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Biomedical subjects

R Galván

Publications and source records attributed to R Galván.

11 recordsLinked to original sources
PubMed2001

Serum leptin and somatotropin components correlate with neonatal birth weight.

OBJECTIVE: To determine whether cord sera leptin and components of the somatotropin axis - growth hormone (GH), total (t) and free (f) insulin-like growth factor (IGF), IGF-binding protein-3 (IGFBP-3), and insulin - correlate with birth weight. DESIGN: Cross-sectional study of 22 newborns, 12 with normal birth weight (NBW) and 10 with low birth weight (LBW), in a population of healthy mothers with an apparent normal pregnancy. METHODS: Paired mother-neonate blood samples were obtained at vaginal delivery in order to measure leptin and the somatotropin axis components. RESULTS: In all cases maternal blood concentrations of leptin, t and fIGF-I, its carrier protein IGFBP-3, and insulin were higher than in the cord sera of the newborns, regardless of their birth weight. On the contrary, maternal GH levels were lower than in their neonates. LBW neonates had decreased levels of leptin, tIGF-I, and IGFBP-3 as compared with those levels in NBW offspring; however, GH concentrations were higher in LBW neonates. Birth weight showed a significant correlation with cord sera leptin, tIGF-I, IGFBP-3, and GH; nevertheless birth weight was neither interrelated with fIGF-I nor with insulin levels. CONCLUSION: These data demonstrate that birth weight is significantly correlated with both leptin and some components of the somatotropin axis; on the other hand, no correlation was observed between leptin concentrations and each one of the components of the somatotropin axis. It is suggested that fetal leptin and the somatotropin axis cooperate in intrauterine growth and birth weight.

Adult↗
PubMed2000

[Circulating leptin doesn not change in postmenopausal women receiving replacement therapy with tibolone].

After informed consent, blood samples were obtained to measure leptin, FSH, LH, insulin, 17-beta-estradiol, and IGF-1. No differences in serum leptin was observed between the women on Tibolone (8.1 +/- 4.2 ng/mL) and the control group (7.4 +/- 3.7 ng/mL). Women on Tibolone had lower insulin levels (16.4 +/- 1.8) than women without therapy (19.4 +/- 1.3 mU/mL) (p < 0.05). On the contrary IGF-I levels were elevated (150.0 +/- 16.4) as compared with those in non-treated women (121.0 +/- 13.4 ng/mL) (p < 0.05). Body weight was similar between the two groups. From these data it is concluded that Tibolone, as replacement therapy, does not increase circulating leptin and seems to have no effect on body weight.

Aged↗
PubMed1999

Increased serum levels of growth hormone and insulin-like growth factor-I associated with simultaneous decrease of circulating insulin in postmenopausal women receiving hormone replacement therapy.

OBJECTIVE: Decreases in circulating growth hormone (GH) and its main biological messenger insulin-like growth factor-I (IGF-I) have been interpreted as part of the aging process. Because estrogens participate in modulating GH synthesis and secretion, hypoestrogenism in menopausal women may lead to GH deficiency. The aim of the present study was to determine the effect of hormone replacement therapy (HRT) on both GH and IGF-I levels as well as insulin concentrations in 50 menopausal women. DESIGN: Patients were assigned randomly into two treatment groups of 25 each; one group received three cycles of conjugated equine estrogen (CEE) 0.625 mg/day for 21 days, and the other, 1.25 mg/day during 21 days. Each also received chlormadinone acetate for 5 days. There was a control group consisting of regularly menstruating women. RESULTS: In the menopausal women, HRT increased significantly (p < 0.001) the low levels of GH and IGF-I; on the contrary the baseline insulin levels declined (p < 0.001) with HRT. A significant linear correlation (r = 0.90) was found between GH and IGF-I as well as with estradiol levels (r = 0.74) in the group of menopausal women receiving CEE 0.625 mg/day. This group of patients had a significant correlation (r = -0.63) between insulin and estradiol levels. No correlation was observed in the group receiving CEE 1.25 mg/day. CONCLUSIONS: HRT restored GH, IGF-I, and insulin levels to normal values in all women. Further research needs to be done to establish the beneficial effect of HRT regarding the prevention of the metabolic effects presumably caused by derangement in the somatotropic axis associated with aging.

Aged↗
PubMed1992

Presynaptic muscarinic receptor subtypes involved in the inhibition of acetylcholine and noradrenaline release in bovine cerebral arteries.

Experiments were performed in bovine cerebral arteries preincubated with [3H]-choline or [3H]-noradrenaline to analyze the presynaptic muscarinic receptors involved in inhibition of acetylcholine and noradrenaline release induced by electrical stimulation (4 Hz, 200 mA, 0.3 ms, 1 min). For this purpose, the actions of several muscarinic receptor antagonists on the 3H overflow and on the carbachol-induced inhibition of this overflow were assessed. The evoked [3H]-acetylcholine release and [3H]-noradrenaline release were markedly reduced by the presence of tetrodotoxin, Ca(2+)-free medium, and the inhibitor of both choline transport and choline acetyltransferase, AF64A. Chemical sympathetic denervation with 6-hydroxydopamine (6-OHDA) decreased the uptake of [3H]-noradrenaline, and AF64A reduced mainly the uptake of [3H]-choline, but also of [3H]-noradrenaline. Carbachol reduced the evoked [3H]-noradrenaline and [3H]-acetylcholine release; the IC50 values were 0.37 and 0.43 mumol/l, respectively. Atropine and 4-DAMP, but not AF-DX 116, methoctramine or pirenzepine, increased the evoked [3H]-acetylcholine release. However, these muscarinic antagonists failed to modify the evoked [3H]-noradrenaline release. Carbachol inhibited the release of both acetylcholine and noradrenaline. The inhibition was blocked by the antagonists. The rank orders of potency (based on plC50 values) were, in the case of [3H]-acetylcholine release, atropine greater than 4-DAMP greater than AF-DX 116 greater than or equal to pirenzepine greater than or equal to methoctramine, and, in the case of [3H]-noradrenaline release, atropine greater than 4-DAMP greater than AF-DX 116 greater than or equal to methoctramine greater than or equal to pirenzepine.(ABSTRACT TRUNCATED AT 250 WORDS)

Acetylcholine↗
PubMed1984

Mechanism of the indirect adrenergic effect of histamine in cat cerebral arteries.

KCl (50 mM), tyramine (10(-7) M), and histamine (10(-4) M) induced an increase in tritium release from cat cerebral arteries preincubated with [3H]noradrenaline, this increase being due in part to noradrenaline. When calcium was absent from the superfusion medium, only tyramine (10(-7) M) enhanced the tritium outflow. Colchicine (10(-3) M) partially inhibited the increase in radioactivity brought about by 10(-4) M histamine. KCl (50 mM) also evoked release of radioactivity from cerebral arteries preloaded with [3H]histamine; this release was unaffected by reserpine pretreatment or removal of both superior cervical sympathetic ganglia. Neither tyramine (10(-7) M) nor compound 48/80 (300 micrograms ml-1) altered the spontaneous tritium outflow from cerebral blood vessels preincubated with [3H]histamine. These results suggest that histamine is not accumulated by sympathetic nerve endings and elicits its noradrenaline-releasing effect by means of an exocytotic process.

Animals↗
PubMedDate not supplied

Correction of insulin resistance in methimazole-treated patients with Graves disease.

The effect of thyroid hormone excess on glucose tolerance as well as insulin secretion and its peripheral action has been a matter of debate for many years. Thyrotoxicosis caused by Graves' disease is associated in some patients with impaired glucose tolerance and insulin resistance. The objective of the present study was to investigate if the insulin sensitivity, assessed by the euglycemic insulin clamp technique, increase after correction of hyperthyroidism due to Graves' disease. After four months of medical treatment, patients became euthyroid and insulin sensitivity increased significantly from 3.47 to 6.39 mg/kg/min; therefore it was concluded that insulin resistance could be improved after successful treatment of hyperthyroidism. The precise mechanism underlying the effect of thyroid hormone excess on insulin sensitivity remains to be elucidated.

Adult↗