Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:3.1.1.8 (cholinesterase)
 12,691 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effects of growth hormone-releasing factor (GHRF) injections to sows during late gestation were investigated in two experiments. In the first one, four treatments were applied to eight catheterized sows according to two 4 x 4 Latin squares: oral administration of 2 mg of pyridostigmine, a cholinesterase inhibitor, per kilogram of BW (PYR group); i.m. injection of 50 micrograms of GHRF/kg BW (GHRF group); a combination of the pyridostigmine and GHRF treatments (PYR+GHRF); or i.m. injection of glucose (control). Pyridostigmine slightly increased the plasma concentration of growth hormone (GH). Growth hormone responses to GHRF and PYR+GHRF treatments were similar, with significantly elevated GH concentrations from 5 to 240 min after GHRF injection. In the second experiment, 36 sows were allocated to two treatments at 102 d of gestation. Until farrowing, they were injected twice daily with 50 micrograms of GHRF/kg BW (GHRF group) or isotonic glucose (control). The DM, N, fat, and energy content of 24 pigs per group was determined at weaning at 22 d. Six pigs per litter had ad libitum access to feed until slaughter at 100 kg BW and their carcasses were evaluated. Treatment with GHRF increased pregnancy duration (114.8 vs 113.6 d, P less than .05), weight of pigs at 13 d (3.69 vs 3.54 kg, P less than .05) and at weaning (5.74 vs 5.48 kg, P less than .05), and improved pig survival (86 vs 71%, P less than .05). Lipid (on a DM basis) and energy contents of the pigs slaughtered at weaning were significantly higher in the GHRF group than in the control group (14.4 vs 12.5% and 2,178 vs 2,029 kcal/kg, respectively).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effects of administration of growth hormone-releasing factor to sows during late gestation on growth hormone secretion, reproductive traits, and performance of progeny from birth to 100 kilograms live weight. 164 96

Neuropathologic data from patients with Alzheimer's disease indicate the presence of neurofibrillary tangles in hypothalamic regions associated with regulation of pituitary hormone release. The authors explored the hypothesis that cholinergic projections to hypothalamic nuclei controlling pituitary growth hormone (GH) release degenerate in Alzheimer's disease. Integrity of cholinergic regulation was tested by assaying the GH response to a presynaptic cholinergic challenge. After administration of the choline esterase inhibitor edrophonium, the peak GH response was 14 ng/ml in healthy elderly control subjects and only 2 ng/ml in Alzheimer's patients. The magnitude of GH blunting was correlated with cognitive and functional deficits. Possible implications of these data for enhanced accuracy in the diagnosis of dementia are discussed.
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PMID:Growth hormone response to edrophonium in Alzheimer's disease. 311 Dec 78

Acylated (octanoylated) ghrelin stimulates food intake and growth hormone secretion and is deacylated into desacyl ghrelin by butyrylcholinesterase. Acylated and desacyl ghrelin both promote adipogenesis. Ghrelin concentrations decrease with hyperglycemia and hyperinsulinism. We hypothesized that 1) acylated ghrelin increases during pregnancy, contributing positively to energy balance, but is lower in women with gestational diabetes and 2) butyrylcholinesterase activity is inversely correlated with acylated ghrelin concentrations. In a first group of subjects, using two-site sandwich ghrelin assays that specifically detect full-length forms, we investigated women with and without gestational diabetes (n = 14/group) during pregnancy and after delivery. We examined whether changes in ghrelin during a test meal were correlated with changes in pituitary growth hormone [assessed through calculation of the area under the curve (AUC) during the test meal]. In postpartum subjects, the percent of total ghrelin that is acylated was four to five times higher than previously observed using single antibody assays. During pregnancy, acylated ghrelin concentrations (mean +/- SE) were lower compared with the postpartum period throughout the meal (AUC 1.2 +/- 0.2 vs. 10.2 +/- 1.9 ng.ml(-1).90 min(-1), P < 0.001). In the postpartum, acylated ghrelin and growth hormone were positively correlated (r = 0.50, P = 0.007). Desacyl (but not acylated) ghrelin was increased in subjects with gestational diabetes during and after pregnancy (AUC 15.4 +/- 1.9 vs. 8.6 +/- 1.2 ng.ml(-1).90 min(-1), P = 0.005). In a second group of subjects (n = 13), acylated ghrelin was similarly suppressed during pregnancy. Circulating octanoate concentrations (3.1 +/- 0.5 vs. 4.5 +/- 0.6 microg/ml, P = 0.029) and cholinesterase activity (705 +/- 33 vs. 1,013 +/- 56 U/ml, P < 0.001) were lower during pregnancy compared with the postpartum period. In conclusion, acylated ghrelin markedly decreases during pregnancy, likely because of a decrease in the acylation process. Desacyl ghrelin increases in gestational diabetes, possibly reflecting resistance to the inhibitory effect of insulin on ghrelin secretion.
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PMID:Acylated ghrelin concentrations are markedly decreased during pregnancy in mothers with and without gestational diabetes: relationship with cholinesterase. 1924 Feb 52