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)

Euthyroid sick syndrome is characterized by low serum T3 and raised reverse T3 (rT3). Most of the states with this syndrome are also documented to manifest hyperglucagonemia. Furthermore, several recent studies have suggested that glucagon may play a role in T4 monodeiodination in some of these states such as starvation and uncontrolled diabetes mellitus. Therefore, hyperglucagonemia was induced by intravenous glucagon administration in euthyroid healthy volunteers and thyroid hormone levels were determined at frequent intervals up to six hours. Plasma glucose and insulin rose promptly on glucagon administration, thus establishing the physiologic effect of glucagon. Serum T4, free T4, T3 resin uptake, and TSH concentrations remained unaltered throughout the study period. Serum T3 declined to a significantly low level (P less than 0.05) between 60-90 minutes. Serum rT3 rose significantly (P less than 0.05) by four hours and the rise was progressive till the end of the study period. Therefore, these results suggest that hyperglucagonemia may be one of the factors responsible for lowering of T3 and a rise in rT3 in euthyroid sick syndrome.
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PMID:Glucagon administration induces lowering of serum T3 and rise in reverse T3 in euthyroid healthy subjects. 391 May 31

The initiation of DNA synthesis has been studied in quiescent primary cultures of fetal rat hepatocytes using defined hormones and chemically defined medium. Preparations of crystalline insulin (0.01-10 microg/ml) or 20,000-fold purified somatomedin (0.01-1 microg/ml) are stimulatory. Growth hormone (0.025 microg/ml) and hydroxycortisone (0.025 microg/ml), 3':5'-GMP! (10(-5) M) fail by themselves to initiate DNA synthesis but added together with insulin, enhance the stimulatory response by 50-100%. Thyroid hormones (L-T(3), L-T(4), 7.5-30 ng/ml) are by themselves without effect, but when they are added to thyroid hormone-depleted serum, the reconstituted mixtures show an enhanced capacity to initiate DNA synthesis. In contrast, glucagon (0.01 microg/ml) inhibits the insulin-stimulated response by about 50% without reducing basal DNA synthesis rates. The results described here and in the accompanying two reports indicate that environmental control over the initiation of DNA synthesis is complex, and can involve the participation of many factors. The in vitro findings are consistent with the concept that liver regeneration is hormonally controlled and raise the possibility that alterations of the intrahepatic ratio of insulin to glucagon are growth regulatory.
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PMID:Growth control of differentiated fetal rat hepatocytes in primary monolayer culture. VII. Hormonal control of DNA synthesis and its possible significance to the problem of liver regeneration. 485 45

The endocrine changes associated with fetal growth retardation caused by unilateral uterine artery ligation of guinea pigs at day 30 of pregnancy were studied. Plasma hormone levels in fetuses that, about 20 or 30 days later, were 35-50% of normal size were measured by radioimmunoassay. The small fetuses were severely hypoglycaemic and hypoinsulinaemic; both showing close correlation and relationship to the degree of growth retardation. Plasma thyroid and cortisol and concentrations were much lower than normal and that glucagon and androstenedione were much higher. Plasma growth hormone level appeared to be unaffected by growth retardation. The developmental changes in glucagon and thyroid hormone concentrations were consistent with a delay in the timing of prenatal events in growth-retarded fetuses. However the late cortisol rise, although somewhat blunted, still occurred at 58-60 in the small fetal guinea pigs.
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PMID:Studies on the growth of the fetal guinea pig. Changes in plasma hormone concentration during normal and abnormal growth. 609 2

After mentioning insulin deficiency diabetes in animals produced by drugs such as Alloxan, Diazoxide or Streptozotocin only drugs are discussed, which are used in elderly patients and may either provoke diabetes mellitus (or temporary hyperglycemia) or may change the clinical course of diabetes. In the first group endocrine products such as corticosteroids, estrogens, somatotrophic hormone, thyroid hormone, glucagon, somatostatin, catecholamines and hormones with anabolic effects are listed. The second group comprises saluretics, salicylates, amphetamines, pentamidine, nicotinic acid and its derivatives, beta-receptor blockers and finally laxatives. Hypopotassemia alone can also be the cause of hyperglycemia. Speaking of the sulfonylureapreparations, their interaction with alcohol, with phenylbutazone, with some sulfonamides and the effect of the sulfonylureas on peripheric insulin-receptors is discussed. In case of severe diabetic vascular disease the use of anticoagulants may lead to hemorrhages. If such an hemorrhage occurs in the eyes, it may lead to blindness. In diabetic nephropathy the use of phenacetine and its derivatives should be substituted by another medication. This review is not at all complete but should only show some of the problems in the treatment of elderly diabetic patients.
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PMID:[Iatrogenic diabetes mellitus (side effects and interactions of drugs during clinical diabetes mellitus (author's transl)]. 612 38

Relative synthesis of malic enzyme is stimulated 25-to 100-fold by feeding neonatal ducklings or by incubating embryonic chick hepatocytes in culture with triiodothyronine. Synthesis of the enzyme is almost completely blocked when fed birds are starved or when triiodothyronine-treated hepatocytes in culture are also treated with glucagon. Cytoplasmic poly(A)+ RNA was isolated from livers of intact ducklings or hepatocytes in culture treated as described above and translated in an mRNA-dependent rabbit reticulocyte lysate. The identity of malic enzyme synthesized in the cell-free system was confirmed by virtue of its antigenicity, subunit molecular weight, and proteolytic peptide pattern. Translatable levels of malic enzyme mRNA paralleled changes in relative synthesis of malic enzyme in vivo and in hepatocytes in culture. Translatable levels od albumin mRNA were either unaffected or changed in a direction opposite to that of malic enzyme mRNA. Thus, both nutritional and hormonal regulation of malic enzyme synthesis involves regulation of cytoplasmic translatable malic enzyme mRNA levels. The hepatocyte culture system is ideally suited for future studies on the regulation of malic enzyme mRNA synthesis and/or degradation by thyroid hormone and glucagon.
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PMID:Nutritional and hormonal regulation of the translatable levels of malic enzyme and albumin mRNAs in avian liver cells in vivo and in culture. 616 81

The plasma adenosine 3', 5' - cyclic monophosphate (cyclic AMP) response to 50 micrograms of intravenous glucagon was examined in 14 normal euthyroid subjects, 15 patients with thyrotoxicosis and 5 patients with myxedema. The cyclic AMP responses to 50 micrograms of intravenous glucagon was significantly higher in the hyperthyroid group than in the euthyroid or hypothyroid group. However, the areas of overlap between all three groups were large and there was little relationship between the plasma cyclic AMP response to glucagon and the biochemical assessment of thyroid function. Serial studies of the response to 50 micrograms glucagon were carried out in four patients receiving treatment for thyrotoxicosis. Again, there was not consistent relationship between the plasma cyclic AMP responsiveness to glucagon and the free thyroxine index. It is concluded that although the plasma cyclic AMP response to glucagon is increased in thyrotoxicosis and decreased in myxedema, the variability of this response in thyroid disease precludes its use as a tissue index of thyroid hormone responsiveness.
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PMID:Investigation of the usefulness of the plasma adenosine 3' 5' - cyclic monophosphate response to glucagon in thyroid disease. 625 51

In vitro studies of nuclear binding of triiodothyronine (T3) in lymphocytes were performed in three members of a family with hereditary peripheral resistance to thyroid hormone action. Ficoll-Hypaque purified lymphocytes were used; the binding characteristics were analyzed by Scatchard's methods. In 5 euthyroid subjects the apparent mean equilibrium association constant (Ka) was 6.2 x 10(9) l/mol and the mean maximal binding capacity (Cap) 14.4 x 10(-15) mol/100 microgram DNA. In the 3 members of the family one single set os saturable T3 nuclear binding sites with affinity constants similar to those in the controls (mean Ka = 3.2 x 10(9) l/mol; mean Cap = 17.4 x 10(-15) mol/100 microgram DNA) were found. The glucagon stimulated increase in plasma cyclic AMP was studied in 6 healthy subjects and the four members of the family. The plasma cyclic AMP levels of the patients with hormone resistance were generally within the normal range. These observations demonstrate that in these patients with peripheral resistance to thyroid hormone binding of T3 to the receptor in the nucleus of lymphocytes is normal; in relation to the high circulating thyroid hormone levels, the thyroid hormone mediated cyclic AMP response is disturbed, suggesting that the defect is at the post-receptor effector level.
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PMID:Triiodothyronine binding to lymphocyte nuclei and plasma cyclic AMP response to intravenous glucagon in patients with peripheral resistance to thyroid hormones. 626 8

The effect of different thyroid states on the oxidation of free fatty acids was investigated in the isolated perfused liver of 24-h-starved rats. 1. Compared with the euthyroid control the oxidation of oleate to ketone bodies as well as to CO2 was increased in hyper-, while it was unchanged in hypothyroid livers. 2. The addition of carnitine stimulated oleate oxidation in livers from eu- and hyperthyroid rats, but was without effect in hypothyroid livers. 3. Glucose did not affect the thyroid hormone-mediated effect of oleate conversion to ketone bodies. 4. Hepatic oxidation of octanoate was similar in all thyroid states. 5. Re-esterification of oleate was enhanced in hypo-, but reduced in hyperthyroidism. 6. The concentration of hepatic malonyl-CoA was decreased in hypo- and unchanged in hyperthyroid livers. 7. The concentration of cyclic AMP was elevated in the liver of hyperthyroid rats, no differences were observed between eu- and hypothyroid livers. However, increasing the hepatic cyclic AMP content by the addition of glucagon did not stimulate ketogenesis in eu- and hypothyroid livers. 8. The results indicate that thyroid hormones stimulate oleate oxidation by an accelerated transport of its CoA derivative into the mitochondrial compartment.
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PMID:Effect of thyroid state on ketogenic capacity of the isolated perfused liver of starved rats. 627 88

Investigation was conducted under in vivo conditions in the adult male rat to determine the basic characteristics of the nuclear thyroid hormone receptors in the cerebral cortex. Equilibrium with cortical nuclei of an intravenous dose of triiodothyronine (T3) occurred 3 h after injection and showed a t1/2 of 1 h for dissociation. Saturation of receptors occurred at 0.5--06. ng/mg DNA. The endogenous level of binding in the normal rat was 0.07--0.1 ng/mg DNA, representing a 15% occupancy of total receptors at a serum concentration of 66 ng/dl. These characteristics were then examined under several pathophysiological conditions. In the hypothyroid rat, an apparent 37% increase in total binding sites occurred. Under either fasting conditions or insulin or glucagon administration declines in serum T3 were noted, and the endogenous binding also decreased in parallel. Only glucagon produced a significant reduction in total binding sites. Under the hypoxic condition produced by maintenance under a 7% oxygen atmosphere, a slight increase in apparent total binding sites was found with no change in endogenous binding level. Severe narcosis resulted in no effects on T3 binding parameters. These results demonstrate specific alterations of thyroid hormone receptors that may be important physiologically.
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PMID:Alterations of nuclear thyroid hormone receptors in cerebral cortex in vivo. 627 8

The effect of different thyroid states on glucose homeostasis was investigated during metabolic adaptation to starvation in the conscious unrestrained miniature pig. Moderate hyperthyroidism increased the rate of glucose turnover, whereas hypothyroidism was without effect. Glucose recycling was elevated in hyperthyroid pigs, and reduced after thyroidectomy. Supplementary doses of T4 normalized total glucose recycling. Glucose metabolic clearance rate and pool size were unaffected by thyroid hormones. During starvation serum insulin showed a similar decrease in all thyroid states; glucagon increased in euthyroid and hypothyroid pigs, although it was already elevated in the hyperthyroid fed state. Serum cortisol levels although varying were enhanced in hyperthyroid and hypothyroid-T4-treated pigs. Glucogenic precursor concentration and cumulative urinary N-excretion were increased in hyperthyroid pigs. It is concluded that 1) even a moderate hyperthyroidism produces an increase in glucose turnover and a concomitant acceleration in protein breakdown, and 2) thyroid hormone is essential for the starvation-induced total glucose recycling.
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PMID:Thyroid hormone regulation of glucose homeostasis in the miniature pig. 634 57


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