The role of ?diabetogenic? hormones on carbohydrate and lipid metabolism following oral glucose loading in insulin dependent diabetics: Effects of acute hormone administration

Bratusch-Marrain, P.; Waldhäusl, W.; Grubeck‐Loebenstein, Beatrix; Korn, A; Vierhapper, H.; Nowotny, Peter

doi:10.1007/bf00252687

Cited by 17 publications

(8 citation statements)

References 47 publications

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“…It is worth noting that in the study of Bratusch-Marrain et a/. [25], elevated levels of plasma NEFA and ketones were reported during the combined administration of the stress hormones despite a high rate insulin infusion: our results are in line with this latter study, demonstrating a potent stimulatory effect of cortisol on adrenaline-induced lipolysis.…”

Section: Discussionsupporting

confidence: 90%

“…Few studies have been designed to examine the metabolic actions of these hormones when administered in combination to reproduce more closely the situation observed in severe stress, and their conclusions are conflicting. A synergistic action of adrenaline, cortisol and glucagon has been demonstrated on glucose metabolism in dogs [23] and in man [24], while no additional effect of either cortisol or glucagon has been reported on adrenaline-induced hyperglycaemia and insulin resistance in ketosis-prone diabetic subjects [25].…”

Section: Introductionmentioning

confidence: 99%

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Interactions of stress hormones on lipid and carbohydrate metabolism in man with partial insulin deficiency

Pernet¹,

Johnston

Hammond³

et al. 1986

Eur J Clin Investigation

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The metabolic responses to 4-h infusions of adrenaline (3 micrograms kg-1 h-1) and cortisol (10 mg m-2 h-1 for 2 h followed by 5 mg m-2 h-1 for 2 h), separately and in combination, have been studied in six healthy subjects with concurrent somatostatin infusion (250 micrograms h-1). A combined infusion of adrenaline, cortisol, glucagon (180 ng kg-1 h-1) and somatostatin has also been studied. Somatostatin plus adrenaline and somatostatin plus cortisol resulted in hyperglycaemia (at 240 min, somatostatin plus adrenaline 11.4 +/- 0.4 mmol l-1, P less than 0.001; somatostatin plus cortisol 6.7 +/- 0.3 mmol l-1, P less than 0.05; somatostatin alone 4.9 +/- 0.4 mmol l-1). No synergistic effect on blood glucose was seen with adrenaline and cortisol together. When glucagon was added, blood glucose rose more rapidly than without glucagon (9.3 +/- 0.4 mmol l-1 v. 7.2 +/- 0.5 mmol l-1 at 45 min, P less than 0.001), but plateau values were similar. Plasma NEFA levels were raised by somatostatin plus adrenaline (0.55 +/- 0.04-1.82 +/- 0.11 mmol l-1 at 60 min). Somatostatin plus cortisol had no more effect on plasma NEFA than somatostatin alone. During the combined infusion of somatostatin plus adrenaline plus cortisol, a synergistic effect on plasma NEFA was observed (2.30 +/- 0.11 mmol l-1 at 60 min, P less than 0.01 v. somatostatin plus adrenaline). This occurred despite a small escape of insulin secretion. The lipolytic actions of adrenaline are potentiated by elevated circulating cortisol levels in insulin-deficient man.(ABSTRACT TRUNCATED AT 250 WORDS)

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Section: Discussionsupporting

confidence: 90%

Section: Introductionmentioning

confidence: 99%

Interactions of stress hormones on lipid and carbohydrate metabolism in man with partial insulin deficiency

Pernet¹,

Johnston

Hammond³

et al. 1986

Eur J Clin Investigation

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“…Any physiological effect of glucagon on glucose tolerance [16] has been questioned on the basis of various experimental approaches with exogenous glucagon administration and suppression of endogenous glucagon secretion [43,44]. Thus, in normal man [45] and insulin-treated diabetic patients [37,46], even significant hyperglucagonaemia fails to impair the disposal of an oral glucose load (Fig. 2).…”

Section: Glucagonmentioning

confidence: 99%

“…This catecholamine excess, which can be rapidly corrected by rehydration and insulin treatment [4,12], may in turn exaggerate and maintain the metabolic abnormality of diabetic ketoacidosis. Our own observations made in diabetic man emphasize the role of adrenaline as the hormone exerting the most pronounced insulin-opposing action [46]. The potency of adrenaline in producing a deterioration in glucose metabolism may explain the known positive relationship between 'stress' of various causes and the onset of deranged control of the diabetic state [59].…”

Section: Glucagonmentioning

confidence: 99%

Insulin-counteracting hormones: Their impact on glucose metabolism

Bratusch-Marrain

1983

Diabetologia

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“…However, in insulin-dependent diabetics whose endogenous GH secretion was blocked by somatostatin, blood glucose remained unchanged regardless of whether basal GH levels were replaced (10). Similarly, short term, low dose GH infusion failed to alter the disposition of an oral glucose load in insulin-dependent diabetics (11). Both latter studies would suggest that short term elevations in plasma GH levels within the physiological range do not adversely affect glucose disposal.…”

mentioning

confidence: 93%

The Effect of Growth Hormone on Glucose Metabolism and Insulin Secretion in Man*

Bratusch-Marrain

Smith

DeFronzo

1982

The Journal of Clinical Endocrinology & Metabolism

319

144

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Pharmacological doses of GH are known to impair glucose tolerance. In the present study we have employed the euglycemic insulin and hyperglycemic clamp techniques to examine the effect of physiological elevations in plasma GH concentrations (27 ± 2 ng/ml) on the tissue responses to insulin and on glucose-stimulated insulin secretion. Three types of studies (low dose insulin clamp, high dose insulin clamp, and hyperglycemic clamp) were performed in young healthy volunteers before and after the infusion of GH (2 /ig/kg-h) for 2 and 12 h. In the low dose insulin clamp studies, the plasma insulin concentration was acutely raised and was maintained at 59 ± 4 juU/ml, while plasma glucose was maintained at basal levels. After 2 h of GH infusion, insulin-mediated glucose metabolism was slightly, although not significantly, decreased (4.48 ± 0.56 vs. 5.04 ± 0.39 mg/kg-min) in the control study. After 12 h of GH infusion, however, insulin-mediated glucose uptake decreased by 32 ± 9% (3.36 ± 0.40 mg/kg-min; P < 0.01). Basal endogenous glucose production (2.02 ± 0.07 mg/kg-min) was suppressed by 89 ± 4% in the control study. After short term GH infusion, the degree of suppression (90 ± 5%) was similar to the control value. After 12 h of GH infusion, however, suppression of endogenous glucose production (78 ± 5%) was slightly less than that in controls (P < 0.05). In the high dose insulin clamp studies, GH was infused for either 2 or 12 h, after which plasma insulin levels were increased to 2292 ± 96 /xU/ml while maintaining euglycemia (high dose insulin clamp study). Insulin-mediated glucose uptake was 11.22 ± 0.53 mg/kg-min in the control study, slightly lower during short term GH infusion (9.56 ± 1.00 mg/kg-min) and significantly diminished after long term GH infusion (7.16 ± 1.12 mg/kg-min; P < 0.02). In the hyperglycemic clamp studies, plasma glucose was raised and maintained at 125 mg/dl above the basal level. Glucose metabolism in controls (8.68 ± 0.53 mg/ kg-min) was decreased by 31 ± 7% after 2 h and by 44 ± 6% after 12 h of GH infusion. The mean increment in plasma insulin in response to hyperglycemia (control, 56 ± 10 juU/ml) was unaltered after 2 and 12 h of GH administration. Total binding of [ 125 I]insulin to monocytes was 7.0 ± 0.5% before GH infusion. After 2 h of GH administration, no change in total specific insulin binding (7.4 ± 0.4%) occurred. After 12 h of exposure to GH, however, total binding was decreased (5.9 ± 0.4%; P < 0.02) due to a decrease in receptor affinity.We conclude that physiological elevations in GH 1) induce a state of insulin resistance within 2-12 h, 2) only slightly impair insulin's suppressive effect on endogenous glucose production, indicating that the primary site of insulin resistance resides in peripheral tissues, 3) do not alter the plasma insulin response to hyperglycemia, and 4) cause a decrease in insulin binding that results from a decrease in receptor affinity. The inability to overcome the defect in glucose metabolism at high plasma insulin concentrations suggests that a...

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The role of ?diabetogenic? hormones on carbohydrate and lipid metabolism following oral glucose loading in insulin dependent diabetics: Effects of acute hormone administration

Cited by 17 publications

References 47 publications

Interactions of stress hormones on lipid and carbohydrate metabolism in man with partial insulin deficiency

Interactions of stress hormones on lipid and carbohydrate metabolism in man with partial insulin deficiency

Insulin-counteracting hormones: Their impact on glucose metabolism

The Effect of Growth Hormone on Glucose Metabolism and Insulin Secretion in Man*

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