Chronic physiologic hyperinsulinemia impairs suppression of plasma free fatty acids and increases de novo lipogenesis but does not cause dyslipidemia in conscious normal rats

Metabolism ◽  
1999 ◽  
Vol 48 (3) ◽  
pp. 330-337 ◽  
Author(s):  
Sietse J. Koopmans ◽  
Rampratap S. Kushwaha ◽  
Ralph A. DeFronzo
Keyword(s):  
Fatty Acids ◽  
Free Fatty Acids ◽  
De Novo ◽  
De Novo Lipogenesis ◽  
Plasma Free Fatty Acids

Model for measuring absolute rates of hepatic de novo lipogenesis and reesterification of free fatty acids

1993 ◽  
Vol 265 (5) ◽  
pp. E814-E820 ◽  
Author(s):  
M. K. Hellerstein ◽  
R. A. Neese ◽  
J. M. Schwarz
Keyword(s):  
Fatty Acids ◽  
Free Fatty Acids ◽  
De Novo ◽  
Human Subjects ◽  
Fat Oxidation ◽  
De Novo Lipogenesis ◽  
Whole Body ◽  
Distribution Analysis ◽  
Oxidation Rates ◽  
Mass Isotopomer Distribution Analysis

We have previously presented a precursor-product stable isotopic technique for measuring in vivo the fraction of very low-density lipoprotein-fatty acids (VLDL-FA) derived from de novo lipogenesis (fractional DNL). Here, we propose a technique for converting fractional DNL into absolute rates of DNL and describe its explicit underlying assumptions. The technique combines the fractional DNL method with a modification of the method of S. Klein, V. R. Young, G. L. A. Blackburn, B. R. Bistrain, and R. R. Wolfe (J. Clin. Invest. 78: 928-933, 1986), for estimating hepatic reesterification of free fatty acids (FFA). Infusions of [1,2,3,4-13C]palmitate and [1-13C]acetate are performed concurrently with indirect calorimetry in human subjects. Fractional DNL (based on mass isotopomer distribution analysis of VLDL-FA), the rate of appearance of plasma FFA (Ra of FFA), and net fat oxidation in the whole body are measured. Equations from the hepatic reesterification model, modified to include the contribution from DNL, allow calculation of absolute DNL (= fractional DNL x [Ra of FFA - net whole body fat oxidation], when respiratory quotient < 1.0). Sample results from human subjects with different dietary energy intakes are presented, with calculations of absolute DNL, absolute reesterification, and absolute fat oxidation rates. The assumptions of this technique (in particular, that all fat oxidized is derived at steady state from circulating FFA and that DNL and reesterification of FFA both occur exclusively in liver) are discussed.(ABSTRACT TRUNCATED AT 250 WORDS)

Source of plasma free fatty acids in dogs receiving fat emulsion and heparin

1963 ◽  
Vol 204 (4) ◽  
pp. 691-695 ◽  
Author(s):  
H. C. Meng ◽  
B. Edgren
Keyword(s):  
Fatty Acids ◽  
Free Fatty Acids ◽  
Lipolytic Activity ◽  
Blocking Agent ◽  
Fat Emulsion ◽  
Similar Reduction ◽  
Plasma Free Fatty Acids ◽  
Fat Infusion ◽  
Plasma Ffa ◽  
Slight Rise

Unanesthetized dogs were given either 3.0 g fat/kg as a 20% fat emulsion or heparin (2 mg/kg) intravenously or both. Plasma free fatty acids (FFA) and lipolytic activity were determined at intervals. In some experiments hexamethonium (5 mg/kg), a sympathetic ganglionic blocking agent, was administered intravenously either before or after fat or heparin. In fasting dogs fat infusion produced a moderate and heparin caused a slight rise in plasma FFA. Heparin given during lipemia produced a marked elevation of plasma FFA. The plasma lipolytic activity was increased after fat emulsion or heparin. Hexamethonium reduced the fasting plasma FFA about 70% or 0.40–0.6 mEq/liter. A similar reduction of plasma FFA also was observed when hexamethonium was administered during fat infusion or after heparin. Hexamethonium did not affect the increase in plasma lipolytic activity following the administration of fat emulsion or heparin. It seems probable that the increase in plasma FFA observed after intravenous infusion of fat emulsion or heparin is mainly due to the result of intravascular lipolysis.

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