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Query: UMLS:C0011849 (diabetes)
 277,896 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Unstable diabetes is characterized by the appearance of irregular and unpredictable variations of the glycemia; because of this it is very difficult to achieve an acceptable metabolic control. There are different criteria (continuous monitorization, M value, MDDG, AMEG, etc.) for the evaluation of the degree of instability. Unstable diabetes may be transitory (generally related to exogenous factors or erroneous management) or permanent. The Somogyi effect must always be taken into account in unstable diabetes. The two most important pathogenic factors could be the absence of the pancreatic insulin reserve and the presence of small quantity of anti-insulin antibodies of high affinity. Other factors such as glucagon, growth hormone, catecholamines, etc. seem to play a secondary role. At the moment the treatment of unstable diabetes is not very satisfactory.
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PMID:[Unstable diabetes (author's transl)]. 52 31

A patient with diabetes mellitus and hypopituitarism developed the Somogyi effect that was characterized by insulin-induced hypoglycemia and rebound insulin-resistant hypoglycemia. This compensatory insulin-resistant hyperglycemia has generally been ascribed to the release of anterior hypophyseal hormones; however, our findings suggest that factors other than anterior hypophyseal hormones are involved.
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PMID:Somogyi effect in patient with hypopituitarism. 94 95

The Somogyi phenomenon or effect is a paradoxical situation of insulin-induced post-hypoglycemic hyperglycemia. The historical aspects of this phenomenon and the subsequent hypotheses and controversy are reviewed. The clinical situation is explained, with regard to its recognition, management and importance as an etiological factor in "brittle" diabetes. Hormone immunoassay techniques at present show human growth hormone (HGH) to be the major consequence of insulin-induced hypoglycemia leading to post-hypoglycemia glucose intolerance, but further studies will probably show glucagon to have a major role.
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PMID:The Somogyi phenomenon. A short review. 97 71

The possible causes of insulin resistance, in particular the production of insulin-antibodies, abnormal factors interfering with the effect of insulin on peripheral tissues and the Somogyi effect, are discussed. Accumulation of insulin antibodies with formation of insulin-antibody complexes is pointed out as the prevalent cause of insulin resistance in advanced age. Intravenous insulin treatment with massive doses ensured a beneficial effect. Achrestic diabetes associated with peripheral resistance is regarded as the cause of insulin resistance in juvenile patients possessing no major amounts of antibody. Muscle tissue obtained from these patients showed an insulin resistant impairment of glucose consumption and of Na-transport. This is consistent with the peripheral pathomechanism underlying this condition. A feedback mechanism elicited by latent hypoglycaemia may be the cause of spurious insulin resistance.
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PMID:Insulin resistance. 123 47

To test the hypothesis that nocturnal hypoglycemia causes postprandial hyperglycemia the next day (the Somogyi phenomenon) in patients with insulin-dependent diabetes mellitus (IDDM), we studied 10 moderately well controlled patients, who were on their usual therapeutic regimens, from 2000 to 2000 on three occasions. On a control day, samples were obtained without intervention. On another day, nocturnal hypoglycemia was prevented (by intravenous infusion of glucose, if necessary, from 2200 to 0400 to keep plasma glucose levels at greater than 5.6 mM). On another day, nocturnal hypoglycemia was induced (by stepped intravenous insulin infusions between 2200 and 0200 to reduce plasma glucose levels to less than 2.8 mM). After nocturnal hypoglycemia (1.9 +/- 0.2 mM), fasting (0800), morning (0800-1100), afternoon (1200-1500), evening (1600-2000), and entire-day (0800-2000) plasma glucose concentrations were no higher than those after prevention of nocturnal hypoglycemia or sampling only. On the control day, fasting and daytime plasma glucose levels were directly related to the preceding 2200 (r = 0.723, P less than 0.02, and r = 0.762, P = 0.01, respectively) and nocturnal nadir (r = 0.714, P less than 0.02, and r = 0.728, P less than 0.02) plasma glucose concentrations. Daytime plasma glucose levels were unrelated to peak nocturnal plasma glucagon, epinephrine, norepinephrine, growth hormone, or cortisol concentrations. We conclude that nocturnal hypoglycemia does not appear to cause clinically important daytime hyperglycemia in patients representative of most patients with IDDM.
Diabetes Care 1990 Feb
PMID:Failure of nocturnal hypoglycemia to cause daytime hyperglycemia in patients with IDDM. 219 Jul 69

The glucose counterregulatory system is one of the most important homeostatic systems in physiology, since it normally prevents hypoglycaemia or, should it occur for any reason such as insulin administration, limits the severity of hypoglycaemia and ultimately may restore normoglycaemia. In normal nondiabetic subjects, activation of counterregulation does not result in overt hyperglycaemia in the post-absorptive state, because the pancreatic beta-cell increases insulin secretion. On the contrary, in subjects with insulin-dependent diabetes mellitus (IDDM) whose pancreatic B-cell cannot respond to an increase in plasma glucose, activated counterregulation may easily result in overt hyperglycaemia. There are two different circumstances under which counterregulation may contribute to excessive hyperglycaemia in IDDM, namely nonhypoglycaemic nocturnal activation of counterregulation (dawn phenomenon), and hypoglycaemic activation of counterregulation (Somogyi phenomenon). The dawn phenomenon is an increase in insulin requirements which occurs between 04.00 and 08.00 h in the absence of preceding hypoglycaemia and concomitant hypoinsulinemia. It is caused by a decrease in hepatic and extrahepatic sensitivity to insulin induced by the nocturnal secretion of growth hormone. The dawn phenomenon may contribute importantly to fasting hyperglycaemia in IDDM, because usually plasma insulin concentration following the pre-supper insulin injection decreases after 04.00 h, i.e. a time at which plasma insulin concentration should instead increase to maintain normoglycaemia. The Somogyi phenomenon is best defined as hyperglycaemia following hypoglycaemia and is caused by the insulin resistance induced by hypoglycaemic-activation of counterregulation. Although insulin resistance following hypoglycaemia is a constant event in IDDM, post-hypoglycaemic hyperglycaemia is not the rule. For example, if the responses of counterregulatory hormones to nocturnal hypoglycaemia are blunted, or plasma insulin concentration following hypoglycaemia is inappropriately high, post-hypoglycaemic insulin resistance is not powerful enough to result in overt hyperglycaemia in the fasting state. However, post-breakfast plasma glucose may be exaggerately elevated following nocturnal hypoglycaemia even in the case that fasting plasma glucose is only modestly increased. It is important to prevent nocturnal hypoglycaemia, not only to protect brain function, but also to prevent insulin resistance which may easily result in exaggerated hyperglycaemia and initiate the vicious circle "hypoglycaemia-hyperglycaemia-increase in insulin dose-risk for subsequent hypoglycaemia", and so on.
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PMID:Impact of activated glucose counterregulation on insulin requirements in insulin-dependent diabetes mellitus. 227 33

Hypoglycemia causes substantial morbidity and some mortality in insulin-dependent diabetes mellitus (IDDM). It is often the limiting factor in attempts to achieve euglycemia. The prevention or correction of hypoglycemia normally involves both dissipation of insulin and activation of glucose counterregulatory systems. Among the latter, glucagon plays a primary role initially, whereas epinephrine is not critical, although it becomes critical when glucagon is deficient. Growth hormone and cortisol play demonstrable roles in recovery from prolonged hypoglycemia. Glucose autoregulation may be involved in defense against severe hypoglycemia. With respect to pathophysiology, counterregulatory systems are involved in at least five clinical glucoregulatory syndromes. Defective glucose counterregulation is associated with, and best attributed to, combined deficiencies of the glucagon and epinephrine responses to plasma glucose decrements. Almost assuredly in concert with hypoglycemia unawareness, it results in a markedly increased frequency of severe hypoglycemia, at least during intensive therapy of IDDM. Defined as a night to morning increase in plasma glucose concentration, the dawn phenomenon is thought to result from dissipation of insulin plus the effects of nocturnal growth hormone secretion. Despite a sound rationale, the clinical relevance of the Somogyi phenomenon has been recently questioned. The clinical impression of altered glycemic thresholds for symptoms, i.e., patients with poorly controlled IDDM suffer symptoms of hypoglycemia at relatively high plasma glucose levels, whereas those with very well-controlled IDDM often tolerate subnormal glucose levels, has received experimental support. Clearly, hypoglycemia in IDDM is a problem that needs to be solved. Numerous issues need to be addressed through both basic and clinical research.(ABSTRACT TRUNCATED AT 250 WORDS)
Diabetes 1989 Sep
PMID:Hypoglycemia in IDDM. 276 40

To assess the effect of asymptomatic nocturnal hypoglycemia on glycemic control in insulin-dependent diabetes mellitus, we studied, on three nights, 10 patients receiving their usual regimens of continuous subcutaneous insulin infusion. During a control night, the patients' mean (+/- SE) plasma glucose level reached a nadir of 4.5 +/- 0.2 mmol per liter at 3 a.m.; the fasting glucose level was 5.9 +/- 0.3 mmol per liter at 7:30 a.m., and a peak glucose level of 8.6 +/- 0.3 mmol per liter was reached at 10 a.m., after breakfast. During nights two and three, supplemental insulin was infused intravenously from 10 p.m. to 2 a.m. to simulate a clinical overdose of insulin. On these nights, either hypoglycemia (2.4 +/- 0.2 mmol per liter) was permitted to occur or a nearly normal glucose level (5.5 mmol per liter) was maintained by infusion of glucose. The subjects were asymptomatic on all three nights. Despite comparable plasma free insulin levels from 4 to 11 a.m., both fasting (7.3 +/- 0.2 mmol per liter) and postbreakfast (12.5 +/- 0.4 mmol per liter) plasma glucose levels were significantly higher after hypoglycemia than when hypoglycemia was prevented (6.2 +/- 0.2 mmol per liter and 8.7 +/- 0.4 mmol per liter, respectively; P less than 0.001 in both cases). Fasting levels of plasma glucose correlated directly with overnight plasma levels of epinephrine (r = 0.78, P less than 0.001), growth hormone (r = 0.57, P less than 0.009), and cortisol (r = 0.52, P less than 0.02) but correlated inversely with the overnight nadir of plasma glucose (r = -0.62, P less than 0.005). We conclude that asymptomatic nocturnal hypoglycemia can cause clinically important deterioration in glycemic control (the Somogyi phenomenon) in patients receiving intensive insulin therapy, and should therefore be considered in the differential diagnosis of unexplained morning hyperglycemia.
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PMID:The effect of asymptomatic nocturnal hypoglycemia on glycemic control in diabetes mellitus. 305 44

Glucose counterregulation is the sum of processes that protect against development of hypoglycemia and that restore euglycemia if hypoglycemia should occur. In order of importance, the key counterregulatory factors are glucagon, epinephrine, growth hormone, cortisol, and hepatic autoregulation. These act primarily by increasing hepatic glucose output, initially via breakdown of glycogen and later by gluconeogenesis. In people without diabetes and in people with type II (non-insulin-dependent) diabetes, suppression of endogenous insulin secretion during hypoglycemia is also important in permitting full expression of the effects of counterregulation. People with diabetes are more prone to develop hypoglycemia for various reasons (e.g., insulin overdose, skipped meals, and intensive exercise); one that has recently been identified is impaired glucose counterregulation: patients with type I (insulin-dependent) diabetes (and to a lesser extent, patients with type II diabetes) lose the glucagon response to hypoglycemia; subsequent development of autonomic neuropathy with concomitant loss of the epinephrine response leads to almost complete paralysis of counterregulation and loss of recognition of hypoglycemia. To make matters worse, an episode of hypoglycemia that causes activation of counterregulation can lead to rebound hyperglycemia (Somogyi phenomenon); if this is improperly treated, brittle diabetes may follow. Thus, abnormalities in glucose counterregulation may predispose to severe hypoglycemia and prevent achievement of optimal glycemic control in patients with diabetes.
Diabetes 1988 Dec
PMID:Lilly lecture 1988. Glucose counterregulation and its impact on diabetes mellitus. 305 59

To estimate the frequency of an early-morning glucose rise (EMR) in relatively unselected children with insulin-dependent diabetes mellitus (IDDM), we assessed capillary blood glucose (CBG) at midsleep (0200-0430) and prebreakfast (0700-0800) in 97 children with diabetes at camp. The EMR (prebreakfast CBG-midsleep CGB) was inversely related to the midsleep CBG level (r = -.45, P less than .001). Of the 49 children with midsleep CBG less than 200 mg/dl, the mean EMR was 34 +/- 60 mg/dl, and 18 of these children had rises of greater than 40 mg/dl. In conclusion, when midsleep glycemia is less than 200 mg/dl, a rise in blood glucose from midsleep to prebreakfast, often greater than 40 mg/dl, is a common element of glycemic control among children with IDDM. The relative importance of the Somogyi phenomenon, the dawn phenomenon, and mere insulin insufficiency in the early-morning hours cannot be determined from these data.
Diabetes Care
PMID:Frequency of early-morning rise in blood glucose in children with diabetes at camp. 320 74


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