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Increased chylomicron triglyceride hydrolysis by connective tissue flow in perfused rat hindlimb: Implications for lipid storage


Clerk, LH and Smith, ME and Rattigan, S and Clark, MG, Increased chylomicron triglyceride hydrolysis by connective tissue flow in perfused rat hindlimb: Implications for lipid storage, Journal of Lipid research, 41, (3) pp. 329-335. ISSN 0022-2275 (2000) [Refereed Article]


Skeletal muscle has two circulatory routes, nutritive (in contact with muscle) and non-nutritive (part of which is located in the connective tissue), and the balance of flow between the two is controlled by neural input and circulating vasomodulators. The purpose of this study was to assess muscle triglyceride hydrolysis given that the two circuits may have a differing vascular distribution of hydrolytic activity. The isolated rat hindlimb was perfused with 6% Ficoll® and a radiolabeled chylomicron-lipid emulsion containing apolipoprotein C-II. Serotonin (0.5-1 μM), a model vasoconstrictor previously shown to preferentially increase connective tissue flow, inhibited hindlimb oxygen uptake (from 16.7 ± 0.6 to 10.2 ± 1.0, mean ± SE, n = 7 (P <0.001)) and stimulated [14C]-labeled fatty acid uptake into muscles (from 184 ± 28 to 602 ± 132, mean ± SE, n = 7 (P = 0.009)). These effects were reversed by the vasodilator carbamyl choline. Vasopressin resulted in increased oxygen consumption but no change in triglyceride hydrolysis. Cholesteryl oleate uptake (an indicator of endocytosis of the chylomicron or remnant particle) was unaltered by serotonin. It is concluded that chylomicron triglyceride hydrolysis is enhanced by vasoconstrictors that increase connective tissue flow in the perfused rat hindlimb. Increased hydrolysis appears to be primarily due to increased access of triglyceride to hydrolytic enzymes, presumably lipoprotein lipase associated with the fat cells commonly observed interlaced amongst bundles of muscle fibers.

Item Details

Item Type:Refereed Article
Research Division:Biomedical and Clinical Sciences
Research Group:Medical biochemistry and metabolomics
Research Field:Medical biochemistry - lipids
Objective Division:Health
Objective Group:Clinical health
Objective Field:Clinical health not elsewhere classified
UTAS Author:Clerk, LH (Ms Lucy Henrietta Clerk)
UTAS Author:Smith, ME (Mrs Maree Smith)
UTAS Author:Rattigan, S (Professor Stephen Rattigan)
UTAS Author:Clark, MG (Professor Michael Clark)
ID Code:19302
Year Published:2000
Web of Science® Times Cited:16
Deposited By:Biochemistry
Deposited On:2000-08-01
Last Modified:2011-11-08

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