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Article: Glucose intolerance in thyrotoxicosis roles of insulin, glucagon and somatostatin

TitleGlucose intolerance in thyrotoxicosis roles of insulin, glucagon and somatostatin
Authors
Issue Date1987
Citation
Acta Endocrinologica, 1987, v. 114 n. 2, p. 228-234 How to Cite?
AbstractThe responses in plasma glucose, insulin, C-peptide, glucagon and somatostatin to an oral glucose load were studied in 10 thyrotoxic patients and 10 matched euthyroid controls. The thyrotoxic patients had higher mean fasting plasma glucose (P < 0.05) and responded to oral glucose with an earlier peak at 30 min which was higher than the corresponding glucose level in the controls (P < 0.05). Impaired glucose tolerance was found in 3 patients. Fasting insulin and C-peptide levels were normal in the thyrotoxic patients when corrected for the higher glucose levels. Following glucose ingestion, there was no significant difference between the areas under the insulin or C-peptide curves in patients and controls, but Seltzer's insulinogenic index was reduced in the patients (P < 0.01) suggesting an impaired pancreatic B-cell response to oral glucose. Mean basal glucagon was normal in the thyrotoxic patients. However, while in the controls plasma glucagon became suppressed following glucose ingestion (P < 0.0001), no significant suppression was found in the patients. In the thyrotoxic patients, mean basal somatostatin was normal, but the area under the somatostatin curve following glucose ingestion was significantly increased (P < 0.02). Our findings suggest that decreased glucagon suppression and impaired insulin response after glucose ingestion are involved in glucose intolerance in thyrotoxicosis. Enhanced somatostatin responses to oral glucose in thyrotoxicosis may have contributed to the observed impairment in pancreatic B-cell responsiveness.
Persistent Identifierhttp://hdl.handle.net/10722/161718
ISSN
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorLam, KSLen_US
dc.contributor.authorYeung, RTTen_US
dc.contributor.authorHo, PWMen_US
dc.contributor.authorLam, SKen_US
dc.date.accessioned2012-09-05T05:14:19Z-
dc.date.available2012-09-05T05:14:19Z-
dc.date.issued1987en_US
dc.identifier.citationActa Endocrinologica, 1987, v. 114 n. 2, p. 228-234en_US
dc.identifier.issn0001-5598en_US
dc.identifier.urihttp://hdl.handle.net/10722/161718-
dc.description.abstractThe responses in plasma glucose, insulin, C-peptide, glucagon and somatostatin to an oral glucose load were studied in 10 thyrotoxic patients and 10 matched euthyroid controls. The thyrotoxic patients had higher mean fasting plasma glucose (P < 0.05) and responded to oral glucose with an earlier peak at 30 min which was higher than the corresponding glucose level in the controls (P < 0.05). Impaired glucose tolerance was found in 3 patients. Fasting insulin and C-peptide levels were normal in the thyrotoxic patients when corrected for the higher glucose levels. Following glucose ingestion, there was no significant difference between the areas under the insulin or C-peptide curves in patients and controls, but Seltzer's insulinogenic index was reduced in the patients (P < 0.01) suggesting an impaired pancreatic B-cell response to oral glucose. Mean basal glucagon was normal in the thyrotoxic patients. However, while in the controls plasma glucagon became suppressed following glucose ingestion (P < 0.0001), no significant suppression was found in the patients. In the thyrotoxic patients, mean basal somatostatin was normal, but the area under the somatostatin curve following glucose ingestion was significantly increased (P < 0.02). Our findings suggest that decreased glucagon suppression and impaired insulin response after glucose ingestion are involved in glucose intolerance in thyrotoxicosis. Enhanced somatostatin responses to oral glucose in thyrotoxicosis may have contributed to the observed impairment in pancreatic B-cell responsiveness.en_US
dc.languageengen_US
dc.relation.ispartofActa Endocrinologicaen_US
dc.subject.meshAdulten_US
dc.subject.meshBlood Glucose - Analysisen_US
dc.subject.meshC-Peptide - Blooden_US
dc.subject.meshFemaleen_US
dc.subject.meshGlucagon - Blooden_US
dc.subject.meshGlucose Tolerance Testen_US
dc.subject.meshHumansen_US
dc.subject.meshInsulin - Blooden_US
dc.subject.meshSomatostatin - Blooden_US
dc.subject.meshThyrotoxicosis - Blooden_US
dc.titleGlucose intolerance in thyrotoxicosis roles of insulin, glucagon and somatostatinen_US
dc.typeArticleen_US
dc.identifier.emailLam, KSL:ksllam@hku.hken_US
dc.identifier.authorityLam, KSL=rp00343en_US
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.pmid2881418-
dc.identifier.scopuseid_2-s2.0-0023119362en_US
dc.identifier.volume114en_US
dc.identifier.issue2en_US
dc.identifier.spage228en_US
dc.identifier.epage234en_US
dc.identifier.isiWOS:A1987F800000011-
dc.identifier.scopusauthoridLam, KSL=8082870600en_US
dc.identifier.scopusauthoridYeung, RTT=7102833337en_US
dc.identifier.scopusauthoridHo, PWM=7402211336en_US
dc.identifier.scopusauthoridLam, SK=7402279473en_US

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