988

Glucose utilization by fetal muscles during maternal fasting.

In utero, glucose utilization by fetal muscles (heart and hindlimb) displays important interspecies differences. In the fed state, it is 5-fold higher in rat than in rabbit fetal muscles. Maternal fasting induces a decrease in glucose utilization in fetal muscles of the rat but not of the rabbit.

Animals↗
PubMed1988

Metabolic fate of a gastric glucose load in unrestrained rats bearing a portal vein catheter.

Metabolic and hormonal responses to the administration of a gastric load of glucose (2.4 mg/g body wt) were evaluated after a fast of 6-7 h in unrestrained rats bearing a portal vein catheter. For the purpose of this study, we have designed a new technique for a direct catheterization of the portal vein that allows serial blood sampling in unrestrained Wistar rats. On the 6th postoperative day, food intake, body weight gain, liver function, histology of the liver, pancreas, intestine, and splanchnic blood flows were similar to those of sham-operated control rats. In the basal state glucose turnover was 21.3 +/- 0.9 mg.kg-1.min-1. After glucose ingestion, a portoperipheral gradient of lactate was present, reflecting the production of lactate by the intestine. Insulin secretion was biphasic and peaked at 12 min (344 +/- 46 microU/ml), whereas portal glucagonemia (400-500 pg/ml) remained unchanged. Sixty minutes after gastric glucose administration, 50% of the load was delivered at the periphery, and glucose utilization was increased by 100%. Hepatic glucose production decreased after 20 min and was inhibited by 30% at 60 min. Liver glycogen concentration remained unchanged during the experiment despite a normal capacity for glycogen synthesis.

Animals↗
PubMed1988

Alanine turnover rate and its hepatic metabolism are increased in midpregnant rat.

At mid pregnancy (12th day) fed rats exhibit a drop of blood alanine level when the weight of the fetoplacental unit is still negligible. A primed infusion A-V method was used to measure alanine kinetics in fed midpregnant rats and virgin controls, using L-[2,3-3H]alanine as a tracer. Alanine turnover and metabolic clearance rates were higher on day 12 than in virgin controls. The increase in alanine turnover rate was accounted for by an increase in alanine degradation. Since the liver is the main site of alanine degradation, alanine uptake was studied in isolated hepatocytes. Hepatocytes isolated from midpregnant rats utilized 50% more alanine than those from virgin controls. This increase was mainly due to metabolism rather than incorporation into proteins. In conclusion, the alanine turnover rate and its hepatic metabolism are increased in fed midpregnant rats, resulting in the decrease in blood alanine.

Alanine↗
PubMed1988

In vivo regulation of glycolytic and gluconeogenic enzyme gene expression in newborn rat liver.

Glucagon and its second messenger, cAMP, are known to rapidly block expression of the L-type pyruvate kinase gene and to stimulate expression of phosphoenolpyruvate (PEP) carboxykinase gene in the liver in vivo. The respective roles, however, of hyperglucagonemia, insulinopenia, and carbohydrate deprivation in the inhibition of L-type pyruvate kinase gene expression during fasting are poorly understood. In addition, the long-term effects of physiological hyperglucagonemia on expression of the two genes are not known. In this study, we investigate the effects of long-term physiological hyperglucagonemia and insulinopenia induced by suckling (which provides a high-fat, low-carbohydrate diet) on expression of the two genes in the liver of normal newborn rats. We show that transcription of the L-type pyruvate kinase gene is inhibited at birth and remains low during the whole suckling period, whereas transcription of the PEP carboxykinase gene is maximal in the neonate, and then decreases despite very high levels of plasma glucagon during suckling. In contrast to the adult, however, in which L-type pyruvate kinase gene expression in the liver is blocked by cAMP and stimulated by carbohydrates, the regulation of L-type pyruvate kinase gene expression in the newborn undergoes a developmental maturation: the inhibitory effect of glucagon is never complete in developing rat liver and the stimulatory effect of glucose could not be detected during suckling, due to either hyperglucagonemia, immaturity of the gene regulatory system, or both.

Animals↗
PubMed1988

Correction of the molecular defect in B lymphocytes from X-linked agammaglobulinemia by cell fusion.

The X chromosome-linked antibody deficiency disease, X-linked agammaglobulinemia (XLA), results from failure of B lymphoid development. In the minor form of XLA, B lymphoid development terminates at the stage of immature B lymphocytes that produce truncated Ig heavy (H) chains composed of D-J-C(mu/delta), resulting from failure of VH gene rearrangement. Fusion of B cells from a patient with the minor form of XLA with mouse myeloma results in complementation of this defect; hybrid cells produce full-length H chains composed of VH-D-JH-C. The VH gene is of human origin. Complementation occurs independent of retention or loss of the human X (XLA) chromosome in the hybrid cells. These results indicate that the D-JH-C structure of the XLA B cells is fully functional for the subsequent rearrangement of a VH gene element, and that failure of immunoglobulin expression is susceptible to correction.

Agammaglobulinemia↗
PubMed1988

Premature appearance of gluconeogenesis and fatty acid oxidation in the liver of the postterm rabbit fetus.

The metabolic consequences of a prolonged gestation (35 vs 32 days) have been studied in the rabbit fetus. Gestation was prolonged by daily subcutaneous injections of progesterone (1.5 mg.kg-1) from day 28 to 34. In control animals, progesterone was injected from day 25 or 28 to day 31 of gestation. When the capacities for gluconeogenesis and fatty acid oxidation, measured on isolated hepatocytes, are normally low in the term control fetus and increase only within the first 24 h after birth, these capacities appear high in the postmature fetus. The rate of glucose production from lactate is 4-fold higher in the postmature fetus than in the normal term fetus. The rate of ketone body production from oleate is also 5-fold higher in the postmature fetus, which results from a switch on of the partition of oleate into esterification and oxidation: 8% of [1-14C]oleate is oxidized in term fetus hepatocytes, but 34% in postmature fetus hepatocytes. As a similar rate of lipogenesis takes place in both stages, this metabolic change could be explained by a 5-fold lower sensitivity of carnitine palmitoyltransferase I to the inhibition by malonyl-coenzyme A. Postmaturity decreases plasma insulin concentrations by 45% and increases plasma glucagon concentrations by 50% which, in turn, induces a 3-fold decrease in the plasma insulin:glucagon molar ratio. As previously shown in fasted or diabetic adult rat, this hormonal change might be a likely candidate for an enhancement of gluconeogenic and ketogenic capacity in the liver of the postterm rabbit fetus.

Animals↗
PubMed1988

Glucose utilization by the placenta and fetal tissues in fed and fasted pregnant rabbits.

Glucose utilization by the placenta and individual fetal tissues was studied in vivo in conscious pregnant rabbits at 29 days of gestation. In the fed state, the rate of glucose utilization was similar in the placenta and the gravid uterus, suggesting that the rate of fetal glucose utilization was approximately 40 nmol/min/g. A 96-h maternal fast induced a significant decrease in glucose utilization by the myoendometrium and in the glucose utilization index by fetal liver and brown adipose tissue. No modification was observed in other fetal tissues. These results indicate that glucose utilization by the placenta and the whole fetus from 96-h fasted rabbits does not decrease despite profound changes in endocrine and metabolic maternal parameters.

Adipose Tissue, Brown↗
PubMed1988

Radioreceptor assay for alpha-MSH using mouse B16 melanoma cells+.

A radioreceptor assay for alpha-MSH is described which is based on cultured mouse B16 melanoma cells and bioactive monoiodinated [Nle4]-alpha-MSH tracer. The assay was used (1) to study the binding characteristics of alpha-MSH to B16 cells, (2) to determine the relative binding activity of MSH peptides, and (3) to measure MSH in tissue extracts. The association of alpha-MSH to B16 cells reached a stable plateau after 3 h at 15 degrees C. At 25 degrees or 37 degrees C, the binding was transient and at 0-1 degree C, the association was very slow. The hormone-receptor complex was relatively stable between 0 degrees and 15 degrees C whereas a 50% dissociation was reached after 90 min at 25 degrees C and after 35 min at 37 degrees C. The mean KD for alpha-MSH of four saturation experiments was 1.3 nM and the number of receptors 9570 per cell. 1,10-Phenanthroline had a stabilizing effect in the binding assay when used at a 0.3 mM concentration. From the MSH peptides tested in the binding assay, some showed similar potencies in three bioassays (tyrosinase, melanin and Anolis skin), whereas others displayed considerably lower bioassay values than expected from the binding data. This shows that binding and bioactivity can be dissociated in some of the MSH peptides. The biological activity of MSH from the neurointermediate lobe of the rat pituitary as measured by its binding to B16 cells corresponds fairly well with RIA results; in the anterior lobe, alpha-MSH values are overestimated because of the large amount of ACTH present.

Animals↗
PubMed1988

[Hormonal control of the development of hepatic gluconeogenesis in the neonate].

Birth in most mammalian species represents an abrupt change from a high-carbohydrate and low-fat diet to a high-fat and low-carbohydrate diet. Gluconeogenesis is absent from the liver of the fetus of well-fed mothers, but can be induced prematurely by prolonged fasting of the mother. Gluconeogenesis increases rapidly in the liver of newborn mammals in parallel with the appearance of phosphoenolpyruvate carboxykinase (PEPCK), the rate-limiting enzyme of this pathway. The rise in plasma glucagon and the fall in plasma insulin which occur immediately after birth are the main determinants of liver PEPCK induction. When liver PEPCK has reached its adult value, i.e. 24 h after birth, other factors are involved in the regulation of hepatic gluconeogenesis. In order to maintain a high gluconeogenic rate, the newborn liver must be supplied with sufficient amount of gluconeogenic substrates and free fatty acids. An active hepatic fatty acid oxidation is necessary to support hepatic gluconeogenesis by providing essential cofactors such as acetyl CoA and NADH. The relevance of animal studies for the understanding of neonatal glucose homeostasis in man is discussed.

Animals↗
PubMed1988

Metabolic and hormonal response to acute cold exposure in newborn pig.

Glucose metabolism and changes in plasma insulin, glucagon and catecholamines were studied in unfed newborn pigs during acute cold exposure immediately after birth. When newborn pigs are exposed to a moderate cold external temperature (20 degrees C), they exhibit a transient thermoregulatory response characterized by an increased liver glycogenolysis, an enhanced blood glucose clearance rate (+35%) and a rise in plasma catecholamine concentrations. When the newborn pigs are exposed to a cold external temperature (12 degrees C), they become rapidly (10-12 h after birth) hypothermic and hyperglycaemic. This results from a fall in blood glucose clearance rate (-40%). Muscle glycogenolysis is low in normothermic animals during the 12 h following birth. Muscle glycogenolysis increases after a delay of 6 h in animals exposed to an external temperature of 20 degrees C or 12 degrees C. These data demonstrate that the failure in the thermoregulatory response in the newborn pig exposed to a cold temperature is not the consequence of a lack of mobilization of energy stores, but results from a defect in glucose utilization.

Adaptation, Physiological↗