Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P01275 (glucagon)
 26,492 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

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

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.
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PMID:Failure of nocturnal hypoglycemia to cause daytime hyperglycemia in patients with IDDM. 219 Jul 69

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)
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PMID:Hypoglycemia in IDDM. 276 40

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.
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PMID:Lilly lecture 1988. Glucose counterregulation and its impact on diabetes mellitus. 305 59

Insulin-treated diabetic patients may show a rapid swing to hyperglycaemia after episodes of hypoglycaemia. This rebound hyperglycaemia, or Somogyi effect, is thought to be caused by the unopposed actions of hormonal antagonists to insulin secreted in response to hypoglycaemia. To test this theory a study was made of 15 patients who had 17 episodes of asymptomatic untreated hypoglycaemia (blood-glucose less than 2 mmol/l) between 11 P.M. and 3 A.M. After nocturnal hypoglycaemia, mean fasting blood-glucose concentrations at 7 A.M. ranged from 0.7-17 mmol/l and were over 7 mmol/l in 6 patients. These 6 patients with apparent rebound hyperglycaemia did not have higher levels of growth hormone, cortisol, or glucagon than those who had little or no recovery of blood-glucose. There was a close inverse correlation (r = -0.996, p < 0.001) between blood-glucose and free insulin, suggesting that hyperglycaemia, when present, was due to relative insulin deficiency in the latter part of the night. Early changes in blood-glucose after untreated hypoglycaemia seem to be primarily due to changes in free insulin rather than a response to antagonist hormones.
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PMID:In search of the Somogyi effect. 610 38