Biomedical subjects
Publications and source records attributed to M Armoni.
Two hundred and sixty-eight children with pediculosis capitis took part in a comparative study to test the efficacy of five different pediculocides commonly used in Israel. The preparations used were pyrethrin shampoo, pyrethroid spray, malathion solution, carbaryl shampoo and carbaryl lotion. Carbaryl lotion and malathion solution were much more efficient when compared to the shampoo and spray preparations.
This study was undertaken to investigate the effect of ketotifen on the immune system of asthmatic children receiving prophylactic treatment with ketotifen. E. rosettes, mitogenic response to phytohemagglutinin (PHA) and concanavalin A (Con A) as well as Con A induced suppression were measured in 15 asthmatic patients before and 1-3 months after treatment with ketotifen (1 mg x 2/day), and in 20 normal healthy controls. No significant difference in immunological parameters studied were found between the pre and post treatment periods in the asthmatic patients, neither was any difference demonstrated between the asthmatic and control group studied.
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We examined the effects of insulin on glucose transport and subcellular glucose transporter distribution in isolated omental adipose cells from men and women. 3-O-Methylglucose transport was measured in intact cells, and the number of glucose transporters in plasma membranes and low density microsomal membranes was determined using the cytochalasin B binding assay. Compared to adipocytes from women, omental adipocytes from men were characterized by 1) 2-fold larger cell volume; 2) 4- to 5- and 2.5-fold higher glucose transport rates when calculated per cell or per cell surface area, respectively, in either basal or insulin-stimulated cells; 3) similar 2-fold insulin stimulating effect per se; and 4) equal concentrations of transporters in both fractions examined, but a 2-fold increase in their total number per cell. Additionally, although not directly measured, the calculated glucose transporter activity in basal plasma membranes prepared from adipocytes from men was 2.7-fold higher than that in women, and insulin further induced a 30% increase in that activity. Thus, a sex-related difference was found between the number of glucose transporters per cell and the resultant glucose transport activity of the intact cells. Together with the increased specific activity of glucose transporters in men compared to women, our findings indicate a sex-related difference in adipocyte glucose transport, mainly due to an increase in the number and modulation of the intrinsic activity of glucose transporters in the plasma membrane.
To determine the role of insulin in reversing the insulin resistance associated with depletion of the intracellular pool of glucose transporters, streptozocin-induced diabetic rats were treated with 5 U/day s.c. of insulin for 0, 8, or 14 days. At each time point, adipose cells were isolated, and 3-O-methylglucose transport was measured in the absence and presence of 1000 microU/ml insulin. With the cytochalasin B-binding assay, concentrations of glucose transporters in the plasma and the low-density microsomal membrane fractions were determined. Eight-day insulin therapy enhanced glucose transport rate (mean +/- SE) from 0.2 +/- 0.0 to 1.1 +/- 0.1 fmol X cell-1 X min-1 in the basal state and from 0.8 +/- 0.1 to 5.5 +/- 0.4 fmol X cell-1 X min-1 in the insulin-stimulated state in untreated and treated diabetic rats, respectively; this is a 3-fold increment of glucose transport rate in both states compared with control rats. After 14-day insulin therapy, glucose-transport activity declined toward normal but still remained approximately 1.5- and 4-fold higher than control and diabetic rats, respectively. Despite the persistent enhancement of glucose transport rate, concentration of glucose transporters in the intracellular pool was restored only to its prediabetic state. Likewise, the increased concentration of glucose transporters in the plasma membranes after insulin stimulation was similar to that of control rats. Thus, we suggest that 8-14 days of insulin therapy reversed the insulin resistance in diabetic rat adipocytes by at least two mechanisms: restoration of the intracellular pool of glucose transporters and enhancement of glucose-transport activity.(ABSTRACT TRUNCATED AT 250 WORDS)
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We examined insulin's effects on glucose transport and on subcellular transporter distribution in isolated human omental adipocytes of various sizes. Insulin stimulated 3-O-methylglucose transport by twofold in small cells, while a smaller and insignificant effect was measured in large cells. In the small cells, basal concentrations of glucose transporters were 2.9 and 17.2 pmol/mg membrane protein in the plasma and the low density microsomal membranes, respectively. Increasing cell size was associated with a 50% decrease in the concentration of transporters in each fraction, with no change in their total number per cell. Insulin stimulated the translocation of transporters from the intracellular pool to the plasma membranes, irrespective of cell size. Thus, insulin resistance at the postreceptor level, observed in human obesity, may be associated with a relative depletion of total transporters per cell together with a reduction in their intrinsic activity at the plasma membrane level.
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Insulin resistance is well established in Cushing's syndrome, but its mechanisms are not completely understood. We performed the euglycemic insulin clamp technique on four patients with Cushing's syndrome, five obese patients and five normal volunteers, in order to determine the role of impairments in insulin responsiveness and insulin clearance in hypercorticism and obesity. Insulin was infused at 0.3, 1, 3 and 10 mU/kg/min, and steady-state glucose-infusion rates required to maintain euglycemia were determined. Glucose disposal at maximal insulin levels was 11.9 +/- 0.4 mg/kg/min in normals, with a 29% decrease in obese and a 42% decrease in Cushing's syndrome patients. Half maximally effective insulin concentrations were increased in both abnormal groups compared to normals. Maximal insulin clearance rates were 1460 +/- 200 ml/min/m2 in normals, not significantly changed in obese and 40% decreased in Cushing's syndrome patients. These results indicate that the insulin resistance in Cushing's syndrome is distinct from that occurring in obesity and is characterized by both decreased insulin responsiveness and decreased insulin clearance. These impairments could be caused by a common defect which may be at or distal to the glucose transport level.
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Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.