Impaired Postprandial Adipose Tissue Blood Flow Response Is Related to Aspects of Insulin Sensitivity

Impaired Postprandial Adipose Tissue Blood Flow Response Is Related to Aspects of Insulin Sensitivity Fredrik Karpe 1 , Barbara A. Fielding 1 , Vera Ilic 1 , Ian A. Macdonald 2 , Lucinda K.M. Summers 1 and Keith N. Frayn 1 1 Oxford Lipid Metabolism Group, Oxford Centre for Diabetes, Endocrinology an...

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Published inDiabetes (New York, N.Y.) Vol. 51; no. 8; pp. 2467 - 2473
Main Authors KARPE, Fredrik, FIELDING, Barbara A, ILIC, Vera, MACDONALD, Ian A, SUMMERS, Lucinda K. M, FRAYN, Keith N
Format Journal Article
LanguageEnglish
Published Alexandria, VA American Diabetes Association 01.08.2002
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Summary:Impaired Postprandial Adipose Tissue Blood Flow Response Is Related to Aspects of Insulin Sensitivity Fredrik Karpe 1 , Barbara A. Fielding 1 , Vera Ilic 1 , Ian A. Macdonald 2 , Lucinda K.M. Summers 1 and Keith N. Frayn 1 1 Oxford Lipid Metabolism Group, Oxford Centre for Diabetes, Endocrinology and Metabolism, Radcliffe Infirmary, Oxford, U.K. 2 University of Nottingham Medical School, Nottingham, U.K. Abstract Obesity has been associated with dysfunctional postprandial adipose tissue blood flow (ATBF), but it has also been recognized that the interindividual response is highly variable. The present work aimed at characterizing this variability. Fifteen subjects were given 75 g oral glucose, and abdominal subcutaneous ATBF was monitored by the 133 Xe washout method. Determinants of insulin sensitivity based on nonesterified fatty acid (NEFA) suppression after oral glucose administration [ISI(NEFA)] were higher in the top tertile ATBF response group (1.29 ± 0.09 vs. 0.90 ± 0.08 in the lower tertiles, P = 0.01). ISI(NEFA) was related to ATBF response ( r s = 0.73, P < 0.002) as well as insulin sensitivity based on postprandial glycemia [ISI(gly), r s = 0.58, P < 0.05], whereas the homeostasis model assessment (HOMA) index ( r s = −0.39, P = 0.16) was not. The relationship between increase in ATBF and ISI(NEFA) was independent of BMI ( P = 0.015) in multivariate analysis. Subjects with a high ATBF response had significantly higher increase of plasma norepinephrine ( P < 0.05), indicating a link between postprandial insulinemia, sympathetic activation, and ATBF response. There is a close relationship between insulin sensitivity and the regulation of postprandial ATBF, independent of adiposity. Impaired regulation of ATBF seems to be another facet of the insulin resistance syndrome. Footnotes Address correspondence and reprint requests to Dr. F Karpe, Oxford Lipid Metabolism Group, Oxford Centre for Diabetes, Endocrinology and Metabolism, Radcliffe Infirmary, Oxford OX2 6HE, U.K. E-mail: fredrik.karpe{at}oxlip.ox.ac.uk . Received for publication 9 January 2002 and accepted in revised form 17 May 2002. ATBF, adipose tissue blood flow; HOMA, homeostasis model assessment; ISI(gly), insulin sensitivity based on postprandial glycemia; ISI(NEFA), insulin sensitivity based on NEFA suppression after oral glucose administration; NEFA, nonesterified fatty acid; RM-ANOVA, repeated-measures ANOVA; TG, triglyceride. DIABETES
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ISSN:0012-1797
1939-327X
DOI:10.2337/diabetes.51.8.2467