Blood glucose and insulin levels, thyroid function, and serology in Ménière's disease, recurrent vestibulopathy, and psychogenic vertigo.

Nineteen patients with unilateral Ménière's disease, 20 with psychogenic dizziness, and 20 with recurrent vestibulopathy (diagnostic criteria in text of paper) were found to have normal five hour glucose tolerance tests, serum thyroxine and effective thyroid indices, and serologic tests for syphilis. Hypothyroidism and hypoglycemia were absent in all groups. An unexplained finding of each diagnostic group was significant increase of fasting blood glucose and insulin levels, and elevated insulin:glucose ratios, compared to a control group. There appears to be no diagnostic indication for performing these chemical and serologic studies in patients with unilateral Ménière's disease, psychogenic vertigo, or recurrent vestibulopathy. Reasons are given to support the view that recurrent vestibulopathy may be a specific vestibular disturbance.

Effect of d- and dl-propranolol on glucose-stimulated insulin release.

The effect of intravenous d- and dl-propranolol on serum insulin levels has been examined before and after the administration of glucose orally to 10 normal subjects. The increase in serum insulin 45 to 90 min after glucose ingestion was reduced during the infusion of either d- or dl-propranolol. The insulin suppression was not accompanied by any alteration in the glucose curves. The insulin/glucose ratios were reduced by both d- and dl-propranolol during the time of maximum glucose and insulin responses. Neither d- nor dl-propranolol induced any significant change in basal glucose or insulin levels before glucose administration. Since d-propranolol has no appreciable beta adrenoceptor blocking activity, it appears that the suppression of glucose-stimulated insulin release by propranolol may be due primarily to local anesthetic properties which are exerted equally by both isomers.

Effects of insulin and procaine hydrochloride on glycogen synthetase activation and adipocyte calcium flux: evidence for a role of calcium in insulin activation of glycogen synthetase.

Observations that insulin-induced stimulation of glycogen synthetase occurs without detectable reduction in cyclic AMP suggests an alternative controlling mechanism. The hypothesis that this stimulation might be mediated through calcium was tested using procaine HC1, a drug whose insulin-like action is not associated with reduction in basal or adrenaline-stimulated cyclic AMP levels. Pretreatment of adipose tissue with insulin or porcaine for 30 minutes increased homogenate glucose-6-phosphate independent ("I") form activity to 58% and 48% respectively with no significant change in total activity. Insulin and procaine also had similar effects on calcium efflux from isolated rat adipocytes. Following an initial displacement of calcium from the adipocytes by insulin (but not by procaine) both agents decreased efflux of calcium, measured following 10, 20 and 30 minutes incubation. In adipose tissue homogenates increasing the free calcium concentration from 10(-8) to 10(-3) M increased "I" form glycogen synthetase activity without significantly altering total activity. A complex interrelationship with ATP and calcium was also observed. In the presence of ATP 0.5 mM maximal activation occurred at 10(-6) M calcium concentration. These findings suggest that insulin-induced activation of glycogen synthetase may be effected by alteration of intracellular free calcium with consequent effects on glycogen synthetase-related enzymes in a mechanism independent of or complementary to effects on cyclic AMP levels.