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Biomedical subjects

S Mora

Publications and source records attributed to S Mora.

At least 19 recordsLinked to original sources
PubMed1995

Insulin and insulin-like growth factor I (IGF-I) stimulate GLUT4 glucose transporter translocation in Xenopus oocytes.

1. The heterologous expression of glucose transporters GLUT4 and GLUT1 in Xenopus oocytes has been shown to cause a differential targeting of these glucose-carrier isoforms to cellular membranes and a distinct induction of glucose transport activity. In this study we have evaluated the effect of insulin and insulin-like growth factor I (IGF-I) on glucose uptake and glucose transporter distribution in Xenopus oocytes expressing mammalian GLUT4 and GLUT1 glucose carriers. 2. Insulin and IGF-I stimulated 2-deoxyglucose uptake in GLUT4-expressing oocytes, but not in GLUT1-expressing oocytes or in water-injected oocytes. The stimulatory effect of insulin and IGF-I on 2-deoxyglucose uptake in GLUT4-expressing oocytes occurred via activation of the IGF-I receptor. 3. Subcellular-fractionation studies indicated that insulin and IGF-I stimulated translocation of GLUT4 to the cell surface of the oocyte. 4. Incubation of intact oocytes with insulin stimulated phosphatidylinositol 3-kinase activity, an effect that was blocked by the additional presence of wortmannin. Furthermore, wortmannin totally abolished the insulin-induced stimulation of 2-deoxyglucose uptake in GLUT4-expressing oocytes. 5. In this study, both the insulin-induced GLUT4 carrier translocation and GLUT4-dependent insulin-stimulated glucose transport have been reconstituted in the Xenopus oocyte. These observations, together with the fact that wortmannin, as found in adipocytes, inhibits insulin-stimulated glucose transport in oocytes, suggest that the heterologous expression of GLUT4 in oocytes is a useful experimental model by which to study the cell biology of insulin-induced GLUT4 translocation.

Androstadienes↗
PubMed1995

Bone mineral metabolism and thyroid replacement therapy in congenital hypothyroid infants and young children.

Impairment of calcium metabolism and low bone density have been found in hypothyroid adults. We investigated the effect of thyroid replacement therapy on calcium metabolism and bone mineralization in congenital hypothyroid (CH) infants and children. One hundred and 16 Caucasian CH consecutive patients were studied and were grouped according to their age: 23 patients at diagnosis, 20 at 3 mo, 24 at 6 mo, 25 at 12 mo and 24 at 36 mo. Thyroid replacement therapy was started at an initial dose of 6-8 micrograms/kg/day of L-thyroxine, and then decreased progressively. Calcium, phosphorus, magnesium, alkaline phosphatase (AP), parathyroid hormone (PTH) and osteocalcin (BGP) were measured as calcium metabolism indices. Bone mineral content (BMC) was measured at the mid-portion of the right radius AP, PTH and BGP concentrations were significantly higher in subjects at 3 mo of age (p < 0.05). This rise coincided with the end of the period of maximum dosage of L-thyroxine. Mild asymptomatic hypercalcemia was observed in 20 patients. All the other indices did not differ between age groups. BMC values and BMC annual increment were not different from those calculated for age-matched controls. We found that L-thyroxine replacement therapy does not alter bone mineralization of CH infants and children. Only a transitory increase of osteoblastic function was observed after the first few months of therapy.

Bone Density↗
PubMed1992

Effect of estrogen replacement therapy on bone mineral content in girls with Turner syndrome.

Because a close relationship between estrogen deficiency and osteoporosis has been proven, it is possible that lifelong estrogen deficiency might be the cause of osteopenia in Turner syndrome. This study was done to characterize the effect of estrogen therapy on bone mineralization in girls with Turner syndrome. Radial bone mineral content values were found to be below the 95% normal confidence interval in 44 of 49 untreated patients, aged 10.82 +/- 3.45 years. An inverse correlation was found between the patients' ages and their delta bone mineral content values. The effect of beginning estrogen treatment early or late was studied in 16 girls who started the treatment before and 11 who started after age 12. Although they were still deficient compared with controls, the first group had better mineralization than the second (P = .0005). Finally, nine patients were followed prospectively during replacement therapy; their bone mineral content delta values changed significantly (P = .02) during the follow-up period (3.17 +/- 0.33 years), but the bone mineral content did not normalize. Our data show that estrogen deficiency per se does not cause osteoporosis in young girls with Turner syndrome. In fact, estrogen therapy prevented bone loss but failed to normalize the low bone mineral content values. Early treatment is preferable because it reduces the bone density deficit present in untreated patients.

Adolescent↗
PubMed1991

Changes in vertebral bone density in black girls and white girls during childhood and puberty.

BACKGROUND: The prevalence of osteoporosis and the incidence of vertebral fractures are lower in black women than in white women, findings generally attributed to racial differences in adult bone mass. Little is known, however, about the factors that contribute to racial variations in bone mass or the time of life when such differences become manifest. This study was done to characterize the changes in vertebral bone density at various stages of sexual development in black and white females. METHODS: We measured cancellous vertebral bone density by quantitative computed tomography in 75 black female subjects between 2 and 20 years old and 75 whites matched for age and stage of sexual development. RESULTS: The vertebral bone density did not differ between black girls and white girls before puberty. Bone density increased during puberty in each racial group, but the magnitude of the increase from prepubertal values was substantially greater in black than in white subjects (34 percent vs. 11 percent). CONCLUSIONS: The marked difference between black and white females in cancellous vertebral bone density occurs during a relatively brief period late in puberty. Metabolic and hormonal events related to the achievement of sexual maturity during adolescence may be important determinants of racial differences in bone mass in women.

Adolescent↗
PubMed1991

Vertebral bone density in insulin-dependent diabetic children.

To determine the effect of insulin-dependent diabetes mellitus (IDDM) on bone mass, we compared the trabecular and cortical bone density in lumbar vertebrae, measured by quantitative computed tomography (CT), in 48 white diabetic patients (23 females, 25 males; 5.2 to 19.6 years of age) with those of a control group of 48 healthy subjects, matched for race, sex, and age. Patients with neuropathy, retinopathy, nephropathy, and those with recent ketoacidosis were excluded from the study. The patient and control groups did not differ in sexual or skeletal maturation, weight, height, surface area, body mass index, abdominal fat, or paraspinal musculature. In diabetic children, cortical bone density was slightly but significantly lower than in controls (3.5% lower, P less than .02); there was no difference between patients and controls regarding trabecular bone density. The decrease in cortical bone density in the diabetic group did not correlate with age, sex, duration of diabetes, or glycosylated hemoglobin levels. These results suggest that in children with uncomplicated IDDM, decreased vertebral bone density is a minor abnormality that only affects cortical bone.

Adolescent↗
PubMed1991

Effects of estradiol replacement in ovariectomized rats on conditioned avoidance responses and other behaviors.

The acquisition of conditioned avoidance responses along with spontaneous behaviors were studied in ovariectomized rats. Fourteen days after ovariectomy, they were injected subcutaneously with one of the following doses of estradiol benzoate: 0.2, 2 or 20 microgram/rat. Behavioral tests were applied 3, 24, 48 or 72 hours after estradiol treatment. Although estradiol 2 microgram/rat induced a decrease in acquisition of conditioned avoidance responses at all times tested, this effect was maximum at 48 h. Estradiol 0.2, and 20 microgram/kg decreased and stimulated, respectively, the acquisition performance, as tested 3 h after injection. All doses increased global motility and rearing behavior. This hypermotility disappeared at 24 h, but it was observed again at 48 and 72 h after estradiol 0.2 and 20 microgram/rat. The hormone also induced an increase in head shaking and a decrease in grooming. Although the behavioral changes are more significant in presence of very low serum levels of estradiol, they seem to be triggered by the previous increase in the estradiol levels. The possible sites and mechanisms of action of estradiol on behavior are discussed.

Animals↗
PubMed1991

Behavioral effects of intracerebral administration of luteinizing hormone releasing hormone (LHRH) in rats.

The effects of LHRH intracerebrally infused on acquisition of conditioned avoidance responses (CARs) and spontaneous motility were studied in adult male rats. The results were the following: 1) LHRH (1 and 2.5 micrograms/rat) administered through a cannula stereotaxically implanted into the lateral ventricle induced an impairment in the acquisition of CARs along with an increase in global motility, rearing, head shaking and grooming behavior; 2) LHRH 1 microgram/rat injected into the hippocampus or nucleus accumbens induced also an impairment in acquisition which is evident 15 min after treatment. In contrast, intrastriatal injection induced an immediate disruption of this behavior; and 3) there is a good dose-response relationship for intrastriatal LHRH between 7.8 and 62.5 ng/rat. The results suggest that the estriatum could be the locus of the LHRH-induced inhibition of CARs. Then the possibility of an involvement of the dopamine nigrostriatal system is discussed.

Animals↗
PubMed1990

Bone mass in young patients with type I diabetes.

We measured bone mineral content (BMC) with single photon absorptiometry in two groups of young patients with type I diabetes: the first group (prospective study) consists of 48 patients followed from onset to the third year of diabetes and the second group (cross-sectional study) consists of 66 long-term diabetics. Bone mineral content at onset of disease was lower than normal in only two cases. After 3 years of diabetes no male revealed BMC below the normal range but two females (6.6%) had low BMC values. In our cross-sectional study we found a BMC reduction in 12% of the cases. We did not find a relationship between bone deficit and duration of diabetes, or bone mass values and HbA1.

Adolescent↗
PubMed1989

Influence of the estrous cycle, ovariectomy and estradiol replacement upon the acquisition of conditioned avoidance responses in rats.

The changes in the acquisition of conditioned avoidance responses (CARs) and the performance of some spontaneous behaviors were examined across the estrous cycle of female rats. CARs were facilitated during diestrus, impaired at proestrus and practically abolished at estrus and metestrus. Motor activity and head shaking were minimally affected with the stages of the cycle. Motor activity was increased at metestrus and head shaking decreased at estrus. At 14 days following ovariectomy, there was a significant enhancement of CARs which was antagonized by the daily administration of estradiol benzoate (10 micrograms/kg) for three days. Ovariectomy also increased grooming behavior and estradiol replacement returned grooming to its basal level. The results suggest an inhibitory control of estradiol on CARs and grooming. The involvement of other hormones which also varied across the estrous cycle and its interaction with brain catecholamine systems, particularly dopamine, are discussed.

Animals↗
PubMed1989

Clinical investigations of medetomidine in dogs.

Experiments with 3 doses of medetomidine (20, 40 and 80 micrograms/kg, iv. and im., respectively) were carried out on 90 dogs of 16 breeds in the Small Animal Surgery of the University of Veterinary Science, Budapest. Changes in hematology as well as in AST, AP, BUN, creatinine were studied. Medetomidine administered iv deepened the sedation and lengthened tranquillization dose-dependently. After im administration the sedative effect was still dose-dependent, but the duration of its clinical effectiveness could not be lengthened significantly. The development of the sedation could however, be quickened. The iv administration increased the level of analgesia in proportion to dosage; the im application could change the level of pain-killing effect of the drug, but could not lengthen it. According to the laboratorical determinations, regardless of the dosage and the route of application, medetomidine did not affect the AST and AP enzyme activities, or the BUN and creatinine values.

Adrenergic alpha-Agonists↗
PubMed1988

LHRH antagonizes yawning and genital grooming induced by apomorphine in rats.

The effects of the pretreatment with LHRH on the behavioral effects induced by low doses of apomorphine were studied in male rats. Three doses of apomorphine (31.25, 62.50 and 125 micrograms/kg) were subcutaneously administered two hours after LHRH 100 micrograms/kg or solvent SC treatment. Apomorphine induced repeated episodes of yawning and genital grooming. Pretreatment with LHRH abolished or reduced yawning and genital grooming induced by the three doses of apomorphine, suggesting that the peptide could induce subsensitivity of DA receptors responsible for yawning and genital grooming.

Animals↗
PubMed1988

Effects of pretreatment with luteinizing hormone releasing hormone (LHRH) on behaviors induced by apomorphine in rats.

The influence of LHRH on the behavioral effects induced by apomorphine (APO) was studied in male rats. Several doses of apomorphine (31.25, 62.5, 125, 250 and 500 micrograms/kg) were administered subcutaneously (SC) after LHRH 100 micrograms/kg or solvent. Low doses of apomorphine induced hypomotility and impaired acquisition of a conditioned avoidance response (CAR). High doses produced hypermotility, stereotyped sniffing and a short lasting increase, followed by a decrease in the acquisition of CARs. Pretreatment with LHRH potentiated the hypomotility induced by low doses of apomorphine (62.5 and 125 micrograms/kg) and the hypermotility, stereotyped sniffing and the enhancement in acquisition of CARs produced by higher doses of apomorphine (250 and 500 micrograms/kg). These findings suggest that LHRH could indirectly regulate dopamine activity through an increase in sensitivity of dopamine receptors (pre- and postsynaptic), which mediate the behavioral effects of APO. It is postulated that this hypersensitivity of DA receptors could be the consequence of an inhibition of presynaptic dopaminergic transmission, induced by LHRH.

Animals↗
PubMed1986

Pharmacological evidence of catecholaminergic involvement in the behavioral effects of luteinizing hormone releasing hormone in rats.

The influence of L-DOPA on the behavioral effects of LHRH was studied in male rats. Subcutaneous administration of LHRH (100 micrograms/kg) caused a significant disruption in the acquisition of a conditioned avoidance response (CAR) and a significant increase in head shaking behavior (HSB). Pretreatment with this hormone antagonized the stimulatory action of amphetamine (1 mg/kg, IP) in acquisition of CARs, spontaneous motor activity (SMA) and rearing behavior (RB). L-DOPA (100 mg/kg, IP), administered after LHRH, stimulated SMA, RB and HSB. In addition L-DOPA antagonized the effect of LHRH on acquisition of CARs and counteracted the antagonism between LHRH and amphetamine in acquisition of CARs and SMA. These findings indicate that LHRH could exert its behavioral effects through an inhibitory action upon brain catecholamine synthesis. The suppression of CARs may be the response to DA antagonism and the interaction with amphetamine could be mediated by an inhibition of both DA and NE activities. The possibility of an interaction between LHRH and central serotonin mechanisms is also discussed.

Amphetamine↗
PubMed1985

Luteinizing-hormone-releasing hormone modifies retention of passive and active avoidance responses in rats.

The influence of posttraining subcutaneous administration of luteinizing-hormone-releasing hormone (LHRH) was tested on the retention of either active or passive avoidance conditioning in male rats. Injection of LHRH (200 micrograms/kg) immediately after the acquisition of an active avoidance response (two-way shuttle behavior) enhanced retention of the response, assessed 7 days later. When the neuropeptide was injected immediately after a passive avoidance conditioning training, the effects varied with the intensity of the footshock applied. LHRH enhanced retention of avoidance training with weak footshock (0.20 and 0.35 mA) but impaired retention of training with strong footshock (0.70 and 1.0 mA). The effects of LHRH seem to be unspecific since they are similar to those observed after treatment with several hormones. The results are discussed based on the interactions between peripherally injected hormones and endogenous substances released following footshock. A modulatory effect on the monoaminergic pathway involved in memory storage processes is postulated.

Animals↗
PubMed1983

LHRH and rat avoidance behavior: influence of castration and testosterone.

Pretraining subcutaneous administration of a high dose of LHRH (100 micrograms/kg) to intact rats impaired acquisition of a conditioned avoidance response (CAR) in a two way shuttle box. Acquisition of a CAR was also decreased when LHRH was administered to castrated rats. LHRH antagonized the dose related impairment in acquisition and retention performance induced by testosterone in castrated animals. The results are discussed based on the interrelationships between castration, testosterone, LHRH and brain monoamines.

Animals↗
PubMed1983

Influence of luteinizing hormone releasing hormone (LHRH) on the behavioral effects of amphetamine in rats.

The influence of luteinizing hormone releasing hormone (LHRH) on the behavioral effects induced by several doses of D-amphetamine (0.25, 0.5, 1.0 and 2.0 mg/kg IP) was studied. A dose response relation was previously established for the effects of LHRH (50, 100 and 200 micrograms/kg SC) on acquisition and retention of conditioned avoidance responses (CARs). The neuropeptide impaired acquisition and improved retention of CARs, without modifying spontaneous motor activity. Pretreatment with 100 micrograms/kg of LHRH antagonizes the enhancement in acquisition of CARs due to D-amphetamine 0.5, 1.0 and 2.0 mg/kg, the impairment in retention induced by amphetamine 1.0 and 2.0 mg/kg, and the hypermotility and the increased rearing behavior induced by amphetamine 1.0 and 2.0 mg/kg. These results suggest that brain catecholamines, particularly dopamine, could play a role in the behavioral effects of LHRH. Interactions between LHRH and central dopaminergic mechanisms are discussed.

Animals↗
PubMed1980

TRH on rat conditioned avoidance behavior: interaction with brain catecholamines.

TRH (10 micrograms) intracerebroventricularly injected improves the acquisition of a two-day avoidance conditioning. This effect is partially antagonized by pretreatment IP with alpha-methyltyrosine (60 mg/kg) or disulfiram (300 mg/kg). L-DOPA (100 mg/kg) administered IP 2 hr after alpha-MT partially restores the facilitatory effect of the hormone. The possible roles of brain catecholamines on the behavioral effect of TRH are analysed. Other tentative mechanisms of action are also discussed.

Animals↗