Effects of hypothyroidism and withholding of feed on plasma lipid concentrations, concentration and composition of very-low-density lipoprotein, and plasma lipase activity in horses

2003 ◽  
Vol 64 (7) ◽  
pp. 823-828 ◽  
Author(s):  
Nicholas Frank ◽  
Janice E. Sojka ◽  
Mickey A. Latour
Keyword(s):  
Lipase Activity ◽  
Low Density Lipoprotein ◽  
Plasma Lipid ◽  
Density Lipoprotein ◽  
Very Low Density Lipoprotein ◽  
Low Density

scholarly journals Estrogen Deficiency after Menopause Does Not Result in Male Very-Low-Density Lipoprotein Metabolism Phenotype

2010 ◽  
Vol 95 (7) ◽  
pp. 3377-3384 ◽  
Author(s):  
Faidon Magkos ◽  
Elisa Fabbrini ◽  
B. Selma Mohammed ◽  
Bruce W. Patterson ◽  
Samuel Klein ◽  
...  
Keyword(s):  
Postmenopausal Women ◽  
Low Density Lipoprotein ◽  
Plasma Lipid ◽  
Lipoprotein Metabolism ◽  
Density Lipoprotein ◽  
Premenopausal Women ◽  
Reproductive Hormones ◽  
Secretion Rate ◽  
Very Low Density Lipoprotein ◽  
Low Density

Context: Sex differences in lipid metabolism result in a less proatherogenic plasma lipid profile in premenopausal women than men. The mechanisms responsible for this are unclear but are thought to be related to differences in the sex hormone milieu in men and women. Objective: Our objective was to evaluate the effect of endogenous sex hormones on very-low-density lipoprotein (VLDL) triglyceride (TG) and apolipoprotein B-100 (apoB-100) metabolism. Experimental Design and Main Outcome Measures: We measured basal VLDL-TG and VLDL-apoB-100 concentrations and kinetics by using stable isotope-labeled tracers. Setting and Participants: Eight premenopausal women [age, 43 ± 8 yr; body mass index (BMI), 35 ± 4 kg/m2; mean ± sd], eight postmenopausal women (age, 55 ± 4 yr; BMI, 34 ± 4 kg/m2), and eight men (age, 41 ± 13 yr; BMI, 34 ± 4 kg/m2) were studied at Washington University School of Medicine, St. Louis, MO. Results: VLDL-TG secretion rate was approximately double (P < 0.05) in postmenopausal women and men compared with premenopausal women but not different in postmenopausal women and men. The secretion rate of VLDL-apoB-100 was not different in pre- and postmenopausal women but was greater (P < 0.05) in men than in women. Conclusions: Endogenous ovarian sex steroids are responsible for sexual dimorphism in VLDL-TG secretion, whereas VLDL-apoB-100 secretion is not regulated by female reproductive hormones.

scholarly journals Low-density lipoprotein is the major carrier of lipid hydroperoxides in plasma. Relevance to determination of total plasma lipid hydroperoxide concentrations

1996 ◽  
Vol 313 (3) ◽  
pp. 781-786 ◽  
Author(s):  
Jaffar NOUROOZ-ZADEH ◽  
Jarad TAJADDINI-SARMADI ◽  
K. L. Eddie LING ◽  
Simon P. WOLFF
Keyword(s):  
Total Lipid ◽  
Xylenol Orange ◽  
Low Density Lipoprotein ◽  
Lipid Hydroperoxide ◽  
Plasma Lipid ◽  
Density Lipoprotein ◽  
Ldl Oxidation ◽  
Lipid Hydroperoxides ◽  
Very Low Density Lipoprotein ◽  
Low Density

High-density lipoprotein (HDL) has been proposed as the principal carrier of hydroperoxides in plasma, based upon data gathered with an HPLC-chemiluminescence technique. To test this hypothesis we have measured total lipid hydroperoxides in native plasma using the ferrous oxidation in Xylenol Orange (FOX) assay and then fractionated plasma into very-low-density lipoprotein, low-density lipoprotein (LDL) and HDL fractions. Hydroperoxides were found to accumulate principally (more than 65%) in LDL, as judged by hydroperoxide content per amount of protein or cholesterol, or expressed as a proportion of total hydroperoxide in plasma. Plasma was also incubated at 37 °C in the presence and absence of 2,2´-azo-bis-(2-amidinopropane) hydrochloride (AAPH), an azo-initiator of lipid peroxidation. The majority of hydroperoxides generated in plasma were recovered in the LDL fraction. Furthermore, when isolated lipoproteins were subject to oxidation initiated by AAPH, very-low-density lipoprotein and LDL showed the greatest propensity for hydroperoxide accumulation, whereas HDL seemed relatively resistant. Estimates for plasma and LDL peroxidation based upon techniques which measure total lipid hydroperoxides suggest that levels of hydroperoxides in plasma and LDL are far higher than that those estimates generated by ostensibly more selective techniques. Higher levels of hydroperoxides in LDL than those reported by HPLC-chemiluminescence also seem in greater accordance with other available data concerning LDL oxidation.

A role for hepatic leptin signaling in lipid metabolism via altered very low density lipoprotein composition and liver lipase activity in mice

Hepatology ◽  
2012 ◽  
Vol 57 (2) ◽  
pp. 543-554 ◽  
Author(s):  
Frank K. Huynh ◽  
Ursula H. Neumann ◽  
Ying Wang ◽  
Brian Rodrigues ◽  
Timothy J. Kieffer ◽  
...  
Keyword(s):  
Lipid Metabolism ◽  
Lipase Activity ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Very Low Density Lipoprotein ◽  
Low Density ◽  
Leptin Signaling ◽  
Lipoprotein Composition

Lipoprotein Profiles in a Family with Two Mutants of Apolipoprotein E: Possible Association with Hypertriglyceridaemia but Not with Dysbetalipoproteinaemia

1994 ◽  
Vol 86 (3) ◽  
pp. 323-329 ◽  
Author(s):  
Shui-Ping Zhao ◽  
Arn M. J. M. Van den Maagdenberg ◽  
Ton F. F. P. Vroom ◽  
Ferdinand M. Van't Hooft ◽  
Jan A. Gevers Leuven ◽  
...  
Keyword(s):  
Apolipoprotein E ◽  
Plasma Cholesterol ◽  
Low Density Lipoprotein ◽  
Family Members ◽  
Plasma Lipid ◽  
Density Lipoprotein ◽  
Molar Ratio ◽  
Very Low Density Lipoprotein ◽  
Low Density ◽  
Lipoprotein Profiles

1. The plasma lipoprotein profiles of eight members of a Dutch pedigree spanning three generations where two rare apolipoprotein E mutants, APOE*3(Cys-112→Arg; Arg-251→Gly) and APOE*2(Val-236 →Glu), segregate were analysed to determine whether the APOE mutants were associated with dyslipidaemia. 2. The proband, a 51-year-old Caucasian male, was a carrier of APOE*3(Cys-112→Arg; Arg-251→Gly) and his spouse was a carrier of APOE*2(Val-236→Glu). Four other family members were carriers of one or both of the mutant APOE genes. 3. The plasma cholesterol and triacylglycerol concentrations were markedly elevated in the proband and were classified as type IV hyperlipoproteinaemia. The plasma triacylglycerol concentration was moderately increased in a sister, who was a carrier of APOE*3(Cys-112→Arg; Arg-251→Gly), and in the son, who was a compound heterozygote for both mutant APOE alleles. Normal plasma lipid levels were observed in all other family members. In the plasma samples of the proband and his family members β-very-low-density lipoprotein was not detectable and the molar ratio of very-low-density lipoprotein-cholesterol to very-low-density lipoprotein-triacylglycerol was less than 0.9. The concentration of intermediate-density lipoprotein was within normal limits. 4. None of the family members carrying APOE*3-(Cys-112→Arg; Arg-251→Gly) and/or APOE*2(Val-236→Glu) exhibited lipoprotein abnormalities characteristic of familial dysbetalipoproteinaemia, although three family members carrying APOE*3-(Cys-112→Arg; Arg-251→Gly) showed hypertriglyceridaemia.

An in vitro model to study lipolysis of rat hepatic very low density lipoprotein using cardiac lipoprotein lipase

1984 ◽  
Vol 62 (11) ◽  
pp. 1076-1080 ◽  
Author(s):  
Louise Brissette ◽  
Simon-Pierre Noël
Keyword(s):  
Lipase Activity ◽  
In Vitro Model ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Very Low Density Lipoprotein ◽  
Low Density ◽  
Triacylglycerol Hydrolysis ◽  
Vitro Model ◽  
Fasted Rats

The purpose of this work was to design an in vitro model for studying the lipolysis of very low density lipoprotein (VLDL) under conditions that approximate those likely to exist in the rat circulation. We first measured the total lipase activity available in the circulation of normal fasted rats. Knowing the VLDL-triacylglycerol concentration and the circulating time of VLDL in rat serum, we calculated that incubating 80 mU of lipoprotein lipase activity per milligram of VLDL triacylglycerols at 37 °C, for 50 min, approximated the in vivo conditions of lipolysis in normal fasted rats. Under these conditions, different concentrations of albumin were tested. The degree of lipolysis gradually increased from 25 ± 10% without albumin to 75 ± 5% (mean ± SD, n = 3) with 4% albumin. No further increase occurred above 4% albumin. The rate of triacylglycerol hydrolysis was faster with VLDL having a high triacylglycerol/protein ratio. However after 50–60 min of incubation, the extent of hydrolysis tended to become similar for all VLDL (75–90%). This suggests that the rate of VLDL hydrolysis differs from one particle to another (depending on the size), but the extent of hydrolysis ends up being approximately the same. Furthermore, addition of high density lipoprotein to the incubation medium did not affect the rate nor the extent of triacylglycerol hydrolysis. We conclude that a large proportion of VLDL triacylglycerols can be hydrolyzed in the normal fasted rat if there is no limitation in the capacity of fatty acid removal from the lipolysis site. The physiological significance of these results obtained in vitro is discussed.

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