Very low density lipoproteins in intestinal lymph: origin, composition, and role in lipid transport in the fasting state

Abstract

A B S T R A C T The transport of endogenous lipids in the lipoproteins of mesenteric lymph was studied in fasting rats with mesenteric lymph fistulas. The lymph was found to contain, in addition to chylomicrons (Sf > 400), a significant amount of another, more dense, triglyceride-rich fraction, the very low density lipoproteins (VLDL), which showed a peak Sf of 102. The VLDL differed from chylomicrons not only in flotation, but also in per cent lipid composition and electrophoretic mobility in agarose gel. The VLDL fraction was found to contain 47% of the triglyceride and 54% of the cholesterol of fasting lymph and, in the fasting state, was the major lipoprotein species present.When cholestyramine resin was administered intraduodenally, or bile flow was acutely diverted from the intestine, it was demonstrated that the lipids in lymph VLDL, like those in chylomicrons, were derived from the intestine and bile. These data indicate that the VLDL in intestinal lymph are not derived from the plasma but are of intestinal origin.Because certain properties of lymph VLDL were similar to those reported for plasma VLDL (per cent lipid composition, flotation coefficient, and continuing entry into plasma in the fasting state), additional comparisons between these fractions were made. Although lymph VLDL moved to the as region in agarose gel, when they were mixed with VLDL-free serum immediately before electrophoresis they showed the a, mobility of rat serum VLDL. Furthermore, immunoelectrophoretic comparison of partially delipidated lymph and serum VLDL revealed that these fractions shared in

The ddY mouse: a model of postprandial hypertriglyceridemia in response to dietary fat

“…FFA released from CM-TG by LPL is converted efficiently to VLDL-TG in the liver (36)(37)(38). In rats, VLDL has been found in mesenteric lymph ( 39 ), and CM and VLDL are packed differently in the intestine ( 40 ), suggesting that increased VLDL production in the small intestine may occur in ddY mice.…”

Chylomicron remnants are increased in the postprandial state in CD36 deficiency

“…Even though this result was observed in an animal model of insulin resistance model, it was suggested that the endogenous production of fatty acids might influence the apoB-48-containing lipoprotein secretion in the small intestine. Endogenous lipids were secreted mainly in the fasting state in the size of VLDL (29), and almost half of total lymphatic TG was derived from endogenously synthesized sources in the postprandial state (30). It is known that PL in CM particles originates from the intestinal epithelium (31); therefore high PL contents of lipoproteins smaller than CM in size indicate that these lipoproteins might be derived from the endogenous source.…”

“…From the tubes that were supposed to contain CM remnants (tubes No. 11,14,17,20,23,26,29,32,35), 15 ml of flow-through (containing ?10 mg protein) was taken, subjected to 4-12% SDS-polyacrylamide gel electrophoresis (SDS-PAGE, TEFCO, Tokyo, Japan) and transferred onto the Immobilon-P Transfer membrane (Millipore Corp., Billerica, MA). This membrane was incubated with anti-human apoB-48 antibody and subsequently with anti-mouse IgG antibody (NA931V, GE Healthcare, Backinghamshire, UK).…”

Apoprotein B in fasting and postprandial human jejunal mucosa.

“…The intestine as a source of plasma lipoReceived for publication 18 August 1975 and in revised form 13 November 1975. proteins was first suggested by biochemical studies which showed that the intestine could incorporate radioactive amino acids into lymph and plasma lipoproteins (1)(2). Studies of the composition of intestinal lymph indicated that the intestine can produce lipoproteins other than chylomicrons (3)(4)(5). Electron microscopic studies of rats have implicated the columnar absorptive cells as the particular site involved in intestinal very low density lipoprotein (VLDL) 1 production (6).…”