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Biomedical subjects

A E Lambert

Publications and source records attributed to A E Lambert.

At least 55 records · Page 3Linked to original sources
PubMed1980

Use of an extracorporeal glucose monitor for the diagnosis and surgical treatment of an insulinoma.

An extracorporeal glucose monitor (EGM) has been used in a patient with an insulinoma. This system, which continuously measures blood glucose, can be used in combination with a feedback-controlled glucose infusion to maintain glycaemia at any preselected level. It prevents the risk of severe hypoglycaemia during diagnostic tests (total fast, tolbutamide and insulin tolerance tests) as well as during surgery. It also helps in determining whether all the insulin-secreting tumour tissue has been removed. The EGM is thus helpful in the diagnosis and surgical treatment of insulinomas.

Adenoma, Islet Cell↗
PubMed1979

Alloxan-induced alteration of insulin release, rubidium efflux and glucose metabolism in rat islets stimulated by various secretagogues.

Insulin release and 86Rb efflux were studied in perifused rat islets exposed in vitro to alloxan (2 mmol/l) for 5 min. At a low glucose concentration, alloxan transiently increased 86Rb efflux. Alloxan immediately and completely abolished the secretory response to glucose (15 mmol/l) and markedly delayed the reduction in 86Rb efflux normally produced by the sugar. 3-O-methylglucose (20 mmol/l) provided complete protection against the alteration of 86Rb efflux and partial protection against the inhibition of insulin release. Immediately after alloxan treatment, glyceraldehyde, alpha-ketoisocaproic acid and tolbutamide still induced a rapid release of insulin, but the late phase normally stimulated by glyceraldehyde and alpha-ketoisocaproic acid was inhibited. If islets were exposed to glyceraldehyde or tolbutamide 15 min after alloxan treatment, the rapid insulin release was also markedly impaired. Alloxan failed, however, to affect the ability of these three stimuli to reduce 86Rb efflux from islet cells. Glucose oxidation and utilization were decreased in alloxan-treated islets and 3-O-methylglucose protected against this effect. The results show that the glucose recognition system in B-cells is the most rapidly and severely affected by alloxan. The drug also alters the response to other secretagogues, the insulin releasing properties of which can be impaired without alteration of their ability to reduce 86Rb efflux.

Alloxan↗
PubMed1979

[Treatment of ambulatory unstable diabetic patients by continuous subcutaneous infusion of insulin: preliminary results (author's transl)].

The aim of the present work was to examine the possibility of improving the metabolic control of ambulatory unstable diabetic patients by continuous subcutaneous infusion of insulin. For this purpose, a simple portable pump infusing insulin at a constant rate of 0.8 or 1.1 U/h was utilized. Pulses of a more concentrated insulin solution were superimposed 30-60 min. before meals. Blood glucose control during conventional insulin therapy and during continuous infusion was compared by measuring the mean blood glucose and the M-value of Schlichtkrull. Blood glucose fluctuations were estimated by the MAGE index of Service and Molnar. Three patients were submitted to continuous subcutaneous infusion of insulin during periods of 1, 5 and 6 weeks. In two cases, the application of this technic considerably improved the metabolic control as evidenced by a remarkable decrease of the three measured parameters. In one patient, continuous infusion of insulin was stopped after one week since it did not lead to an improvement of diabetic equilibrium. This failure was apparently due to emotional intolerance of the new technic. On two occasions, infection at the site of infusion was noted. These results should encourage longer-term studies involving a larger number of patients.

Ambulatory Care↗
PubMed1978

Growth hormone secretion in Addison's disease.

Growth hormone secretion has been evaluated in patients with Addison's disease given T.R.H., A.C.T.H. or Glucagon i.v., or L-DOPA p.o. In those with the idiopathic, auto-immune variety the mean response to glucagon and L-DOPA was reduced when compared with that documented for patients in whom tuberculosis caused the lesion. Growth hormone plasma concentrations barely changed after T.R.H. and A.C.T.H., irrespective of the aetiology of the disease.

Addison Disease↗
PubMed1976

Bicarbonate modulation of glucose-9nduced biphasic insulin release by rat islets.

The role of HCO3 ions in pancreatic beta-cell functions was evaluated with isolated rat islets. The early phase of insulin release was absent when HCO3 ions were omitted from the medium prior to glucose stimuation, but was augmented if HCO3- withdrawal or reintroduction coincided with glucose increase. The inhibition of the late phase augmented as a function of the duration of HCO3- absence, and its reversibility upon readmission of the anion was delayed. Theophylline and cytochalasin B partially corrected the inhibition of the late phase but failed to restore a rapid response. In the presence of 5 mM NaHCO3, the early response was delayed but the total response was normal. In a HCO3--free medium, glucose oxidation and utilization and glucose transport in islet cells were unaltered. Uptake of calcium was reduced in the absence of HCO3 ions, but normal in 5 mM HCO3-. The results document the importance of HCO3- in insulin release and show that the two phases of glucose-induced secretion are differentially modified by its omission. Some of these findings may be explained by alterations in Ca++ uptake by islet cells. It is suggested that the mechanisms regulating insulin granule extrusion upon stimulation by glucose may be partially different for the two phases of release.

Animals↗
PubMed1976

Potassium ions and insulin release.

This article briefly reviews the effects of potassium on insulin release. Omission of extracellular potassium in vitro is followed by a delayed impairment of the release. At low concentrations of potassium, the insulinotropic effect of glucose is reduced in vivo and in vitro. In vivo, high concentrations of potassium increase insulin secretion, but, in vitro, supraphysiological concentrations of the ion first activate and then inactivate the releasing process.

Animals↗
PubMed1975

Extracellular bicarbonate ions and insulin secretion.

The role of bicarbonate ions in insulin release was studied with incubated and perifused isolated rat islets of Langerhans. In the absence of NaHC03, the early phase of glucose-induced secretion was completely abolished and the second phase inhibited by approximately 65%. The insulinotropic effect of the sugar was totally restored after reintroduction of the ion in the medium. The monophasic secretory after reintroduction of the ion in the medium. The monophasic secretory response to tolbutamide was also markedly diminished by omission of NaHC03, WHereas the release evoked by a high concentration of K+ was very little affected. CO2 wwas unable to substitute for HC03minus, but small concentrations of the anion (3to 5mM) WEre sufficient to ensure a normal response to glucose.

Animals↗