Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0432222 (SEM)
 47,337 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Mononuclear leukocytes from 25 children (16 with normal pituitary ACTH production and 9 with ACTH deficiency) were examined for in vivo ACTH production by immunofluorescence with antiserum to ACTH-(1-13) amide. The protocol included 3 study periods: control, after administration of insulin, and after administration of typhoid vaccine (an interferon-alpha inducer). Plasma cortisol and mononuclear leukocyte ACTH immunofluorescence were measured before (0900 h) and 1, 2, 4, 6, 8, and 10 h after treatment on each of the 3 study days. In vitro studies with human leukocytes from normal subjects incubated with ACTH, insulin, or typhoid vaccine were also performed. Patients with normal pituitary ACTH production had an increase in the number of ACTH immunofluorescence-positive cells 1 h after insulin administration [25 +/- 5% (+/- SEM) to 44 +/- 6% P less than 0.05], and no change after typhoid administration. ACTH-deficient patients had no change after insulin administration and a significant rise 6 h after typhoid vaccine treatment (24 +/- 12% to 50 +/- 6%; P less than 0.05). The number of ACTH immunofluorescence-positive cells did not increase when mononuclear leukocytes were incubated in vitro with ACTH or insulin (with or without glucose deprivation). However, typhoid antigen enhanced this response from 8% to 55%. These data suggest that the number of human mononuclear leukocytes containing immunoreactive ACTH is increased by at least 2 stimuli: 1) a central factor(s), such as CRH, accounting for the in vivo rise 1 h after insulin administration in patients with an intact hypothalamic-pituitary axis, and 2) an interferon inducer (e.g. typhoid antigen), accounting for the typhoid antigen-induced rise in the number of ACTH-positive cells in vivo in ACTH-deficient patients and in vitro.
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PMID:In vivo immunoreactive adrenocorticotropin (ACTH) production by human mononuclear leukocytes from normal and ACTH-deficient individuals. 243 Sep 92

We have measured plasma 7B2 (a novel pituitary protein)-immunoreactivity (IR) concentrations in patients with various endocrine disorders. Mean (+/- SEM) basal plasma 7B2-IR concentrations (ng/L) in patients with acromegaly (81 +/- 14.6), Cushing's disease (57.2 +/- 8.5), prolactinoma (71.4 +/- 9.5), panhypopituitarism (50.6 +/- 7.6), isolated ACTH deficiency (47.9 +/- 11.6), hyperthyroidism (57.9 +/- 6.7) and hypothyroidism (60.8 +/- 9.4) were on the same levels as those in age-matched normal subjects. However, basal plasma 7B2-IR concentrations were increased to more than 100 ng/L in 5 out of 25 patients with acromegaly (20%). Mean basal plasma 7B2-IR concentrations in patients with medullary carcinoma of the thyroid and pheochromocytoma were 293 +/- 38.1 ng/L (range: 225.7-357.4 ng/L, n = 3) and 221 +/- 82.8 ng/L (range: 48.5-527.8 ng/L, n = 5), respectively, and significantly higher than those in age-matched normal subjects (P less than 0.001). These results suggest that plasma 7B2-IR may have some diagnostic value for acromegaly and may be useful as a marker for medullary carcinoma of the thyroid and pheochromocytoma.
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PMID:Plasma 7B2 (a novel pituitary protein) immunoreactivity concentrations in patients with various endocrine disorders. 285 Sep 8

Glucose metabolism during fasting was investigated in 10 children aged 1.5 month-11.5 yr with deficiency of GH with or without other pituitary hormone deficiencies. After 10-16 h of fasting, mean plasma glucose was 56 +/- 4 (SEM) mg/dl, the result of decreased hepatic production of glucose (3.3 +/- 0.3 mg kg-1 min-1) insufficient to match glucose utilization (3.6 +/- 0.4 mg kg-1 min-1). The diminution of plasma glucose and of glucose production was similar whether ACTH deficiency was present (3.2 +/- mg kg-1 min-1) or not (3.5 +/- 0.6 mg kg-1 min-1). These results indicate that the lack of GH was the primary cause of hypoglycemia. Fasting plasma alanine (212 +/- 41 mumol/liter) and lactate (1222 +/- 136 mumol/liter), the main gluconeogenic substrates, were normal and did not correlate with the decrease of hepatic glucose release. Both plasma FFA (552 +/- 35 microM) and beta-hydroxybutyrate (654 +/- 158 microM) were in the low normal range, and neither correlated with the rate of glucose utilization. hGH replacement therapy resulted in a normalization of fasting plasma glucose concentration (78.5 +/- 6 mg/dl, P less than 0.005) and hepatic glucose production (6.1 +/- 1.2 mg kg-1 min-1). No significant changes occurred in the plasma concentrations of gluconeogenic or lipid substrates. These results, together with the known stimulatory effects of GH on carbohydrate-induced insulin secretion and storage of hepatic glycogen, suggest that the changes in glucose production in untreated and GH treated patients reflect the degree of hepatic glycogen replenishment.
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PMID:Effects of hypopituitarism and growth hormone replacement therapy on the production and utilization of glucose in childhood. 390 70