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Article: Postprandial lipid metabolism and β-cell function in non-insulin-dependent (Type 2) diabetes mellitus after a mixed meal with a high fat content

TitlePostprandial lipid metabolism and β-cell function in non-insulin-dependent (Type 2) diabetes mellitus after a mixed meal with a high fat content
Authors
Issue Date1996
PublisherBlackwell Publishing Ltd. The Journal's web site is located at http://www.blackwellpublishing.com/journals/DME
Citation
Diabetic Medicine, 1996, v. 13 n. 9, p. 816-827 How to Cite?
AbstractPostprandial lipid profiles and release of insulin (INS), intact proinsulin (PI), and 32-33 split proinsulin (SPI) in response to a mixed meal with a high fat content were determined over a 12h period in non-obese control subjects (n = 10) and non-insulin-dependent (Type 2) diabetic (NIDDM) patients with normotriglyceridaemia (NTG; n = 11) and hypertriglyceridaemia (HTG; n = 10), by calculation of the 'areas under the curves' (AUC). The postprandial triglyceride-AUC was significantly greater in HTG-NIDDM patients (p < 0.05) than in NTG-NIDDM or control subjects. Chylomicron clearance was impaired only in HTG-NIDDM patients (p < 0.05). Chylomicron-remnant clearance was impaired in both groups of NIDDM patients (p < 0.05). The postprandial suppression of plasma non-esterified fatty acid (NEFA) content was impaired in HTG-NIDDM patients (p < 0.05). The postprandial INS-, PI- and SPI-AUCS were significantly greater than in the control subjects (p < 0.05). In NIDDM, triglyceride-AUC correlated significantly with PI and SPI release (triglyceride-AUC vs PI, p < 0.05; triglyceride-AUC vs SPI, p < 0.01). Chylomicron AUC was unrelated to the fasting plasma INS, PI or SPI content, unlike chylomicron-remnant-AUC (Chylomicron-remnant-AUC vs INS, p = NS; chylomicronremnant-AUC vs PI, p < 0.01; chylomicron-remnant-AUC vs SPI, p < 0.01). The NEFA response was associated with fasting plasma SPI content (NEFA-AUC vs SPI, p < 0.05). Postprandial chylomicron AUC was not related to the overall secretion of INS, PI or SPI. However, triglyceride-, chylomicron-remnant- and NEFA-AUCs were all associated positively with the release of PI and SPI (p < 0.05). In multivariate analyses, chylomicron-remnant clearance had the major relationship with the release of insulin precursors, accounting for 23 % of the variability (p < 0.01). Inclusion of overall response of free fatty acids improved the model, with both parameters together accounting for 30 % of the variability (p < 0.01). The output of the β-cell over the postprandial period differed between the NIDDM patients and the control subjects in that when glycaemic stimulation was moderate, the proportion of insulin-like molecules as a percentage of the total output was greater than in control subjects but this was not the situation when glycaemia was greatest. We conclude that abnormal postprandial lipaemia in NIDDM is associated with β-cell output, possibly mediated by the availability of free fatty acids.
Persistent Identifierhttp://hdl.handle.net/10722/162124
ISSN
2015 Impact Factor: 3.152
2015 SCImago Journal Rankings: 1.654
References

 

DC FieldValueLanguage
dc.contributor.authorCooper, MBen_US
dc.contributor.authorTan, KCBen_US
dc.contributor.authorHales, CNen_US
dc.contributor.authorBetteridge, DJen_US
dc.date.accessioned2012-09-05T05:17:28Z-
dc.date.available2012-09-05T05:17:28Z-
dc.date.issued1996en_US
dc.identifier.citationDiabetic Medicine, 1996, v. 13 n. 9, p. 816-827en_US
dc.identifier.issn0742-3071en_US
dc.identifier.urihttp://hdl.handle.net/10722/162124-
dc.description.abstractPostprandial lipid profiles and release of insulin (INS), intact proinsulin (PI), and 32-33 split proinsulin (SPI) in response to a mixed meal with a high fat content were determined over a 12h period in non-obese control subjects (n = 10) and non-insulin-dependent (Type 2) diabetic (NIDDM) patients with normotriglyceridaemia (NTG; n = 11) and hypertriglyceridaemia (HTG; n = 10), by calculation of the 'areas under the curves' (AUC). The postprandial triglyceride-AUC was significantly greater in HTG-NIDDM patients (p < 0.05) than in NTG-NIDDM or control subjects. Chylomicron clearance was impaired only in HTG-NIDDM patients (p < 0.05). Chylomicron-remnant clearance was impaired in both groups of NIDDM patients (p < 0.05). The postprandial suppression of plasma non-esterified fatty acid (NEFA) content was impaired in HTG-NIDDM patients (p < 0.05). The postprandial INS-, PI- and SPI-AUCS were significantly greater than in the control subjects (p < 0.05). In NIDDM, triglyceride-AUC correlated significantly with PI and SPI release (triglyceride-AUC vs PI, p < 0.05; triglyceride-AUC vs SPI, p < 0.01). Chylomicron AUC was unrelated to the fasting plasma INS, PI or SPI content, unlike chylomicron-remnant-AUC (Chylomicron-remnant-AUC vs INS, p = NS; chylomicronremnant-AUC vs PI, p < 0.01; chylomicron-remnant-AUC vs SPI, p < 0.01). The NEFA response was associated with fasting plasma SPI content (NEFA-AUC vs SPI, p < 0.05). Postprandial chylomicron AUC was not related to the overall secretion of INS, PI or SPI. However, triglyceride-, chylomicron-remnant- and NEFA-AUCs were all associated positively with the release of PI and SPI (p < 0.05). In multivariate analyses, chylomicron-remnant clearance had the major relationship with the release of insulin precursors, accounting for 23 % of the variability (p < 0.01). Inclusion of overall response of free fatty acids improved the model, with both parameters together accounting for 30 % of the variability (p < 0.01). The output of the β-cell over the postprandial period differed between the NIDDM patients and the control subjects in that when glycaemic stimulation was moderate, the proportion of insulin-like molecules as a percentage of the total output was greater than in control subjects but this was not the situation when glycaemia was greatest. We conclude that abnormal postprandial lipaemia in NIDDM is associated with β-cell output, possibly mediated by the availability of free fatty acids.en_US
dc.languageengen_US
dc.publisherBlackwell Publishing Ltd. The Journal's web site is located at http://www.blackwellpublishing.com/journals/DMEen_US
dc.relation.ispartofDiabetic Medicineen_US
dc.rightsDiabetic Medicine. Copyright © Blackwell Publishing Ltd.-
dc.subject.meshBlood Glucose - Metabolismen_US
dc.subject.meshChylomicrons - Blooden_US
dc.subject.meshDiabetes Mellitus, Type 2 - Blood - Physiopathology - Therapyen_US
dc.subject.meshDiabetic Angiopathies - Blood - Epidemiology - Physiopathologyen_US
dc.subject.meshDiabetic Dieten_US
dc.subject.meshDietary Fatsen_US
dc.subject.meshFastingen_US
dc.subject.meshFatty Acids, Nonesterified - Blooden_US
dc.subject.meshHemoglobin A, Glycosylated - Analysisen_US
dc.subject.meshHumansen_US
dc.subject.meshHypertriglyceridemia - Blood - Physiopathologyen_US
dc.subject.meshHypoglycemic Agents - Therapeutic Useen_US
dc.subject.meshInsulin - Blood - Secretionen_US
dc.subject.meshIslets Of Langerhans - Secretionen_US
dc.subject.meshMaleen_US
dc.subject.meshMiddle Ageden_US
dc.subject.meshPostprandial Perioden_US
dc.subject.meshProinsulin - Blood - Secretionen_US
dc.subject.meshProtein Precursors - Blood - Secretionen_US
dc.subject.meshReference Valuesen_US
dc.subject.meshTime Factorsen_US
dc.subject.meshTriglycerides - Blooden_US
dc.titlePostprandial lipid metabolism and β-cell function in non-insulin-dependent (Type 2) diabetes mellitus after a mixed meal with a high fat contenten_US
dc.typeArticleen_US
dc.identifier.emailTan, KCB:kcbtan@hku.hken_US
dc.identifier.authorityTan, KCB=rp00402en_US
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.doi10.1002/(SICI)1096-9136(199609)13:9<816::AID-DIA183>3.0.CO;2-Len_US
dc.identifier.pmid8891457-
dc.identifier.scopuseid_2-s2.0-0029791120en_US
dc.identifier.hkuros22829-
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-0029791120&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume13en_US
dc.identifier.issue9en_US
dc.identifier.spage816en_US
dc.identifier.epage827en_US
dc.publisher.placeUnited Kingdomen_US
dc.identifier.scopusauthoridCooper, MB=7404410514en_US
dc.identifier.scopusauthoridTan, KCB=8082703100en_US
dc.identifier.scopusauthoridHales, CN=7103213698en_US
dc.identifier.scopusauthoridBetteridge, DJ=34973752700en_US

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