Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P01350 (gastrin)
 9,683 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The gastro-entero-pancreatic (GEP) hormone response to glucose ingestion is considerably altered in pregnancy in normal women and gestational diabetics. In normal women, also the GEP hormone response to protein is changed in pregnancy. In the present investigation, the gastrin, gastric inhibitory polypeptide (GIP), gut glucagon-like-immunoreactivity (gut GLI), insulin, pancreatic glucagon, and pancreatic polypeptide (PP) responses to a protein rich meal in pregnancy and postpartum were studied in 10 women with gestational diabetes. Five of the women were overweight and five were normal weight. Fasting and postprandial gut GLI and PP levels were reduced and insulin levels enhanced in pregnancy. No effect of pregnancy on fasting or postprandial gastrin, GIP, or glucagon levels was found. In pregnancy as well as postpartum, insulin levels were higher in the overweight than in the normal weight patients, whereas the concentrations of the other hormones were similar in the two subgroups of gestational diabetics. It is concluded that the GEP hormone response to a protein rich meal is influenced by late pregnancy in gestational diabetics in the same way as in normal women. The physiological consequences of the findings are not known in detail as yet but they may be important to carbohydrate metabolism and gastrointestinal physiology in pregnancy.
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PMID:Gastro-entero-pancreatic hormones in gestational diabetes: response to a protein rich meal. 711 58

At present the physiological role of gastrin, neurotensin and somatostatin in pregnancy and gestational diabetes is scarcely known. We have measured their different molecular forms in plasma of six female controls, six normal pregnant (NP) women and six gestational diabetic (GD) women under basal conditions and 30 min after an oral glucose load (100 g) and a liquid mixed meal in order to study if their alteration could contribute to the impaired glucose tolerance in GD. Total basal concentrations of neurotensin and somatostatin were higher in GD than in controls and NP, and no change was found after the glucose load or mixed meal in GD. Neurotensin-1-13 was the main molecular form of all neurotensins at basal time in the three groups studied, being higher in GD in comparison with controls and NP. Somatostatin-1-14 was the predominant molecular form in controls and GD under basal conditions and did not show any change any change after stimuli. In NP, somatostatin-1-14 showed a significant increase following both kinds of stimuli. Total gastrin concentrations in NP and GD showed a significant increase after the glucose load, which was not observed in controls. Gastrin-17 was the main molecular form at basal time and 30 min post-stimuli in GD but not in NP and controls. We suggest that the basal elevation of neurotensin and somatostatin levels could contribute to the impaired glucose tolerance observed in gestational diabetes, as well as to the lack of post-stimuli responses for neurotensin and somatostatin in GD.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Plasma molecular forms of gastrin, neurotensin and somatostatin in pregnancy and gestational diabetes after an oral glucose load or a mixed meal. 810 15