Mechanism of the Cortisone-Modified Glucose Tolerance Test

Berger, Sheldon; Downey, James L.; Traisman, Howard S.; Metz, Robert

doi:10.1056/nejm196606302742602

Cited by 23 publications

(9 citation statements)

References 12 publications

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“…The response did not appear to be significantly enhanced by a larger (8o mg.) or more prolonged (3 days x 20 mg.) dosage schedule. The findings of Berger et al 3 who studied the glucose tolerance and IRI responses of subjects who had a diabetic relative are similar to those of the present study, although our subjects were not selected on the basis of family history. They also found that impairment of glucose tolerance after corticosteroid administration was associated with an enhanced plasma IRI response.…”

Section: Methodssupporting

confidence: 89%

Serum Immunoreactive Insulin Levels During Glucose Tolerance and Intensive Islet Stimulation: Effect of Prednisone

1971

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The effects of a potent glucocorticoid (prednisone) on hlood sugar and serum immunoreactive insulin (IRI) levels during glucose tolerance and intensive islet stimulation were studied in forty-two subjects whose glucose tolerance ranged from well-within-normal limits to frankly diabetic. The ability to maintain "normal" glucose tolerance under this added stress was not directly related to capacity for increasing serum IRI levels. "Diabetic" subjects were not more susceptible to degeneration of glucose tolerance after prednisone even though serum IRI levels increased little 01 even decreased in several subjects. The data make it difficult to directly relate the magnitude of serum IRI levels at the times measured to degree of glucose intolerance and suggest that other factors (possibly insulin resistance), as yet unknown, are operative. DIABETES 20: 410-15, June, 1971. In a preceding report 1 we discussed the relationships between plasma immunoreactive insulin (IRI) and blood sugar levels during intensive islet stimulation. The multiple factors that should be considered in their interpretation were discussed and it was noted that among individuals there was a wide range of IRI response until high fasting blood sugar levels were reached, at which levels there was definite diminution of IRI response to the stimuli given.

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Section: Methodssupporting

confidence: 89%

Serum Immunoreactive Insulin Levels During Glucose Tolerance and Intensive Islet Stimulation: Effect of Prednisone

1971

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“…In patients with tularemia of similar severity to those reported in this study, maximum urinary 17-hydroxycorticosteroid excretion at the height of fever approached twice baseline; this output of 17-hydroxycorticosteroids in typical tularemia was reproduced in a control study in normal subjects by orally administered cortisol, with a maximum dose of 72 mg. per day. 28 Berger et al 21 used a comparable dose during their cortisone-modified glucose tolerance studies in which serum insulin responses were calculated. The dose of dexamethasone used by Perley and Kipnis 16 to alter the insulin response was severalfold greater in potency.…”

Section: Discussionmentioning

confidence: 99%

Insulin Response during Tularemia in Man

Shambaugh

Beisel

1967

Diabetes

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Serum insulin concentrations were measured serially in seven nondiabetic subjects following a rapid intravenous glucose load during a preinfection control period, during early clinical respiratory tularemia, and again in convalescence following therapy. Within twenty-four hours of onset of clinical illness the rate of glucose disappearance from the blood had diminished significantly (p<0.05). At the same time there was a brisk rise in insulin levels reaching higher peak concentrations and falling more slowly than the response observed during the preinfection control period. The pattern during clinical illness was different from that described after intravenous glucose loading in maturity onset diabetes or obesity and may have been influenced by glucocorticoid excess. Increased whole blood pyruvate concentrations following glucose loading during clinical illness were compatible with heightened glucocorticoid ction. The magnitude of insulin clinical illness was significantly increased (p<0.02) and was directly related to height of fever In contrast, the rate of glucose disappearance was inversely related to fever. The inverse relationship of the magnitude of insulin output to the rate of glucose reappearance suggested a peripheral inhibition of insulin action during infection. Although fever may have played a role during acute illness, the persistence of an abnormal insulin response in one patient during convalescence suggested that this change was not dependent upon fever alone. Other factors that may have contributed to the peripheral inhibition of insulin action during clinical illness are briefly discussed.

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“…Treatment with glucocorticoids is characterized by the coexistence of hyperinsulinemia with hyperglycemia which suggests an insulin-resistant state (1)(2)(3). However, the impairment of carbohydrate tolerance in normal subjects tends to improve during chronic glucocorticoid administration (1,4).…”

mentioning

confidence: 99%

Insulin Resistance in Cushing’s Syndrome*

Nosadini

Prato

Tiengo

et al. 1983

The Journal of Clinical Endocrinology & Metabolism

143

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It is well established that cortisol excess causes insulin resistance in man, but the mechanisms responsible for this insulin resistance are poorly understood. We studied five women with Cushing's syndrome with impaired oral glucose tolerance tests and seven normal subjects, plotting the shape of the insulin-induced disposal dose-response curve obtained by means of the euglycemic clamp procedure during four different plasma insulin plateaus at four infusion rates of 21, 73, 760, and 1200 mU/M2 . min. Glucose disposal (M = mg/M2 . min) was calculated as glucose amount infused to maintain euglycemia. In Cushing's syndrome the dose-response curve was shifted to the right in comparison with normal subjects, with a significantly lower M (337 +/- 35 vs. 657 +/- 76 P less than 0.01) during the highest insulin infusion rate [maximal glucose disposal (MGD)] without any significant difference in the levels of insulin half-maximally effective in the stimulation of glucose utilization. Neither erythrocyte nor monocyte maximum insulin receptor binding were different between the two populations. Four Cushing's syndrome patients were studied again after surgical treatment. A marked improvement of MGD was observed without any significant change in insulin-binding capacity. These results, particularly the marked decrease in MGD, a typical feature of postreceptor defects, indicate that cortisol-induced insulin resistance in man is due to an impairment of peripheral insulin action located beyond the hormone-receptor binding step.

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Mechanism of the Cortisone-Modified Glucose Tolerance Test

Cited by 23 publications

References 12 publications

Serum Immunoreactive Insulin Levels During Glucose Tolerance and Intensive Islet Stimulation: Effect of Prednisone

Serum Immunoreactive Insulin Levels During Glucose Tolerance and Intensive Islet Stimulation: Effect of Prednisone

Insulin Response during Tularemia in Man

Insulin Resistance in Cushing’s Syndrome*

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