Insulin-induced posthypoglycemic hyperglycemia as a cause of “brittle” diabetes

Bloom, Marvin E.; Mintz, Daniel H.; Field, James B.

doi:10.1016/0002-9343(69)90203-4

Cited by 54 publications

(14 citation statements)

References 13 publications

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“…The acute release of diabetogenic hormones in response to insulin-induced hypoglycaemia [10,19,20,40] has been presumed to contribute also to insulin resistance and impaired glucose tolerance with subsequent hyperglycaemia ("Somogyi effect") [41]. On the basis of the present results, it would seem that only catecholamines possess the potency to normalize rapidly blood glucose concentration after insulin-induced hypoglycaemia, whereas glucagon, cortisol, and growth hormone seem to be of no major relevance to the acute restoration of glucose homeostasis.…”

Section: Discussionmentioning

confidence: 99%

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

et al. 1981

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Summary. To evaluate the relative role of "diabetogenic" hormones as insulin antagonists in severe derangements of diabetic control, glucagon, cortisol, growth hormone and adrenaline were administered by continuous intravenous infusion, separately and in combination, to ketosis-prone insulin-dependent diabetics (n = 11). The amount of insulin required for the assimilation of a 50 g glucose load during the various hormone infusions was determined by means of an automated glucose-controlled insulin infusion system and used as an index of insulin effectiveness. Raising plasma hormone concentrations acutely into the range seen in severe diabetic states (glucagon 517+_70pg/ml; cortisol 32-+3gg/dl; growth hormone 14+3ng/ml) did not alter significantly blood glucose profile and insulin requirement (control ll.3_l.lU; glucagon 11.6-+2.0U; cortisol 11.1_+0.4 U; growth hormone 12.9___1.4 U), except for adrenaline (plasma level 550_+ 192 pg/ml), which caused a marked rise in blood glucose levels and a threefold increase in insulin demand (31.1_+ 3.7 U). Combined infusion of all hormones did not potentiate significantly the latter effect (38.3___4.7 U). The effectiveness of metabolic control by insulin was assessed by a marked decrease in plasma nonesterified free fatty acids and ketone bodies upon its administration after glucose ingestion in all groups studied. It is concluded that from the hormones investigated within this study adrenaline exerts the strongest diabetogenic action during its short term administration followed by that of growth hormone. Whereas it may well be that over-insulinization of the patients by the glucose controlled insulin infusion system has overcome and disguised the smaller diabetogenic effects of cortisol and glucagon.Key words: Diabetes mellitus, counter-regulatory hormones, glucagon, cortisol, growth hormone, adrenaline, insulin, non-esterified fatty acids, ketone bodies.Excess secretion of insulin-counteracting hormones is claimed to be important in the metabolic changes and insulin resistance in diabetic ketoacidosis [1,2]. The observations in severe derangements of diabetic control include elevated plasma levels of glucagon [3], cortisol [4], growth hormone [5,6], and catecholamines [7,8]. The hierachy of their pathogenetic significance, however, remains to be established. Hyperglycaemia, decreased glucose tolerance and insulin resistance have been demonstrated under certain circumstances after exogenous administration of these hormones [9][10][11][12]. Furthermore, the above mentioned counter-regulatory hormones are known to exert lipolytic and ketogenic activity when elevated to high physiological concentrations in insulin deficient diabetic man [12][13][14][15][16]. The delay in the development of ketoacidosis in insulin-withdrawn diabetics by either somatostatin-induced suppression of growth hormone and glucagon [17] or following pituitary ablation [1] serves as further support for implicating these hormones as pathogenic factors of deranged metabolic control. In addition, circulator...

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Section: Discussionmentioning

confidence: 99%

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

et al. 1981

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“…As has already been reported (Wrenshall et al 1952;Rastogi et al 1973;Tasaka et al 1979 (Shima et al 1977;Yue et al 1978;Tasaka et al 1978), emotional problems (Citrin et al 1981), defective subcutaneous insulin absorption (Home et al 1982), Somogyi phenomenon (post-hypoglycaemic hyperglycaemia) (Somogyi 1959;Bloom et al 1969;Gale et al 1980), and lacking response of pancreatic hormones to hypoglycaemia (Hilsted et al 1982), but no investigation has been done from the viewpoint of the amount of pancreatic insulin (IRI) or C-peptide-like immunoreactivity (CPR).…”

mentioning

confidence: 99%

C-peptide immunoreactivity and insulin content in the diabetic human pancreas and the relation to the stability of diabetic serum glucose level

Tasaka

Marumo

Inoue

et al. 1986

Acta Endocrinologica

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The content of insulin and C-peptide-like immunoreactivity (CPR) were determined in the tail of pancreas from 35 autopsied diabetic and 21 non-diabetic subjects. In the 28 diabetics who had been followed for more than 6 months, the relation between the amount of insulin or CPR in the pancreas and the stability of fasting serum glucose during diabetic life before death was analyzed together with the relation between the serum CPR response to the breakfast tolerance test before death and insulin content at autopsy. As an index of the instability of the blood sugar level, the standard deviation of the mean of 15 successive determinations of fasting serum glucose was used. Both insulin and CPR content in the pancreas were significantly decreased in diabetics as compared with non-diabetics. sd of the mean fasting serum glucose and insulin or CPR content in the tail of pancreas showed a significant inverse correlation on a logarithmic scale (P < 0.01, r = \m=-\0.704and P < 0.01, \g=g\ = \m=-\0.757,respectively). Serum CPR value during the breakfast tolerance test correlated significantly with the insulin content in the pancreas of diabetic subjects.These findings suggest that one of the causes of the instability of fasting serum glucose levels is the devastation of pancreatic \g=b\-cellsand that the pancreatic insulin content is logarithmically and inversely related to fluctuations in fasting serum glucose.

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“…The chemical events in insulin-induced instability have been difficult to document because the hypoglycémie episode can be quite brief as well as asymptomatic while the rebound hyperglycemia (and keto¬ sis) can endure for longer than a day. 3 cernia can occur at elevated glucose levels as a result of rapid decline from even higher levels.7 We have thus sought to systematically define useful clinical criteria for overinsulinization and to determine the factors that lead to the development of overtreatment in order to work toward preventing its occurrence. An additional goal of this study was the development of a strat¬ egy for reducing the insulin dosage.…”

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confidence: 99%

Chronic Overtreatment With Insulin in Children and Adolescents

Rosenbloom¹

1977

Arch Pediatr Adolesc Med

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\s=b\ We have recorded clues to the clinical recognition of chronic insulin overdosage in 101 pediatric patients with diabetes mellitus, identified predisposing circumstances, and reconsidered the traditional strategy of slow reduction in insulin dose. Overtreatment occurred in 70%, overall, and in 90% of those referred for instability; mean overdose was 38% of the readjusted dose. The most common findings were frank hypoglycemic episodes, polyuria/nocturia/enuresis despite increasing insulin dosage, excessive appetite, hepatomegaly, weight gain, headaches, exercise intolerance, marked variation in glucosuria, mood swings, and frequent bouts of rapidly developing ketoacidosis. Overtreatment usually developed because of attempts to achieve metabolic control using glucosuria as principal criterion. One fourth of those observed became overtreated during periods of emotional turmoil when need for increased insulin to counter stressinduced hyperglycemia and ketosis led to chronic increase in dosage. Persistent glucosuria/ketonuria and exacerbation of hypoglycemic symptoms were more frequent with slow than with rapid reduction in insulin dosage.(Am J Dis Child 131: [881][882][883][884][885] 1977)

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Insulin-induced posthypoglycemic hyperglycemia as a cause of “brittle” diabetes

Cited by 54 publications

References 13 publications

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

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

C-peptide immunoreactivity and insulin content in the diabetic human pancreas and the relation to the stability of diabetic serum glucose level

Chronic Overtreatment With Insulin in Children and Adolescents

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