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F J Arrieta

Publications and source records attributed to F J Arrieta.

9 recordsLinked to original sources

Sulphonylurea stimulates glucose uptake in rats through an ATP-sensitive K+ channel dependent mechanism.

We studied the effect of gliclazide, a second-generation sulphonylurea, on rat skeletal muscle glucose uptake using perfused hindquarter muscle preparations. Gliclazide at concentrations of 10 to 1000 microgram/ml increased (p < 0.05) the basal glucose uptake. The effect of gliclazide on glucose uptake was immediate and dose-dependent, reaching a plateau at a concentration of 300 micrograms/ml; the half-maximal effect was obtained between 25 and 50 micrograms/ml. The glucose uptake stimulated by gliclazide (300-1000 micrograms/ml) did not differ from that achieved by 10(-9) mol/l insulin, and was lower (p < 0.05) than that obtained with 10(-7) mol/l insulin. The combination of gliclazide (300 micrograms/ml) and 10(-9) mol/l insulin produced an increase in glucose uptake (7.7 +/- 0.6 mumol.g-1.h-1, n = 8, mean +/- SEM) which was higher (p < 0.05) than that achieved with 10(-9) mol/l insulin (5.6 +/- 0.7 mumol.g-1.h-1, n = 11) and not different from that obtained with 10(-7) mol/l insulin (9.8 +/- 1.0 mumol.g-1.h-1, n = 11). Diazoxide (100 mumol/l), an ATP-sensitive K+ channel opener, reversed the stimulatory effect of gliclazide (100 microgram/ml) on muscle glucose uptake from 3.1 +/- 0.4 to 0.5 +/- 0.2 mumol.g-1.h-1, (n = 7, p < 0.001). The addition of diazoxide prior to gliclazide into the perfusion medium blocked the gliclazide-induced glucose uptake by the hindquarter muscle preparations. In conclusion, gliclazide alone has an immediate stimulatory effect on glucose uptake by skeletal muscle and together with insulin has an additive effect on muscle glucose uptake. The effect of gliclazide on muscle glucose uptake seems to be due to the inhibition of ATP-sensitive K+ channels.

Adenosine Triphosphate

Impaired tyrosine-kinase activity of muscle insulin receptors from hypomagnesaemic rats.

The effect of magnesium deficiency on glucose disposal, glucose-stimulated insulin secretion and insulin action on skeletal muscle was investigated in rats which were fed a low magnesium-containing diet for 4 days. Control rats were fed a standard diet. Compared to the control rats, the rats fed with low magnesium diet presented: 1) lower serum magnesium levels (0.45 +/- 0.02 vs 0.78 +/- 0.01 mmol/l, p < 0.001), 2) higher basal serum glucose (6.8 +/- 0.02 vs 5.5 +/- 0.2 mmol/l, p < 0.05) and similar basal serum insulin, 3) 40% reduction (p < 0.001) in the glucose disappearance rate after its i.v. administration, and 4) 45% reduction (p < 0.05) in the glucose-stimulated insulin secretion. The insulin action upon the glucose uptake by skeletal muscle was determined by means of hindquarter perfusions. Compared with control rats, magnesium-deficient rats presented: 1) normal basal glucose uptake, 2) lower stimulatory effect on the glucose uptake by insulin at the concentrations of 5 x 10(-10) mol/l (3.0 +/- 0.9 vs 5.4 +/- 0.6, p < 0.05) and 5 x 10(-9) mol/l (6.3 +/- 0.5 vs 8.0 +/- 0.5, p < 0.05), 3) normal glucose uptake at a maximal insulin concentration of 1 x 10(-7) mol/l, and 4) 50% reduction in the insulin sensitivity (ED50: 1.3 +/- 0.3 vs 0.55 +/- 0.1 mol/l, p < 0.05). In partially purified insulin receptors prepared from gastrocnemius muscle, 125I-insulin binding was similar in both groups of rats. However, the autophosphorylation of the beta-subunit of the insulin receptor was significantly reduced by 50% in magnesium-deficient rats and the tyrosine kinase activity of insulin receptors toward the exogenous substrate Poly Glu4; Tyr 1 was also reduced (p < 0.05) by hypomagnesaemia. The abundance of the insulin-sensitive glucose transporter protein (muscle/fat GLUT4), measured by Western blot analysis using polyclonal antisera, was similar in muscles of control and hypomagnesaemic rats. These findings indicate that hypomagnesaemia has a deleterious effect on glucose metabolism due to an impairment of both insulin secretion and action. The insulin resistance observed in skeletal muscle of magnesium-deficient rats may be attributed, at least in part, to a defective tyrosine kinase activity of insulin receptors.

Animals

Serum and urinary manganese levels in patients with Parkinson's disease.

To elucidate the possible role of manganese in the risk of developing Parkinson's disease (PD), we compared serum levels of manganese, and 24-h manganese excretion by urine in 29 PD patients and in 27 matched controls. We also measured chromium and cobalt in the same samples. All these values did not differ significantly between the groups, they were not influenced by antiparkinsonian drugs, and they did not correlate with age, age at onset and duration of the PD, scores of the Unified PD Rating Scale or the Hoehn & Yahr staging in the PD group. These results might suggest that serum levels and urinary excretion of manganese are apparently unrelated to the risk of developing PD.

Activities of Daily Living

[Type I familial pseudohypoparathyroidism: clinical and hormonal study].

Pseudohypoparathyroidism is a rare disease characterized by a target tissue resistance to the action of the parathyroid hormone (PTH). Frequently, others hormonal disorders can be associated. We report a family with pseudohypoparathyroidism type I, and discuss the clinical-hormonal alterations founded; it is emphasized that while there were no phenotypical differences among the family members; from the hormonal features point of view, some differences do exist, and several degrees of peripheral resistance were noted.

Adult

[Empty sella turcica with intrasellar herniation of the optic chiasm].

We here present the case of a patient who starts with a progressive vision loss, observing in the radiologic exam herniation of optic chiasma in a primary empty sella turcica. Based on this case, we have performed a review of this clinical picture and point out the most important aspects in the literature.

Cranial Nerve Diseases

[Adrenal gland masses and Addison's disease of tuberculous origin: apropos of 2 cases].

Two cases of confirmed tuberculous Addison disease, with an increase in size of the adrenal glands are presented. One patient presented also a renal adenocarcinoma; this association is very rare given the small frequency of these diseases. Based on these two cases we emphasize the utility of puncture aspiration with a fine needle (PAFN), echography and TC Scan in the study of Addison disease.

Addison Disease