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N Pulido

Publications and source records attributed to N Pulido.

11 recordsLinked to original sources
PubMed2000

Stimulation of glucose transport by thyroid hormone in 3T3-L1 adipocytes: increased abundance of GLUT1 and GLUT4 glucose transporter proteins.

In 3T3-L1 adipocytes we have examined the effect of tri-iodothyronine (T(3)) on glucose transport, total protein content and subcellular distribution of GLUT1 and GLUT4 glucose transporters. Cells incubated in T(3)-depleted serum were used as controls. Cells treated with T(3) (50 nM) for three days had a 3.6-fold increase in glucose uptake (P<0.05), and also presented a higher insulin sensitivity, without changes in insulin binding. The two glucose carriers, GLUT1 and GLUT4, increased by 87% (P<0.05) and 90% (P<0. 05), respectively, in cells treated with T(3). Under non-insulin-stimulated conditions, plasma membrane fractions obtained from cells exposed to T(3) were enriched with both GLUT1 (3. 29+/-0.69 vs 1.20+/-0.29 arbitrary units (A.U.)/5 microg protein, P<0.05) and GLUT4 (3.50+/-1.16 vs 0.82+/-0.28 A.U./5 microg protein, P<0.03). The incubation of cells with insulin produced the translocation of both glucose transporters to plasma membranes, and again cells treated with T(3) presented a higher amount of GLUT1 and GLUT4 in the plasma membrane fractions (P<0.05 and P<0.03 respectively). These data indicate that T(3) has a direct stimulatory effect on glucose transport in 3T3-L1 adipocytes due to an increase in GLUT1 and GLUT4, and by favouring their partitioning to plasma membranes. The effect of T(3) on glucose uptake induced by insulin can also be explained by the high expression of both glucose transporters.

3T3 Cells↗
PubMed1998

High glucose uptake by adipocytes in a type 1 diabetic patient with a partial 'honeymoon' period.

Hypoglycaemic episodes and low insulin requirements are frequently seen in the early phase of treatment of Type 1 diabetes mellitus but the mechanism is not clear. We present a diabetic patient with recurrent hypoglycaemia in the early phase of insulin treatment. A very high glucose transport in adipocytes (basal: 176 and insulin stimulated glucose transport 10(-7) mol l(-1): 335 fl cell(-1) s(-1)) was found when compared with reference laboratory diabetic patients (basal: 59 +/- 10 and insulin 10(-7) mol l(-1): 106 +/- 7 fl cell(-1) s(-1), mean +/- SE) and with reference laboratory of non-diabetic subjects (basal: 106 +/- 6 and insulin 10(-7) mol l(-1): 188 +/- 15 fl cell(-1) s(-1)). Insulin binding to adipocytes was in the normal range. The patient was studied again 1 year later when the partial clinical remission had disappeared, and the glucose transport in adipocytes had decreased. In conclusion, an increase in glucose uptake by peripheral tissues may be among the mechanisms of the partial 'honeymoon' period of diabetic patients.

Adipocytes↗
PubMed1998

[Body mass index influence in the insulin action mechanisms].

OBJECTIVE: Improve the knowledge of the "in vitro" insulin action in healthy subjects with different body mass index (BMI), in order to know the role of obesity in the diabetes mellitus. MATERIAL: In 12 healthy subjects with different BMI and normal oral glucose test we made a gluteal biopsy to obtain adipose tissue. In the isolated adipocytes we studied the interaction of insulin with its receptor and the glucose transport. RESULTS: BMI was not correlated with the maximal specific 125I-insulin binding but was negative when correlated with the glucose transport in basal situation (r = -0.63, p < 0.05) as well as when stimulated with insulin (r = -0.67, p < 0.05), when the results were expressed as number of cells. When the data were expressed as surface, BMI was negative correlated with the percentage of maximal specific 125I-insulin binding (r = -0.81, p < 0.05), and also with the basal glucose transport (r = -0.69, p < 0.05) and stimulated with insulin (r = -0.77, p < 0.01). CONCLUSION: The increase of BMI is an important diabetogenic agent, acting at receptor as well as at postreceptor level, and the data should be expressed according to the cellular diameter rather than to the number of cells in subjects with different BMI. A cutting point was established at the 30 BMI level after which the described alterations could be observed.

Adult↗
PubMed1997

Gliclazide treatment of streptozotocin diabetic rats restores GLUT4 protein content and basal glucose uptake in skeletal muscle.

This study examined whether the treatment of streptozotocin (STZ)-diabetic rats with gliclazide (5 mg/kg body weight twice daily orally) increases muscle glucose uptake. Rats were treated (group G, n = 10) or untreated (group D, n = 11) for 12 days. Normal rats served as controls (group C, n = 11). At the end of the treatment, both basal and insulin-stimulated glucose uptake by the perfused hindquarters were measured. In gastrocnemious muscles, the protein content of GLUT4 and the insulin binding and tyrosine kinase activity of partially purified solubilized insulin receptors were measured. Group G had a lower mean glycemic value during the treatment period than group D (mean +/- SEM, 17 +/- 0.6 v 19.7 +/- 0.5 mmol/L, P < .05), without differences in serum insulin levels. Basal glucose uptake by the hindquarters was significantly higher in group G versus group D (2.8 +/- 0.3 v 1.3 +/- 0.2 mumol/g/h, P < .05), and was not different versus group C (3.6 +/- 0.2 mumol/g/h). Insulin-stimulated glucose uptake was higher (P < .05) in group C compared with the two groups of diabetic rats. Glucose uptake at 10(-7) mol/L insulin was higher in group G than in group D (9.2 +/- 0.6 v 7.0 +/- 0.6 mumol/g/h, P < .05). Both insulin binding and tyrosine kinase activity were similar in muscle insulin receptors from both groups of diabetic rats. The GLUT4 protein content was higher in group G than in group D (95 +/- 10 v 57 +/- 7 arbitrary units [AU]/microgram protein, P < .05) and similar to that of group C (113 +/- 13 AU/microgram protein). In conclusion, gliclazide has a glucose-lowering effect in STZ-diabetic rats that could be attributed to an increase in muscle glucose clearance by a post-insulin receptor mechanism, probably related to a normalization of GLUT4 content.

Animals↗
PubMed1996

Sulfonylureas stimulate glucose uptake through GLUT4 transporter translocation in rat skeletal muscle.

We studied the effect of gliclazide on glucose uptake and GLUT4 translocation in skeletal muscle. Rat hindquarters were perfused in the absence or presence of gliclazide (300 micrograms/ml), insulin or both drugs. The basal glucose uptake was increased 2.7-fold by gliclazide (p < 0.05). Gastrocnemius muscles perfused with gliclazide had a significant increase (2.4-fold) in the GLUT4 content in plasma membranes compared to basal conditions (p < 0.05). The stimulations produced by 1 nM insulin on muscle glucose uptake (2.8-fold) and on GLUT4 level in plasma membranes (2.5-fold) were similar to those produced by gliclazide. The effect of insulin on the glucose uptake and on the GLUT 4 translocation was significantly enhanced by gliclazide (3.4-fold and 3.7-fold vs basal, respectively). These data show that sulfonylureas stimulate glucose uptake in skeletal muscle by promoting the movement of GLUT4 to the plasma membrane.

Animals↗
PubMed1996

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↗
PubMed1995

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↗
PubMed1994

Intracranial pressure dynamics in clinical practice: online PC-based ICP monitoring system.

Correct patient management involves determining the exact point on the intracranial pressure/volume (P/V) curve that corresponds to the patient; this requires calculating intracranial elastance (IE). Intracranial pressure (ICP) monitoring systems should provide the necessary information for this purpose. An ICP monitoring unit is presented that acquires ICP, systemic arterial pressure (SAP) and airway pressure (AWP). The cerebral perfusion pressure (CPP) and the mean values and the peak-to-peak values of the two of them (ICPmean, SAPmean, ICPp-p, SAPp-p,) are calculated. Graphs display the temporal evolution (TE) of the ICP and SAP, as well as histograms of the ICP (%) and intracranial pulse amplitude (ICPAmP) with respect to the ICP or CPP during the preceding 3, 6, 12 or 24 h of monitoring. By digital filtering the ICP respiratory and cardiac components (RCICP, CCICP) are calculated. Finally, the pulse amplitudes (AmP) of the ICP, CCICP and RCICP are computed, as well as the average pulses per minute of SAP, CCICP, AWP and RCICP. Two off-line pulse-amplitude and pulse-morphology oriented toolkits display the afore-mentioned curves, histograms and average pulses per minute, and other additional ones, in order to achieve a deeper patient monitoring study.

Blood Pressure Determination↗
PubMed1993

An ODA-based coder/decoder for multimedia medical documents.

This paper describes the prototype of a coder/decoder based on the Open Document Architecture (ODA) standard for management of medical documents, as well as the working environment in which it has been developed. The prototype has been assessed in an X-Windows-equipped workstation with a relational database containing patient folders (text and still images) from the departmental information system of the liver transplantation unit.

Humans↗