title: Increased chylomicron triglyceride hydrolysis by connective tissue flow in perfused rat hindlimb. Implications for lipid storage.
abstract: 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((R)) and a radiolabeled chylomicron;-lipid emulsion containing apolipoprotein C-II. Serotonin (0.5-1 micrometer), 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 [(14)C]-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 an increased access of triglyceride to hydrolytic enzymes, presumably lipoprotein lipase associated with the fat cells commonly observed interlaced amongst bundles of muscle fibers.
authors.affiliation: Division of Biochemistry, Medical School, University of Tasmania, Hobart, Australia 7001.
authors.forename: L H
authors.initials: LH
authors.lastname: Clerk
authors.forename: M E
authors.initials: ME
authors.lastname: Smith
authors.forename: S
authors.initials: S
authors.lastname: Rattigan
authors.forename: M G
authors.initials: MG
authors.lastname: Clark
mesh_terms: D000818:Animals; D002217:Carbachol / Q000494:pharmacology; D002914:Chylomicrons / Q000378:metabolism*; D006614:Hindlimb; D006868:Hydrolysis; D007700:Kinetics; D008297:Male; D018482:Muscle, Skeletal / Q000098:blood supply / Q000187:drug effects / Q000378:metabolism*; D010477:Perfusion; D051381:Rats; D017208:Rats, Wistar; D012701:Serotonin / Q000494:pharmacology; D014280:Triglycerides / Q000378:metabolism*; D014665:Vasodilator Agents / Q000494:pharmacology; D014667:Vasopressins / Q000494:pharmacology
chemical_list: D002914:Chylomicrons; D014280:Triglycerides; D014665:Vasodilator Agents; D014667:Vasopressins; D012701:Serotonin; D002217:Carbachol