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)

A new syndrome in two siblings with primordial birdheaded nanism, progressive ataxia, goiter, primary gonadal insufficiency and insulin resistant diabetes mellitus is presented. Plasma concentrations of TSH, PTH, LH, FSH, ACTH, glucagon and insulin all working through cell membrane receptors were elevated. A generalized cell membrane defect was suggested to be the pathophysiological abnormality in these patients.
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PMID:Primordial birdheaded nanism associated with progressive ataxia, early onset insulin resistant diabetes, goiter and primary gonadal insufficiency. A new syndrome. 266 2

The examination of 28 children with diffuse toxic goiter showed disturbance of glucose tolerance with a significant decrease in the level of C-peptide in the blood serum and its response to glucose. The concentration of immunoreactive insulin (IRI) and its increment under the influence of a glucose tolerance test in children was much above the normal. At the same time the molar C-peptide/IRI ratio in the patients' sera both on an empty stomach and during the glucose tolerance test showed a dramatic decrease indicating the reduction of insulin extraction by the liver as a cause of peripheral hyperinsulinemia. Distortion of the plasma immunoreactive glucagon reaction to a glucose tolerance test was observed in children with diffuse toxic goiter.
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PMID:[Characteristics of the endocrine function of the pancreas in diffuse toxic goiter in children]. 354 91

The increase in plasma cyclic adenosine-3':5'-monophosphate (cAMP) was measured after intravenous injection of 1 mg of glucagon in 26 normal subjects, 36 patients with hyperthyroidism, 35 patients with hypothyroidism and 24 patients with euthyroid goitre. While patients with euthyroid goitre responded normally, the plasma cyclic AMP response in patients with hyperthyroidism was considerably increased and in those with hypothyroidism decreased. 4 patients with cirrhosis of the liver had reduced responses and 1 patient with extrahepatic obstructive jaundice an enhanced response. This test seems to be a valuable additional parameter for the description of the thyroid-dependent metabolic situation. However, because of its unspecificity it cannot replace the measurement of serum T3, T4 and thyrotropin (TSH) response to thyroliberin (TRH).
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PMID:[The effect of thyroid function on the increase of plasma cyclic AMP following glucagon injection (author's transl)]. 625 72

Significant amounts of immunoreactive glucagon (IRG) were determined in acid-ethanol and acid-saline extracts of human thyroid. Glucagon content of healthy thyroid, expressed as ng/g wet tissue or pg/mg protein, was significantly greater after an acid-alcohol extraction than after an acid-saline one. Furthermore IRG in acid-alcohol extracts of healthy tissue was greater than in acid alcohol extracts of diseased thyroid, while with an acid-saline procedure glucagon content was greater in the extracts of pathological tissues. No significant differences in the IRG content between calcified or follicular thyroid nodules and nodular goiter were found. Aliquots of the tissue extracts, fractionated on Bio-Gel P-30 or Sephadex G-100 columns, gave a 3,500 mol wt immunoreactive peak suggesting the existence of a polypeptide with the same size and immunological properties as pancreatic glucagon. Also, active glucagon synthesis by pieces of thyroid was established by the incorporation of L3-H-tryptophan into a 3,500 mol wt polypeptide with specific immune reaction to 30K antiserum. These results suggest that thyroid gland could represent a source of extrapancreatic glucagon in men, and therefore contribute to the circulating levels of this hormone.
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PMID:Presence of immunoreactive glucagon in healthy and diseased human thyroid. Evidence of glucagon synthesis by this gland. 648 80

The case of a 27 year-old woman with typical manifestations of multiple endocrine neoplasia type II b is reported. Medullary carcinoma of the thyroid was detected on the occasion of an operation for goiter when she was 22 years of age. Constipation due to megacolon caused by intestinal neuroma had persisted since childhood. Neuroma of the tongue and lips, hypertrophic corneal nerve and Marfanoid habitus were also found. The presence of pheochromocytoma was suggested in view of the positive cold pressor and results of glucagon loading tests, but this remains inconclusive. There was prolonged and exaggerated response of growth hormone and luteinizing hormone after provocative tests for anterior pituitary gland, in spite of normal basal levels. Screening of her family members for medullary carcinoma of the thyroid was carried out by measurement of immunoreactive calcitonin. Two siblings were shown to be hypercalcitoninemic, presumably due to occult medullary carcinoma of the thyroid. This case appeared to be the first in Japan showing multiple endocrine neoplasia type II b accompanied by familial hypercalcitoninemia.
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PMID:A case of multiple endocrine neoplasia type II b: endocrinological evaluation and family screening. 710 60

Accelerated metabolism is a hallmark of thyrotoxicosis, but the underlying biochemical mechanisms are incompletely understood. In order to elucidate these metabolic events further, we studied 12 patients with newly diagnosed diffuse (10 patients) or nodular (two patients) toxic goitre (ten women, two men; age 42.8 +/- 3.2 yr; BMI: 21.6 +/- 0.7 kg/m2) before ("TOX") and after ("TRE") 11.2 +/- 1.0 weeks treatment with methimazole and compared these patients to a control group ("CTR") of 11 subjects (nine women, two men; age 40.5 +/- 3.9 yr; BMI 22.5 +/- 1.0 kg/m2). All were studied for three hours in the basal state, using indirect calorimetry, isotope dilution for measurement of glucose turnover and the forearm technique for assessment of muscle metabolism. Prior to treatment patients with thyrotoxicosis were characterized by: Increased (p < 0.05) levels of T3 (3.75 +/- 0.23 [TOX], 1.89 +/- 0.08 [TRE] and 1.75 +/- 0.11 [CTR] nmol/l), resting energy expenditure (130.5 +/- 3.5 [TOX], 107.7 +/- 2.7 [TRE] and 106.3 +/- 3.1 [CTR] percent of predicted), protein oxidation (0.67 +/- 0.03 [TOX], 0.54 +/- 0.06 [TRE] and 0.46 +/- 0.05 [CTR] mg/kg/min), lipid oxidation (1.34 +/- 0.08 [TOX], 1.00 +/- 0.06 [TRE] and 1.02 +/- 0.04 [CTR] mg/kg/min), endogenous glucose production (2.51 +/- 0.13 [TOX], 1.86 +/- 0.12 [TRE] and 1.85 +/- 0.12 [CTR] mg/kg/min), non-oxidative glucose turnover (1.28 +/- 0.16 [TOX], 0.75 +/- 0.18 [TRE] and 0.71 +/- 0.11 [CTR] mg/kg/min) and a 50% increase in total forearm blood flow. Glucose oxidation (1.23 +/- 0.09 [TOX], 1.13 +/- 0.10 [TRE] and 1.13 +/- 0.09 [CTR] mg/kg/min), exchange of substrates in the muscles of the forearm and circulating levels of insulin, C-peptide, growth hormone or glucagon were not influenced by hyperthyroidism. Propranolol (20 mg thrice daily) given to seven of the patients for two days did not affect circulating levels of thyroid hormones, energy expenditure or glucose turnover rates. These results suggest that all major fuel sources contribute to the hypermetabolism of thyrotoxicosis and that augmented non-oxidative glucose metabolism may further aggravate the condition. All abnormalities recede with medical treatment of the disease.
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PMID:[Substrate metabolism in untreated and treated thyrotoxicosis]. 952 Jun 16

A 24-year-old female suffered from acute pancreatitis, followed by simultaneous onset of painless goiter, elevation of thyroid hormones and diabetic ketoacidosis. Two months later, her insulin secreting function was severely decreased and positive for anti-GAD and anti-islet cell antibodies, whereas the serum glucagon level was normal, suggesting an autoimmune-related destruction specifically of beta cells. In addition, the initial hyperthyroid state was followed by a hypothyroid phase which later recovered to an euthyroid state, suggesting an initial destruction of thyroid cells. Because anti-thyroidal antibodies were positive, it is likely that the thyroidal destruction was also autoimmune-related. This case implies common pathogenic mechanisms in the autoimmunity related destruction of beta cells and thyroid cells.
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PMID:Simultaneous onset of type 1 diabetes mellitus and painless thyroiditis following acute pancreatitis. 1144 77