Metabolism of triglyceride-rich lipoproteins during alimentary lipemia.

Abstract

The metabolism of chylomicron remnants and VLDL was studied in healthy controls and normo-(NTG) and hypertriglyceridemic (HTG) patients with coronary artery disease after intake of an oral fat load. Specific determination of apo B-48 and B-100 enabled separation of the respective contribution of the two lipoprotein species. The postprandial plasma levels of small (Sf 20-60) and large (Sf 60-400) chylomicron remnants increased in controls and NTG patients. In contrast, only large chylomicron remnants increased in the HTG patients. An increase of large VLDL was seen in response to the oral fat load in all groups, whereas small VLDL were either unchanged in the controls and the NTG patients, or decreased in the HTG patient group. The whole plasma concentration of C apolipoproteins was essentially uninfluenced by the oral fat load, whereas the content in large triglyceride-rich lipoproteins paralleled the apo B elevations in controls and NTG patients. An even more prominent increase of apo B in large triglyceriderich lipoproteins in the HTG group was not accompanied by an increase of C apolipoproteins. These findings indicate that chylomicrons compete with VLDL for removal of triglycerides by lipoprotein lipase and that the postprandial metabolism of triglyceride-rich lipoproteins is severely defective in hypertriglyceridemia. (J. Clin. Invest. 1993.91:748-758.) Key words: chylomicron remnants * very low density lipoprotein -apolipoprotein B-48 * apolipoprotein B-100 * apolipoprotein C-I1

Methodology for studying postprandial lipid metabolism

“…When groups are studied where there is greater variability in body weight (i.e., with large range of body weights and therefore blood volumes), it may be preferable to use the alternative approach in which the amount of nutrients/ energy in the test meal is estimated as unit amount per kg body weight (Cohn et al, 1988a(Cohn et al, , b, 1993Lopez-Miranda et al, 1997;Shishebor et al, 1999) or body surface area (Weintraub et al, 1988;Karpe et al, 1993). Although this may be considered a more valid approach because it takes account of greater blood volume in larger subjects, it should be considered that in adults the main variable influencing body weight is variation in fat mass.…”

“…The concept behind this type of approach is that a large fat load will overwhelm the normal capacity of lipoprotein handling postprandially and thus, will reveal those subjects with reduced capacity (linked to disturbed metabolism and/or diet), whereas a smaller meal may be insufficient to challenge the metabolic capacity to its limit. Cohen et al (1988) 40-120 Weintraub et al (1988) 50 g/m 2 body surface area Cohn et al (1988aCohn et al ( , 1993 1 g/kg body weight Schneeman (1990) 43 Cara et al (1992) 70 Karpe et al (1993) 50 g/m 2 body surface area Dubois et al (1994a, b) 31/42, 45 Zampelas et al (1994) 40 Frayn et al (1994) 80 Murphy et al (1995) 20-80 Fielding et al (1996) 61 Lopez-Miranda et al (1997) 1 g/kg body weight Lovegrove et al (1997) 82 Roche and Gibney, 1997;Roche et al, 1998a, b 40 Dubois et al (1998 15-50 Couillard et al (1998) 60/m 2 Shishebor et al (1999) 0.5 g/kg body weight Guerci et al (2001) 80 Harbis et al (2001) 40 Dallongeville et al (2002) 70 Harbis et al (2004) 28-29…”

“…As mentioned above, postprandial changes in triglyceridaemia are essentially because of TRLs, that is, both intestinally derived chylomicrons and hepatically derived VLDL (Cohn et al, 1993;Schneeman et al, 1993;Karpe et al, 1993Karpe et al, , 1995Roche et al, 1998a;Mekki et al, 1999;Harbis et al, 2001Harbis et al, , 2004. The two main components of these TRL species are triglycerides and apoB.…”

“…Because all classes of lipoproteins are interrelated, every kind of lipoprotein can be altered postprandially (Patsch et al, 1983;Weintraub et al, 1987;Cohn et al, 1988a, b;Karpe et al, 1993Karpe et al, , 1995Dubois et al, 1994Dubois et al, , 1998. If the full pattern of lipoprotein parameters, including LDL and HDL particles, is required, these can be separated from plasma samples by a more prolonged ultracentrifugation and components assayed (triglycerides, cholesterol and phospholipidsapolipoproteins).…”

Insulin and non-esterified fatty acid relations to alimentary lipaemia and plasma concentrations of postprandial triglyceride-rich lipoproteins in healthy middle-aged men

“…Fasting plasma concentrations of cholesterol and triglycerides in VLDL, LDL and HDL were determined by a combination of preparative ultracentrifugation, precipitation of apo B-containing lipoproteins and lipid analyses [17]. Triglyceride-rich lipoproteins were subfractionated by cumulative density gradient ultracentrifugation [18]. Consecutive runs calculated to float Sf over 400, Sf 60±400 and Sf 20±60 particles were made and the Sf 12±20 fraction was recovered by slicing the tube after the Sf 20±60 lipoproteins had been aspirated.…”