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Article: Does abnormal insulin action or insulin secretion explain the increase in prevalence of impaired glucose metabolism with age in populations of different ethnicities?

TitleDoes abnormal insulin action or insulin secretion explain the increase in prevalence of impaired glucose metabolism with age in populations of different ethnicities?
Authors
Keywordsβ-cell function
Age
Impaired fasting glucose
Impaired glucose tolerance
Insulin resistance
Issue Date2010
PublisherJohn Wiley & Sons Ltd. The Journal's web site is located at http://www3.interscience.wiley.com/cgi-bin/jhome/10009394
Citation
Diabetes/Metabolism Research And Reviews, 2010, v. 26 n. 4, p. 245-253 How to Cite?
AbstractBackground: Age is associated with both impaired glucose and insulin metabolism. To what extent the age-related changes in insulin resistance (IR) and β-cell function contribute to the increase in prevalence of impaired fasting glucose (IFG) and impaired glucose tolerance (IGT) is less known, and this is investigated in this study. Methods: This study included 6610 men and 7664 women of different ethnic groups aged 30-69 years. IR and β-cell function were examined by the homeostasis model assessment of insulin resistance (HOMA-IR) and homeostasis model assessment of β-cell function (HOMA-B). Odds ratios (ORs) and 95% confidence intervals (95% CIs) were estimated using logistic regression analysis adjusting for body mass index and study. Results: In Chinese men, the ORs (95% CIs) for IFG were 2.69 (1.70, 4.26), 2.51 (1.49, 4.21) and 2.89 (1.68, 4.97), respectively, in age groups of 40-49, 50-59 and 60-69 years compared with 30-39 years (p < 0.001 for trend); the corresponding figures for IGT were 1.73 (1.25, 2.38), 2.54 (1.78, 3.63) and 3.57 (2.46, 5.19) (p < 0.001 for trend). Similar trends for IGT were observed also in Chinese women and other ethnic groups, but not for IFG in Mauritius Indian and Creole men. Adjustment for HOMA-IR and HOMA-B reduced the ORs in all age groups of all ethnicities for both IFG and IGT, but the risk gradient between age groups remained particularly for the IGT. Conclusions: The age-related increase in glucose intolerance may not be fully explained by the defect in HOMA-IR and HOMA-B. As HOMA-IR and HOMA-B are only surrogate measures of insulin sensitivity and insulin secretion, the results need to be further investigated. Copyright © 2010 John Wiley & Sons, Ltd.
Persistent Identifierhttp://hdl.handle.net/10722/151713
ISSN
2023 Impact Factor: 4.6
2023 SCImago Journal Rankings: 1.991
ISI Accession Number ID
Funding AgencyGrant Number
Academy of Finland118492
129197
Finnish Centre for International Mobility Fellowship (CIMO)TM-08-5694
Funding Information:

This study was supported by grants from Academy of Finland (118492, 129197) and Finnish Centre for International Mobility Fellowship (CIMO TM-08-5694); Unrestricted grants from AstraZeneca R&D, Molndal, Sweden for data analysis are also acknowledged.

References

 

DC FieldValueLanguage
dc.contributor.authorNing, Fen_US
dc.contributor.authorQiao, Qen_US
dc.contributor.authorTuomilehto, Jen_US
dc.contributor.authorHammar, Nen_US
dc.contributor.authorHo, SYen_US
dc.contributor.authorSöderberg, Sen_US
dc.contributor.authorZimmet, PZen_US
dc.contributor.authorShaw, JEen_US
dc.contributor.authorNakagami, Ten_US
dc.contributor.authorMohan, Ven_US
dc.contributor.authorRamachandran, Aen_US
dc.contributor.authorLam, THen_US
dc.contributor.authorAndersson, SWen_US
dc.contributor.authorJanus, EDen_US
dc.contributor.authorBoyko, EJen_US
dc.contributor.authorFujimoto, WYen_US
dc.contributor.authorPang, ZCen_US
dc.date.accessioned2012-06-26T06:27:00Z-
dc.date.available2012-06-26T06:27:00Z-
dc.date.issued2010en_US
dc.identifier.citationDiabetes/Metabolism Research And Reviews, 2010, v. 26 n. 4, p. 245-253en_US
dc.identifier.issn1520-7552en_US
dc.identifier.urihttp://hdl.handle.net/10722/151713-
dc.description.abstractBackground: Age is associated with both impaired glucose and insulin metabolism. To what extent the age-related changes in insulin resistance (IR) and β-cell function contribute to the increase in prevalence of impaired fasting glucose (IFG) and impaired glucose tolerance (IGT) is less known, and this is investigated in this study. Methods: This study included 6610 men and 7664 women of different ethnic groups aged 30-69 years. IR and β-cell function were examined by the homeostasis model assessment of insulin resistance (HOMA-IR) and homeostasis model assessment of β-cell function (HOMA-B). Odds ratios (ORs) and 95% confidence intervals (95% CIs) were estimated using logistic regression analysis adjusting for body mass index and study. Results: In Chinese men, the ORs (95% CIs) for IFG were 2.69 (1.70, 4.26), 2.51 (1.49, 4.21) and 2.89 (1.68, 4.97), respectively, in age groups of 40-49, 50-59 and 60-69 years compared with 30-39 years (p < 0.001 for trend); the corresponding figures for IGT were 1.73 (1.25, 2.38), 2.54 (1.78, 3.63) and 3.57 (2.46, 5.19) (p < 0.001 for trend). Similar trends for IGT were observed also in Chinese women and other ethnic groups, but not for IFG in Mauritius Indian and Creole men. Adjustment for HOMA-IR and HOMA-B reduced the ORs in all age groups of all ethnicities for both IFG and IGT, but the risk gradient between age groups remained particularly for the IGT. Conclusions: The age-related increase in glucose intolerance may not be fully explained by the defect in HOMA-IR and HOMA-B. As HOMA-IR and HOMA-B are only surrogate measures of insulin sensitivity and insulin secretion, the results need to be further investigated. Copyright © 2010 John Wiley & Sons, Ltd.en_US
dc.languageengen_US
dc.publisherJohn Wiley & Sons Ltd. The Journal's web site is located at http://www3.interscience.wiley.com/cgi-bin/jhome/10009394en_US
dc.relation.ispartofDiabetes/Metabolism Research and Reviewsen_US
dc.subjectβ-cell function-
dc.subjectAge-
dc.subjectImpaired fasting glucose-
dc.subjectImpaired glucose tolerance-
dc.subjectInsulin resistance-
dc.subject.meshAdulten_US
dc.subject.meshAge Factorsen_US
dc.subject.meshAgeden_US
dc.subject.meshBlood Glucose - Metabolismen_US
dc.subject.meshDiabetes Mellitus, Type 2 - Ethnologyen_US
dc.subject.meshFemaleen_US
dc.subject.meshGlucose Intolerance - Ethnologyen_US
dc.subject.meshHumansen_US
dc.subject.meshInsulin - Secretionen_US
dc.subject.meshInsulin Resistance - Ethnologyen_US
dc.subject.meshMaleen_US
dc.subject.meshMiddle Ageden_US
dc.subject.meshPrevalenceen_US
dc.titleDoes abnormal insulin action or insulin secretion explain the increase in prevalence of impaired glucose metabolism with age in populations of different ethnicities?en_US
dc.typeArticleen_US
dc.identifier.emailHo, SY:syho@hku.hken_US
dc.identifier.emailLam, TH:hrmrlth@hkucc.hku.hken_US
dc.identifier.authorityHo, SY=rp00427en_US
dc.identifier.authorityLam, TH=rp00326en_US
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.doi10.1002/dmrr.1078en_US
dc.identifier.pmid20503256-
dc.identifier.scopuseid_2-s2.0-77952783736en_US
dc.identifier.hkuros170701-
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-77952783736&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume26en_US
dc.identifier.issue4en_US
dc.identifier.spage245en_US
dc.identifier.epage253en_US
dc.identifier.isiWOS:000278660400003-
dc.publisher.placeUnited Kingdomen_US
dc.identifier.scopusauthoridNing, F=33667824300en_US
dc.identifier.scopusauthoridQiao, Q=7005824706en_US
dc.identifier.scopusauthoridTuomilehto, J=36012823000en_US
dc.identifier.scopusauthoridHammar, N=7006083229en_US
dc.identifier.scopusauthoridHo, SY=7403716884en_US
dc.identifier.scopusauthoridSöderberg, S=35463005200en_US
dc.identifier.scopusauthoridZimmet, PZ=7102179242en_US
dc.identifier.scopusauthoridShaw, JE=35563820200en_US
dc.identifier.scopusauthoridNakagami, T=7006023112en_US
dc.identifier.scopusauthoridMohan, V=35509595400en_US
dc.identifier.scopusauthoridRamachandran, A=7102252827en_US
dc.identifier.scopusauthoridLam, TH=7202522876en_US
dc.identifier.scopusauthoridAndersson, SW=55166010800en_US
dc.identifier.scopusauthoridJanus, ED=7006936536en_US
dc.identifier.scopusauthoridBoyko, EJ=7005703432en_US
dc.identifier.scopusauthoridFujimoto, WY=7101642681en_US
dc.identifier.scopusauthoridPang, ZC=12806211900en_US
dc.identifier.citeulike7224282-
dc.identifier.issnl1520-7552-

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