Intrahepatic Lipid Content and Insulin Resistance Are More Strongly Associated with Impaired NEFA Suppression after Oral Glucose Loading Than with Fasting NEFA Levels in Healthy Older Individuals

Introduction. The mechanisms underlying the association between insulin resistance and intrahepatic lipid (IHL) accumulation are not completely understood. We sought to determine whether this association was explained by differences in fasting non-esterified fatty acid (NEFA) levels and/or NEFA supp...

Full description

Saved in:
Bibliographic Details
Main Authors: Francis M. Finucane, Stephen J. Sharp, Mensud Hatunic, Alison Sleigh, Ema De Lucia Rolfe, Avan Aihie Sayer, Cyrus Cooper, Simon J. Griffin, David B. Savage, Nicholas J. Wareham
Format: Article
Language:English
Published: Wiley 2013-01-01
Series:International Journal of Endocrinology
Online Access:http://dx.doi.org/10.1155/2013/870487
Tags: Add Tag
No Tags, Be the first to tag this record!
_version_ 1832554871261233152
author Francis M. Finucane
Stephen J. Sharp
Mensud Hatunic
Alison Sleigh
Ema De Lucia Rolfe
Avan Aihie Sayer
Cyrus Cooper
Simon J. Griffin
David B. Savage
Nicholas J. Wareham
author_facet Francis M. Finucane
Stephen J. Sharp
Mensud Hatunic
Alison Sleigh
Ema De Lucia Rolfe
Avan Aihie Sayer
Cyrus Cooper
Simon J. Griffin
David B. Savage
Nicholas J. Wareham
author_sort Francis M. Finucane
collection DOAJ
description Introduction. The mechanisms underlying the association between insulin resistance and intrahepatic lipid (IHL) accumulation are not completely understood. We sought to determine whether this association was explained by differences in fasting non-esterified fatty acid (NEFA) levels and/or NEFA suppression after oral glucose loading. Materials and Methods. We performed a cross-sectional analysis of 70 healthy participants in the Hertfordshire Physical Activity Trial (39 males, age 71.3 ± 2.4 years) who underwent oral glucose tolerance testing with glucose, insulin, and NEFA levels measured over two hours. IHL was quantified with magnetic resonance spectroscopy. Insulin sensitivity was measured with the oral glucose insulin sensitivity (OGIS) model, the leptin: adiponectin ratio (LAR), and the homeostasis model assessment (HOMA). Results. Measures of insulin sensitivity were not associated with fasting NEFA levels, but OGIS was strongly associated with NEFA suppression at 30 minutes and strongly inversely associated with IHL. Moreover, LAR was strongly inversely associated with NEFA suppression and strongly associated with IHL. This latter association (beta = 1.11 [1.01, 1.21], ) was explained by reduced NEFA suppression ( after adjustment). Conclusions. Impaired postprandial NEFA suppression, but not fasting NEFA, contributes to the strong and well-established association between whole body insulin resistance and liver fat accumulation.
format Article
id doaj-art-f1258a5f005a484cb2c94e58e3ea88e2
institution Kabale University
issn 1687-8337
1687-8345
language English
publishDate 2013-01-01
publisher Wiley
record_format Article
series International Journal of Endocrinology
spelling doaj-art-f1258a5f005a484cb2c94e58e3ea88e22025-02-03T05:50:21ZengWileyInternational Journal of Endocrinology1687-83371687-83452013-01-01201310.1155/2013/870487870487Intrahepatic Lipid Content and Insulin Resistance Are More Strongly Associated with Impaired NEFA Suppression after Oral Glucose Loading Than with Fasting NEFA Levels in Healthy Older IndividualsFrancis M. Finucane0Stephen J. Sharp1Mensud Hatunic2Alison Sleigh3Ema De Lucia Rolfe4Avan Aihie Sayer5Cyrus Cooper6Simon J. Griffin7David B. Savage8Nicholas J. Wareham9MRC Epidemiology Unit, Institute of Metabolic Science, Addenbrooke's Hospital, P.O. Box 285 Hills Road, Cambridge CB20QQ, UKMRC Epidemiology Unit, Institute of Metabolic Science, Addenbrooke's Hospital, P.O. Box 285 Hills Road, Cambridge CB20QQ, UKMetabolic Research Laboratories, Institute of Metabolic Science, Cambridge CB20QQ, UKWolfson Brain Imaging Centre, University of Cambridge, Cambridge CB20QQ, UKMRC Epidemiology Unit, Institute of Metabolic Science, Addenbrooke's Hospital, P.O. Box 285 Hills Road, Cambridge CB20QQ, UKMRC Lifecourse Epidemiology Unit, University of Southampton, Southampton SO166YD, UKMRC Lifecourse Epidemiology Unit, University of Southampton, Southampton SO166YD, UKMRC Epidemiology Unit, Institute of Metabolic Science, Addenbrooke's Hospital, P.O. Box 285 Hills Road, Cambridge CB20QQ, UKMetabolic Research Laboratories, Institute of Metabolic Science, Cambridge CB20QQ, UKMRC Epidemiology Unit, Institute of Metabolic Science, Addenbrooke's Hospital, P.O. Box 285 Hills Road, Cambridge CB20QQ, UKIntroduction. The mechanisms underlying the association between insulin resistance and intrahepatic lipid (IHL) accumulation are not completely understood. We sought to determine whether this association was explained by differences in fasting non-esterified fatty acid (NEFA) levels and/or NEFA suppression after oral glucose loading. Materials and Methods. We performed a cross-sectional analysis of 70 healthy participants in the Hertfordshire Physical Activity Trial (39 males, age 71.3 ± 2.4 years) who underwent oral glucose tolerance testing with glucose, insulin, and NEFA levels measured over two hours. IHL was quantified with magnetic resonance spectroscopy. Insulin sensitivity was measured with the oral glucose insulin sensitivity (OGIS) model, the leptin: adiponectin ratio (LAR), and the homeostasis model assessment (HOMA). Results. Measures of insulin sensitivity were not associated with fasting NEFA levels, but OGIS was strongly associated with NEFA suppression at 30 minutes and strongly inversely associated with IHL. Moreover, LAR was strongly inversely associated with NEFA suppression and strongly associated with IHL. This latter association (beta = 1.11 [1.01, 1.21], ) was explained by reduced NEFA suppression ( after adjustment). Conclusions. Impaired postprandial NEFA suppression, but not fasting NEFA, contributes to the strong and well-established association between whole body insulin resistance and liver fat accumulation.http://dx.doi.org/10.1155/2013/870487
spellingShingle Francis M. Finucane
Stephen J. Sharp
Mensud Hatunic
Alison Sleigh
Ema De Lucia Rolfe
Avan Aihie Sayer
Cyrus Cooper
Simon J. Griffin
David B. Savage
Nicholas J. Wareham
Intrahepatic Lipid Content and Insulin Resistance Are More Strongly Associated with Impaired NEFA Suppression after Oral Glucose Loading Than with Fasting NEFA Levels in Healthy Older Individuals
International Journal of Endocrinology
title Intrahepatic Lipid Content and Insulin Resistance Are More Strongly Associated with Impaired NEFA Suppression after Oral Glucose Loading Than with Fasting NEFA Levels in Healthy Older Individuals
title_full Intrahepatic Lipid Content and Insulin Resistance Are More Strongly Associated with Impaired NEFA Suppression after Oral Glucose Loading Than with Fasting NEFA Levels in Healthy Older Individuals
title_fullStr Intrahepatic Lipid Content and Insulin Resistance Are More Strongly Associated with Impaired NEFA Suppression after Oral Glucose Loading Than with Fasting NEFA Levels in Healthy Older Individuals
title_full_unstemmed Intrahepatic Lipid Content and Insulin Resistance Are More Strongly Associated with Impaired NEFA Suppression after Oral Glucose Loading Than with Fasting NEFA Levels in Healthy Older Individuals
title_short Intrahepatic Lipid Content and Insulin Resistance Are More Strongly Associated with Impaired NEFA Suppression after Oral Glucose Loading Than with Fasting NEFA Levels in Healthy Older Individuals
title_sort intrahepatic lipid content and insulin resistance are more strongly associated with impaired nefa suppression after oral glucose loading than with fasting nefa levels in healthy older individuals
url http://dx.doi.org/10.1155/2013/870487
work_keys_str_mv AT francismfinucane intrahepaticlipidcontentandinsulinresistancearemorestronglyassociatedwithimpairednefasuppressionafteroralglucoseloadingthanwithfastingnefalevelsinhealthyolderindividuals
AT stephenjsharp intrahepaticlipidcontentandinsulinresistancearemorestronglyassociatedwithimpairednefasuppressionafteroralglucoseloadingthanwithfastingnefalevelsinhealthyolderindividuals
AT mensudhatunic intrahepaticlipidcontentandinsulinresistancearemorestronglyassociatedwithimpairednefasuppressionafteroralglucoseloadingthanwithfastingnefalevelsinhealthyolderindividuals
AT alisonsleigh intrahepaticlipidcontentandinsulinresistancearemorestronglyassociatedwithimpairednefasuppressionafteroralglucoseloadingthanwithfastingnefalevelsinhealthyolderindividuals
AT emadeluciarolfe intrahepaticlipidcontentandinsulinresistancearemorestronglyassociatedwithimpairednefasuppressionafteroralglucoseloadingthanwithfastingnefalevelsinhealthyolderindividuals
AT avanaihiesayer intrahepaticlipidcontentandinsulinresistancearemorestronglyassociatedwithimpairednefasuppressionafteroralglucoseloadingthanwithfastingnefalevelsinhealthyolderindividuals
AT cyruscooper intrahepaticlipidcontentandinsulinresistancearemorestronglyassociatedwithimpairednefasuppressionafteroralglucoseloadingthanwithfastingnefalevelsinhealthyolderindividuals
AT simonjgriffin intrahepaticlipidcontentandinsulinresistancearemorestronglyassociatedwithimpairednefasuppressionafteroralglucoseloadingthanwithfastingnefalevelsinhealthyolderindividuals
AT davidbsavage intrahepaticlipidcontentandinsulinresistancearemorestronglyassociatedwithimpairednefasuppressionafteroralglucoseloadingthanwithfastingnefalevelsinhealthyolderindividuals
AT nicholasjwareham intrahepaticlipidcontentandinsulinresistancearemorestronglyassociatedwithimpairednefasuppressionafteroralglucoseloadingthanwithfastingnefalevelsinhealthyolderindividuals