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)

Secretory protein-I (SP-I) of parathyroid glands and chromogranin A ( CGA ) of adrenal medullary chromaffin cells are chemically similar if not identical proteins. Both proteins are contained within secretory granules and appear to be cosecreted with granule contents, for example, in the parathyroid with PTH and in the adrenal with epinephrine and dopamine beta-hydroxylase. Antisera to bovine SP-I and porcine CGA , together with antisera to a variety of peptide hormones, were used in an immunofluorescence study of rat tissues in order to determine the probable distribution and cellular localization of these proteins. In addition to their previously demonstrated presence in parathyroid and adrenal cells, the SP-I/ CGA protein family was detected in cells of the thyroid that contained calcitonin and often SRIF but not thyroglobulin; in cells of the anterior pituitary staining for the alpha-subunit of TSH/FSH/LH but not in cells staining for GH, PRL, ACTH, or beta-endorphin; in pancreatic islet cells staining for SRIF and pancreatic polypeptide-related peptides, but not for insulin or glucagon; in the celiac and mesenteric ganglia in cells some of which contained SRIF; and in the gastric antrum in cells containing SRIF, but not gastrin. SP-I/ CGA was not detected in cells of the liver, kidney, parotid gland, or acinar pancreas or in the intermediate or posterior lobes of the pituitary. These results suggest that this protein family enjoys a widespread but highly restricted distribution in many different endocrine-peptide cells of the rat, many that are believed to be of the APUD cell series. The possibility is raised that SP-I/ CGA plays some physiological role in the secretory process or exerts an effect of its own in the periphery after secretion.
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PMID:Selective localization of the parathyroid secretory protein-I/adrenal medulla chromogranin A protein family in a wide variety of endocrine cells of the rat. 623 31

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

The endocrine profile of FK 33-824, 0.5 mg i.m., was determined in comparison with placebo or pretreatment with naloxone, 4 mg i.v., in 14 healthy men. Prolactin (PRL), growth hormone (GH), ACTH, cortisol, gonadotropins (LH, FSH), thyrotropin (TSH), thyroxine (T4), triiodothyronine (T3), insulin and glucagon were measured and free water clearance was calculated from urine volumes and osmolar clearances. FK 33-824 increased PRL and GH (p less than 0.001). ACTH was below assay sensitivity but cortisol was significantly lowered (p less than 0.001). Free water clearance was enhanced (p less than 0.01) and the remaining parameters were unchanged. Naloxone alone had no hormonal effect but abolished the increase in PRL and GH following injection of FK 33-824 without modifying the decrease in plasma cortisol or the increase in free water clearance following the same treatment. The results indicate that the effect of FK 33-824 on PRL and GH release is mediated by opiate receptors. Other mechanisms or naloxone nonsensitive receptors may be implicated in the effects recorded on cortisol and FWC.
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PMID:Endocrine effect of a methionine-enkephalin derivative (FK 33-824) in man. 626 6

We have evaluated the responsiveness of hypocalcemic magnesium-deficient patients to ACTH, TRH, gonadotropin-releasing hormone, and glucagon as determined by the rise in serum cortisol, TSH, LH, and plasma cAMP concentrations, respectively. It was previously been shown that the hypocalcemia of magnesium deficiency is secondary to impaired secretion of parathyroid hormone (PTH) along with renal and skeletal resistance to the action of PTH. Since PTH secretion and action are though to be effected through the intermediary action of cAMP, and magnesium is a required cofactor for adenylate cyclase, defective generation of cAMP could account for the observed defects in PTH secretion and action. Other hormonal systems requiring the intermediary action of cAMP may be similarly affected by magnesium deficiency. The results of the present study, however, demonstrate normal responsiveness of the adrenal cortex, thyrotrophs, gonadotrophs, and liver to their respective trophic hormones in hypocalcemic magnesium-deficient patients. The reason why these responses are intact while PTH secretion and action are impaired is unknown but may be accounted for by differing magnesium requirements of the adenylate cyclase complex in these tissues.
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PMID:End-organ response to adrenocorticotropin, thyrotropin, gonadotropin-releasing hormone, and glucagon in hypocalcemic magnesium deficient patients. 627 86

Experiments were performed to determine whether the TSH receptor-adenylate cyclase (AC) system in benign and malignant thyroid neoplasms differs from the TSH receptor-AC system in normal thyroid tissue removed from the same patients. TSH binding and AC assays were performed using the same in vitro conditions. TSH binding was rapid, reversible, saturable, and hormone specific in particulate fractions from both normal and neoplastic thyroid tissue. A positive correlation existed between the equilibrium constants for [125I]bovine ([125I]bTSH) TSH binding and the concentration of TSH required to activate AC, suggesting that binding sites were coupled to AC in neoplastic thyroid tissue. Mean values for dissociation constants (Kd1 and Kd2), capacity (site 2), as determined by Scatchard analysis, and nonspecific binding (NSB) for the TSH receptors were lower in neoplastic thyroid. Some normal thyroid tissue appeared to lack a high affinity site, and some tumors lacked a low affinity binding site. Hormone specificities (bTSH, human (h) TSH, hLH, hFSH, hGH, hACTH, and glucagon) in normal thyroid and neoplastic tissue were virtually identical. hFSH, hACTH, hGH, and glucagon failed to inhibit [125I]bTSH binding or stimulate AC in either normal or neoplastic thyroid tissue, whereas hLH inhibited [125I]bTSH binding and stimulated AC, but required 10- to 100-fold higher concentrations than hTSH or bTSH. The specific binding and NSB of [125I]bTSH in both normal and neoplastic thyroid tissue was highest at pH 7.0 and lowest at pH 8.3. In contrast to bTSH binding, TSH stimulation of AC was lowest at pH 7.0 in both normal and neoplastic tissues and highest at pH levels of 7.5-8.0. TSH binding and TSH stimulation of AC activity were highest in the absence of NaCl and decreased progressively as the salt concentration was increased in both normal and neoplastic thyroid tissues. Increasing the sucrose concentration and, thus, the osmolarity of the system had a minimal effect on the binding of [125I]bTSH. Preincubation with ammonium sulfate did not significantly influence binding. Basal AC activity and the AC response to TSH were greater in neoplastic thyroid than in normal tissues. These studies demonstrate that changes in salt concentration and pH affect the TSH receptor-cyclase system in a comparable fashion in normal and neoplastic thyroid tissues. The discriminatory properties of the TSH receptor are also maintained in thyroid neoplasms. Thyroid tumors, however, have a higher affinity for TSH and display a greater AC response to TSH than normal thyroid tissue.
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PMID:Characterization of the thyrotropin receptor-adenylate cyclase system in neoplastic human thyroid tissue. 630 32

Oral glucose tolerance, plasma insulin and basal levels of glucagon, hGH, hPRL, hPL, TSH, T4, T3, thyroxine-binding globulin (TBG), cortisol, corticosteroid-binding globulin (CBG) and estriol were measured in 23 normal pregnant women in late gestation (31 +/- 0.4 weeks of pregnancy). Twelve of these subjects could be re-examined 14 +/- 2 weeks postpartum. Blood glucose was lower basal and after glucose load (100 g) in the pregnant group. Fasting plasma insulin and glucose-induced insulin release were higher in pregnancy. The insulinogenic index and the beta cell response were significantly greater antepartum, while peripheral insulin activity was unchanged. The insulin:glucagon ratio as well as TSH and hGH showed no significant differences between ante- and postpartum values. However, T4, T3, TBG, cortisol, CBG, estriol, hPRL and hPL were significantly higher during gestation than after delivery. T4:TBG and T3:TBG ratios were much lower antepartum, while the cortisol:CBG ratio was comparable ante- and postpartum. To our knowledge this is the first report in which such an extensive hormonal and metabolic analysis was performed in the same women ante- and postpartum. It could be shown that glucose tolerance is not worsened during pregnancy in healthy subjects. The higher gestational insulin values are discussed with respect to the various significant hormonal changes.
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PMID:Hormonal profile and glucose tolerance in late pregnancy and postpartum. 635 85

Since no data are available concerning thyroid hormone levels in Snell dwarf mice from birth on, a cross-sectional study was performed of L-thyroxine (T4) and L-triiodothyronine (T3) levels in blood or serum as a function of age of several litters, starting at birth. In normal Snell mice T4 levels in blood and serum are changing with age. T4 increases during the first 2 weeks of age and declines thereafter, until adult levels of about 50 nmol/l are reached at 21 days of age. Serum T3 values are in the range of 2-3 nmol/l. They do not show such an age-related pattern. From birth on in each litter there was a clear separation between animals with low T4 levels in blood and the others. This separation was possible at all subsequent days until 9 days of age, when dwarfs can be recognized by eye. Above that age the low T4 values were associated with dwarfism. This suggests that dwarfs are hypothyroid already at birth. Serum T3 in dwarfs falls below the normal range only after 4 weeks of age, resulting in a lower T4/T3 ratio than normal. The half life time of exogenous T4 in serum of dwarfs is in the range of 13-18 h and not different from normal. For T3 t1/2 is 9.5-11.1 h. Dwarf mice become euthyroid by treatment with 0.1 microgram T4 per day. 1 microgram T4 was needed to reach a physiological level of T3. These data suggest that the peripheral conversion of T4 to T3 is slower in dwarfs than in normals. Treatment with hGH, prolactin, glucagon, insulin, testosterone and oestradiol had no influence on serum T4. As expected TSH was stimulatory. Similar results were obtained for serum T3, with the exception of prolactin which caused slightly increased levels of serum T3.
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PMID:Thyroxine and triiodothyronine levels in Snell mice. 640 74

The influence of iv administration of 0.2 mg thyrotropin-releasing hormone (TRH) on serum calcium was examined in 20 subjects divided into three different groups: one, comprising patients with primary hypothyroidism (A), another, containing euthyroid patients with various diseases (B), and a third, including healthy volunteers (C). Ninety min after the TRH injection total serum calcium (T-Ca) had fallen by 0.19 +/- 0.03 mmol/l in group A (p less than 0.01), by 0.10 +/- 0.02 mmol/l in group B (p less than 0.01), and by 0.08 +/- 0.02 mmol/l in group C (p less than 0.02). Ionized serum calcium (I-Ca) fell in parallel with T-Ca in group A and B. In contrast, serum magnesium was unaffected in all groups. Neither the renal excretion of calcium nor the serum concentration of parathyroid hormone, glucagon or calcitonin changed significantly in response to TRH. These results indicate that TRH has a slight hypocalcemic effect in man which is not caused by plasma dilution, direct influence on the kidneys, or TRH effects on the major calcium regulating hormones. Whether TRH per se, or an increased serum TSH level, induces calcium to leave the vascular space remains to be elucidated.
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PMID:Serum calcium decline after intravenous administration of thyrotropin-releasing hormone in man. 640 74

Synthetic human pancreatic GRF (hpGRF-44) was administered as an iv bolus to 28 normal children with short stature and 27 patients with GH deficiency. After a dose of 1 or 2 micrograms hpGRF-44/kg BW, mean plasma GH levels peaked at 15 and 30 min, respectively, with corresponding values of 30.1 +/- 4.7 and 33.2 +/- 3.7 ( +/- SE) ng/ml in normal but short children. The overall plasma GH response was greater than that of other GH stimulation tests such as insulin-induced hypoglycemia, glucagon-propranolol or L-dopa administration. Plasma LH, FSH, TSH, PRL, and cortisol levels were not altered by hpGRF-44 injection. Sixteen of 27 patients with GH deficiency did not respond to a 2 micrograms/kg BW hpGRF-44. However, plasma GH increases to greater than 5 ng/ml occurred in the remaining 11 patients. Their GH levels reached peaks between 15 and 90 min, with values ranging between 5.8 and 17.8 ng/ml. Two of these responding patients were infused iv with hpGRF-44 at 2.5 micrograms/min for 90 min after receiving an iv bolus injection of 2 micrograms/kg BW. Their plasma GH levels increased and remained near peak values throughout the infusion period. However, no increase in plasma GH levels occurred after a second bolus injection of hpGRF-44 given at the end of the infusion. These results suggest that hpGRF-44 is useful for the diagnosis of GH deficiency in individuals with short stature and that some patients with GH deficiency, diagnosed on the basis of established tests, have GH responses to hpGRF-44.
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PMID:Plasma growth hormone (GH) response to GH-releasing factor in normal children with short stature and patients with pituitary dwarfism. 642 Apr 32

Forty-one endocrine and biochemical serum parameters were studied over a 24-hour span with 6 samples at 4-hour intervals in 20 non-insulin dependent (Type II) diabetics and in 20 non-diabetic subjects matched for sex, age, height and weight. Circadian rhythms were verified by cosinor analysis. Group-synchronized circadian rhythms were detected in diabetic and non-diabetic subjects with no statistically significant difference in any of the rhythm parameters (rhythm adjusted mean, amplitude and acrophase) in: Aldosterone, cortisol, insulin, 17-OH progesterone, prolactin, testosterone, TSH, and in serum albumin, creatine phosphokinase (CPK), serum iron, inorganic phosphate and total protein. Statistically significant (p less than .05) circadian rhythms in both groups with a difference in some parameters between the diabetic and the non-diabetic subjects, which were verified by the Bingham Test (p less than .05) were found with a difference in the mesor in cholesterol, glucose, urea nitrogen (BUN), in the amplitude in C-peptide and in the acrophase in triglycerides, globulin and reverse T3 (rT3). Statistically significant circadian rhythms were detected as a group phenomenon for the diabetics only in progesterone, free and total T4, chloride, calcium, bilirubin and LDH and in the non-diabetic subjects only in ACTH, LH, total T3, alkaline phosphatase, uric acid and potassium. In the remainder of the functions studied, a circadian rhythm was detectable with statistical significance by cosinor analysis as a group phenomenon neither in the diabetics nor in the matched non-diabetic controls (DHEA-S, estradiol, FSH, GH, glucagon, free T3, sodium, GOT and gamma GT). In the absence of a detectable circadian rhythm as group phenomenon, the circadian mean was different between the diabetics and the non-diabetic subjects in sodium, chloride and calcium which were higher in the diabetic patients and serum LDH which was lower. In a comparison of endocrine determinations in the two groups, the circadian mean or mesor in T3 was lower in the diabetics and ACTH higher, without corresponding changes in TSH or in corticosteroids. The circadian time structure of Type II diabetic patients thus seems to be very similar to that seen in non-diabetic subjects of the same sex, age, weight and height. The minor differences found in some rhythm parameters will have to be confirmed or excluded in larger numbers of subjects. The higher circadian mean ACTH concentrations without change in steroid rhythm parameters observed in this group is interesting but will also require confirmation.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Circadian time structure of endocrine and biochemical parameters in adult onset (type II) diabetic patients. 652 19


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