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Biomedical subjects

L L Ng

Publications and source records attributed to L L Ng.

At least 127 records · Page 7Linked to original sources
PubMed1988

The human leucocyte sodium pump in Cushing's syndrome.

Because corticosteroids have important effects on sodium homeostasis, we studied leucocyte 22Na efflux in patients with Cushing's syndrome. The ouabain-sensitive 22Na+ efflux rate constant was raised in Cushing's syndrome (mean +/- SD 2.84 +/- 0.32 vs 2.35 +/- 0.53/h, P less than 0.001, n = 15). This efflux rate constant correlated with the urinary free cortisol (rs = 0.61, P less than 0.02), but less significantly with the 0900 h plasma cortisol (rs = 0.46, P less than 0.08). There was no correlation with the supine plasma aldosterone. Intracellular sodium content was significantly lower in Cushing's syndrome (21.1 +/- 4.6 vs 27.8 +/- 9.5 mmol/kg dry weight, P less than 0.01), with a raised intracellular potassium to sodium content ratio (16.1 +/- 3.3 vs 12.9 +/- 3.6, P less than 0.01). After treatment of the Cushing's syndrome by trans-sphenoidal adenomectomy or adrenalectomy, these defects in cellular sodium balance were corrected. Thus, the distribution of sodium between intra- and extracellular fluid may be affected by adrenal corticosteroids via an action on the sodium pump.

Adult↗
PubMed1987

Leucocyte sodium pump activity after meals or insulin in normal and obese subjects: cause for increased energetic efficiency in obesity?

As cellular sodium pumping is an energy consuming process and differences in the obese may account for their energetic efficiency, leucocyte sodium-22 efflux was studied in obese and normal volunteers both in the fasting state and after a test meal or infusion of glucose and insulin intravenously. The 22Na ouabain sensitive efflux rate constant was significantly higher in obese subjects than normal (mean (1 SD) 2.69 (0.40)/h v 2.35 (0.49)/h). Two hours after a 4.2 MJ (1000 kcal) meal there was an increase in the efflux rate constant from its fasting value in normal weight subjects (2.39 (0.33)/h to 2.71 (0.40)/h) but not in obese subjects (2.65 (0.54)/h to 2.61 (0.58)/h). The rise in ouabain sensitive efflux rates was significantly higher in normal than obese subjects. Both groups showed a rise in intracellular sodium concentrations. The euglycaemic clamp produced similar results. Feeding or infusion of insulin increases sodium pump activity more in normal than obese subjects. This difference may contribute to any defective dietary thermogenesis in obesity, which may lead to energetic efficiency and a tendency to gain weight.

Adult↗
PubMed1987

Analysis of sulindac and metabolites in plasma and urine by high-performance liquid chromatography.

A reversed-phase high-performance liquid chromatographic method with ultraviolet detection is described for the quantification of sulindac, sulindac sulfone and sulindac sulfide in plasma and sulindac, trans-sulindac, sulindac sulfone and sulindac sulfide in urine. Plasma samples are de-proteinized with acetonitrile and urine samples are injected directly following enzymatic hydrolysis of glucuronide metabolites. The resulting chromatograms are essentially free from endogenous interference and the limits of detection are 0.1 microgram/ml for plasma and 0.2 microgram/ml for urine for all of the above compounds.

Chromatography, High Pressure Liquid↗
PubMed1987

Leucocyte sodium transport in acromegaly.

The leucocyte sodium pump was studied in patients with active and treated acromegaly. The ouabain-sensitive 22Na+ efflux rate constant was significantly raised in active acromegaly (median 2.71 [range 2.33-3.20] vs 2.32 [1.55-3.67] h-1, P less than 0.008) and was lowered into the normal range with successful treatment. Plasma GH and insulin levels and skin fold thickness on the dorsum of the hand were positively correlated with this efflux rate constant (rs = 0.06 P less than 0.02; rs = 0.57, P less than 0.02; rs = 0.57 P less than 0.04, respectively). GH, in vitro, stimulated ouabain-sensitive efflux in leucocytes at a concentration of 25 mU/l. We propose that this action of GH may explain the sodium retaining and calorigenic effects and possibly the stimulation of amino acid uptake by the hormone. The activity of the leucocyte sodium pump in acromegaly may be associated with other indices of disease activity.

Acromegaly↗
PubMed1987

The human leucocyte sodium pump in adrenocortical insufficiency.

In view of the known effects of cortisol and related compounds on sodium balance, we examined leucocyte 22Na+ efflux in patients with adrenocortical insufficiency. The ouabain-sensitive 22Na+ efflux rate constant, which reflects sodium pump activity, was lowered in secondary hypoadrenalism (mean 1.95 +/- SD 0.25 vs 2.33 +/- 0.45 h-1, P less than 0.002, n = 6). Patients with hypoadrenalism also had higher intracellular sodium content (mean 34.9 +/- SD 3.5 vs 27.8 +/- 9.5 mmol/kg dry weight, P less than 0.008) and lower intracellular potassium to sodium ratios (mean 9.7 +/- SD 0.7 vs 12.9 +/- 3.6, P less than 0.001). These defects in cellular sodium balance were corrected following replacement therapy with cortisol, prednisolone or dexamethasone. In-vitro incubation of normal leucocytes with 5-20 nmol/l dexamethasone led to an increase in the Na+/K+-ATPase activity. The effect of cortisol and related compounds on the distribution of sodium between intra- and extra-cellular fluid may be mediated by their action on the sodium pump.

Adrenal Insufficiency↗
PubMed1987

The effect of oral glucose on the leucocyte sodium pump in normal and obese subjects.

The effect of oral glucose (40 g/m2 body surface area) on the leucocyte 22Na efflux rate constants (ERC) was studied in 13 normal weight and 10 obese subjects. The ouabain-sensitive 22Na ERC was higher in leucocytes isolated from fasting obese subjects (median [range] for obese 2.77 [2.33-3.11] vs normals 1.91 [1.57-2.77] h-1, P less than 0.001). There was no difference in the ouabain-resistant 22Na ERC. Oral glucose raised the ouabain-sensitive 22Na ERC after 2 h in normal subjects (1.91 [1.57-2.77] to 2.41 [2.11-3.02] h-1, P less than 0.001). The ouabain-resistant 22Na ERC fell from 0.71 [0.32-1.10] to 0.46 [0.35-0.68] h-1, P less than 0.008. Conversely, in obese subjects, the ouabain-sensitive ERC fell (2.77 [2.33-3.11] to 2.59 [2.11-2.92] h-1, P less than 0.06). There was no significant change in ouabain-resistant 22Na ERC 2 h after oral glucose. The fasting leucocyte 22Na ouabain-sensitive ERC correlated with fasting plasma insulin levels and insulin resistance (rs = 0.48, P less than 0.01 for both). The change in this ERC with oral glucose correlated with the incremental insulin response over 2 h (rs = -0.53, P less than 0.006) and to the insulin resistance (rs = -0.56, P less than 0.003). The failure of oral glucose to stimulate the leucocyte sodium pump in obesity could partially account for the defect in dietary thermogenesis in obesity. This defect in stimulation of the sodium pump is related to insulin resistance.

Adult↗
PubMed1986

Non-esterified fatty acids may regulate human leucocyte sodium pump activity.

Human leucocyte sodium pump activity was studied in normal fasting subjects by measuring the ouabain-sensitive 22Na+ efflux rate constants. This 22Na+ efflux rate constant was inversely related to the fasting plasma non-esterified fatty acid level (rs = -0.73, P less than 0.0001). An oral glucose load (40 g/m2 surface area) led to an increase in the leucocyte ouabain-sensitive 22Na+ efflux rate constant after 2 h (1.97 +/- 0.25 to 2.44 +/- 0.19 h-1, P less than 0.0001, n = 11). There was a concomitant fall in the plasma non-esterified fatty acid level. Incubation of leucocytes in vitro with 100 mumol/l linoleic acid inhibited the leucocyte ouabain-sensitive 22Na+ efflux rate constant (1.52 +/- 0.27 vs 0.84 +/- 0.24 h-1, P less than 0.001, n = 8). The leucocyte Na+,K+-dependent adenosine triphosphatase (Na+,K+-ATPase) activity was inhibited in vitro by long chain non-esterified fatty acids, especially when unsaturated. Non-esterified fatty acids may account for some of the Na+,K+-ATPase inhibitory activity of plasma.

Biological Transport, Active↗
PubMed1986

The leucocyte sodium pump in healthy and obese subjects: the association of insulin with its activity.

Leucocyte ouabain-sensitive 22Na+ efflux was studied in 35 normal and 12 obese subjects. This efflux rate constant was raised in the obese (2.72 +/- SEM 0.13 vs 2.31 +/- 0.08 h-1, P less than 0.006), indicating a higher activity of the sodium pump in vivo, There was a significant correlation between this efflux rate constant and fasting insulin level in both the whole population and in the normals alone (rs = 0.36, P less than 0.007, and rs = 0.40, P less than 0.009 respectively). A hyperinsulinaemic-euglycaemic clamp was performed on seven normal volunteers. After 2 h, there was a significant stimulation of the leucocyte efflux rate constant (from 2.86 +/- 0.17 to 3.33 +/- 0.18 h-1, P less than 0.01). In-vitro incubation of leucocytes with insulin produced a maximal stimulation of the Na+-K+-ATPase activity of about 35% at 2 h with half-maximal stimulation achieved at 46 mU/l. Insulin (100 mU/l) also stimulated the leucocyte ouabain-sensitive 22Na+ efflux rate constant in vitro by about 11% with or without 1 h of preincubation with the insulin. These findings may explain the hypokalaemic and sodium retaining effects of insulin in man; they may also partially explain the raised Na+ efflux rate constants in obesity.

Adolescent↗
PubMed1985

Interval between insulin injection and eating in relation to blood glucose control in adult diabetics.

In a survey of 225 diabetics treated with insulin 24 (10.6%) claimed never to have received advice concerning the interval between insulin injection and eating. Of the remainder, 67 (33%) admitted disregarding advice and using shorter intervals. There was a significant (p less than 0.01) difference between the reported frequencies of clinical hypoglycaemia in patients using different intervals. The effects on glucose control of intervals between insulin injection and breakfast of zero, 15, 30, and 45 minutes were studied for periods of one week in 11 patients with type I diabetes who were receiving twice daily injections of monocomponent porcine insulins and high fibre, high carbohydrate diets, using standard home blood glucose monitoring techniques to measure blood glucose concentrations each morning. The delay of 45 minutes resulted in the lowest frequency of hypoglycaemia and the most acceptable pattern of glucose concentrations measured one and two hours after breakfast and before lunch. Combining results obtained at these three times, the mean increment in blood glucose concentration was smaller after allowing a delay of 45 minutes than after delays of zero (p less than 0.001), 15 (p less than 0.03), and 30 (NS) minutes. A delay of 30 minutes resulted in smaller mean increments in blood glucose concentration than did delays of zero (p less than 0.001) and 15 (NS) minutes. These results suggest that this aspect of diabetic management may be neglected, with important consequences for blood glucose control. An increase in delay between insulin injection and eating to 45 minutes would be a simple and safe way of improving blood glucose control in at least the 37% of the diabetic population surveyed in this study who currently allow less than 15 minutes.

Adolescent↗