Literature DB >> 14564717

Endogenous triglyceride turnover in liver and plasma of the dog.

R C Gross1, E H Eigenbrodt, J W Farquhar.   

Abstract

Radioactive glycerol and S(f) > 20 lipoproteins labeled with it were used to study turnover of plasma S(f) > 20 and hepatic triglyceride in anesthetized dogs. From specific activity-time curves of these lipids after an injection of labeled material, a tentative and incomplete model for the kinetics of endogenous hepatic and plasma triglyceride was defined and partially validated. Pool sizes and turnover rates of triglyceride in liver and S(f) > 20 lipoproteins of plasma were then calculated in seven dogs. Hepatic triglyceride was composed of two compartments: 60% metabolically inert and 40% metabolically active. Although communication between these hepatic compartments surely occurred during the time course of these studies, it was not sufficient to be detected by our present methods. The metabolically active compartment turned over as a single pool but with two destinations: a quite variable proportion (an average of 61%) was secreted into plasma as S(f) > 20 triglyceride, and an average of 39% was presumably hydrolyzed within the liver. The fractional turnover rate of plasma S(f) > 20 triglyceride was 2-3 times that of hepatic triglyceride. This finding, and the parallel decline of specific activities of plasma S(f) > 20 and liver triglyceride after injection of labeled glycerol, confirm the rate-determining role of hepatic triglyceride. In this respect the dog differs importantly from man. Though turnover rates of plasma S(f) > 20 triglyceride fell in the same range in men and dogs, the relationship of turnover rate to plasma concentration of this lipid differed greatly between them. The model for the dog does resemble that previously reported for man, however, in the lack of major recycling of intact plasma triglyceride between the liver and plasma. Lack of such recycling, however, does not exclude return of plasma triglyceride into a hepatic triglyceride sink. The amount of such unidirectional uptake, if any, could not be determined by these techniques.

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Year:  1967        PMID: 14564717

Source DB:  PubMed          Journal:  J Lipid Res        ISSN: 0022-2275            Impact factor:   5.922


  8 in total

1.  Plasma triacylglycerol turnover in rats using labeled glycerol.

Authors:  N Baker
Journal:  Lipids       Date:  1984-02       Impact factor: 1.880

2.  Role of insulin in endogenous hypertriglyceridemia.

Authors:  G M Reaven; R L Lerner; M P Stern; J W Farquhar
Journal:  J Clin Invest       Date:  1967-11       Impact factor: 14.808

3.  The effect of high-carbohydrate diets on liver triglyceride formation in the rat.

Authors:  M Waddell; H J Fallon
Journal:  J Clin Invest       Date:  1973-11       Impact factor: 14.808

4.  Transport of plasma free fatty acids and triglycerides in man: a theoretical analysis.

Authors:  D M Shames; A Frank; D Steinberg; M Berman
Journal:  J Clin Invest       Date:  1970-12       Impact factor: 14.808

5.  Inhibition of hepatic triglyceride formation by clofibrate.

Authors:  L L Adams; W W Webb; H J Fallon
Journal:  J Clin Invest       Date:  1971-11       Impact factor: 14.808

6.  Kinetic studies of plasma free fatty acid and triglyceride metabolism in man.

Authors:  R P Eaton; M Berman; D Steinberg
Journal:  J Clin Invest       Date:  1969-08       Impact factor: 14.808

7.  Plasma lipoproteins and the synthesis and turnover of plasma triglyceride in normal and genetically obese mice.

Authors:  D M Salmon; D A Hems
Journal:  Biochem J       Date:  1973-11       Impact factor: 3.857

8.  Fatty liver disrupts glycerol metabolism in gluconeogenic and lipogenic pathways in humans.

Authors:  Eunsook S Jin; Jeffrey D Browning; Rebecca E Murphy; Craig R Malloy
Journal:  J Lipid Res       Date:  2018-07-27       Impact factor: 5.922

  8 in total

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