The intestinal absorption and metabolism of micellar solutions of lipids

doi:10.1016/0926-6542(64)90005-8

Biochimica et Biophysica Acta (BBA) - Specialized Section on Lipids and Related Subjects

Volume 84, Issue 4, 5 August 1964, Pages 412-423

https://doi.org/10.1016/0926-6542(64)90005-8 Get rights and content

Abstract

1.
1. The absorption of micellar solutions of conjugated bile salts and labeled fatty acids and/or monoglycerides have been demonstrated employing intestinal slices and brush border preparations.
2.
2. the absorption of the lipid from these solutions appears to be enzymical energetically independent and occurs from these solutions appears to be enzymically and energetically independent and occurs at a faster rate than corresponding solutions bound to albumin or in the emulsified state.
3.
3. The resynthesis of the abosorbed micellar lipids into triglycerides has been demonstrated and the relationship of these findings to the mechanism of the absorption of fats in vivo discussed.

References (31)

J.M. Johnston
J. Biol. Chem.
(1959)
B. Clark et al.
Biochim. Biophys. Acta
(1961)
J.R. Senior et al.
J. Biol. Chem.
(1962)
J.M. Johnston et al.
Biochim. Biophys. Acta
(1962)
J.M. Johnston et al.
Acta Chem. Scand.
(1963)
D. Miller et al.
Anal. Biochem.
(1961)
H.C. Tidwell et al.
Arch. Biochem. Biophys.
(1960)
J.R. Senior et al.
J. Clin. Invest.
(1963)
F.H. Mattson et al.
J. Biol. Chem.
(1962)
E. Overton
Arch. Ges. Physiol.
(1902)

J.L. Brown et al.

Biochim. Biophys. Acta

(1963)

B. Borström, F. Kern and K. Ekbom, unpublished...

B. Clark et al.

Nature

(1960)

A.M. Dawson et al.

J. Clin. Invest.

(1960)

C.M. Dowes et al.

J. Physiol. London

(1956)

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The intestine is a primary site of nutrient absorption and a critical defense barrier against dietary-derived mutagens, carcinogens, and oxidants. Accumulation of oxidants like peroxidized lipids in the gut lumen can contribute to impairment of mucosal metabolic pathways, enterocyte dysfunction independent of cell injury, and development of gut pathologies, such as inflammation and cancer. Despite this recognition, we know little of the pathways of intestinal transport, metabolism, and luminal disposition of dietary peroxides in vivo or of the underlying mechanisms of lipid peroxide-induced genesis of intestinal disease processes. This chapter summarizes our current understanding of the determinants of intestinal absorption and metabolism of peroxidized lipids. I will review experimental evidence from our laboratory and others (Table 1) supporting the pivotal role that glutathione (GSH) and reduced nicotinamide adenine dinucleotide phosphate (NADPH) play in mucosal transport and metabolism of lipid hydroperoxides and how reductant availability can be compromised under chronic stress such as hypoxia, and the influence of GSH on oxidative susceptibility, and redox contribution to genesis of gut disorders. The discussion is pertinent to understanding dietary lipid peroxides and GSH redox balance in intestinal physiology and pathophysiology and the significance of luminal GSH in preserving the integrity of the intestinal epithelium.
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Citation Excerpt :
Because there is one apoB48 molecule per particle and because the efficiency of apoB48 incorporation into the particle is highly dependent on lipid availability in the intestinal cell, the increased number of lipoprotein particles may be because of more efficient intestinal fat absorption in the FF hamster, or other factors. The former possibility is less likely because fat absorption is known to be highly efficient and is rarely the rate-limiting factor in determining the postprandial TG excursion (48, 49). A series of ex vivo experiments were also conducted in enterocytes from fasted hamsters that allowed us to address the mechanism, independent of dietary fat consumption.
Insulin-resistant states are characterized by hypertriglyceridemia, predominantly because of overproduction of hepatic very low density lipoprotein particles. The additional contribution of intestinal lipoprotein overproduction to the dyslipidemia of insulin-resistant states has not been previously appreciated. Here, we have investigated intestinal lipoprotein production in a fructose-fed hamster model of insulin resistance previously documented to have whole body and hepatic insulin resistance, and hepatic very low density lipoprotein overproduction. Chronic fructose feeding for 3 weeks induced significant oversecretion of apolipoprotein B48 (apoB48)-containing lipoproteins in the fasting state and during steady state fat feeding, based on (a)in vivo Triton WR1339 studies of apoB48 production as well as (b) ex vivo pulse-chase labeling of intestinal enterocytes from fasted and fed hamsters. ApoB48 particle overproduction was accompanied by increased intracellular apoB48 stability, enhanced lipid synthesis, higher abundance of microsomal triglyceride transfer protein mass, and a significant shift toward the secretion of larger chylomicron-like particles. ApoB48 particle overproduction was not observed with short-term fructose feeding orin vitro incubation of enterocytes with fructose. Secretion of intestinal apoB48 and triglyceride was closely linked to intestinal enterocyte de novo lipogenesis, which was up-regulated in fructose-fed hamsters. Inhibition of fatty acid synthesis by cerulenin, a fatty acid synthase inhibitor, resulted in a dose-dependent decrease in intestinal apoB48 secretion. Overall, these findings further suggest that intestinal overproduction of apoB48 lipoproteins should also be considered as a major contributor to the fasting and postprandial dyslipidemia observed in response to chronic fructose feeding and development of an insulin-resistant state.
The lymphatic absorption of lipids is normalized by enteral phosphatidylcholine infusion in ovariectomized rats with estrogen replacement
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Estrogen (ES) replacement previously was shown to decrease the lymphatic absorption of fat with a simultaneous decrease in phospholipid (PL) output in ovariectomized (OX) rats. The present study was conducted to investigate whether intraduodenal infusion of phosphatidylcholine (PC) would normalize the absorption of ¹⁴C-linoleic acid (¹⁴C-LA) and unlabeled oleic acid (OA) in OX rats implanted s.c. with an estradiol pellet (OXE; 25 μg/day/rat), compared with OX rats implanted with a placebo pellet (OXP). Additionally, this study examined whether ES would alter the rate of fatty acid esterification into various lipids in the intestinal mucosa. Both groups were meal-trained and pair-fed for 7 weeks. Each rat with a lymph cannula was infused at 3 mL/hr via a duodenal catheter with a lipid emulsion containing ¹⁴C-LA and triolein (380 μmol) with or without PC (41 μmol). Lymph was collected hourly for 8 hr via a lymph fistula. Without PC infusion, the total lymphatic absorption of ¹⁴C-LA was significantly lower (26.0 ± 3.4% dose) in OXE rats than in OXP rats (31.8 ± 2.0% dose) with a close parallel decrease in OA output at 2 hr and thereafter. Also, the total lymphatic secretion of PL was significantly lower in OXE rats (26.5 ± 2.4 μmol) compared with OXP rats (37.1 ± 4.1 μmol). When PC was infused, the total lymphatic absorption of ¹⁴C-LA and OA in OXE rats was restored completely to normal, whereas PC infusion had no effect on the lymphatic outputs of ¹⁴C-LA or OA in OXP rats. The lymphatic outputs of PL were enhanced markedly in both groups with PC infusion. The hourly output of PL was correlated highly with the absorption of ¹⁴C-LA (r = 0.81) and OA (r = 0.78). Regardless of whether lysophosphatidylcholine (lysoPC) was present in the intestinal lumen, the rates of mucosal ¹⁴C-LA incorporation into triglycerides (TG), PL, and other lipids were not affected by ES treatment. The results indicate that the slower rate of lymphatic absorption of fatty acids in ES-treated rats is not due to alteration in mucosal fatty-acid esterification, but to a limited availability of PL to the enterocyte. This may be associated with an inhibitory effect of ES on the hepatic secretion of PL via the biliary route.
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Effects of zinc (Zn) and essential fatty acid (EFA) deficiencies on the rates of lymphatic absorption of vitamin A and output of phospholipid (LP) were investigated. Twenty male rats were divided into four groups in a 2 × 2 factorial design: (1) Zn and EFA deficient (−Zn−EFA), (2) Zn deficient and EFA adequate (−Zn+EFA), (3) Zn adequate and EFA deficient (+Zn−EFA), and (4) Zn and EFA adequate (+Zn+EFA). At 9 weeks, rats with lymph cannula were infused at 3 mL/hr via an intraduodenal catheter with a triolein emulsion containing 5.4 μCi ³H-retinol (³H-ROH). The lymphatic absorption of ³H-ROH was lowered markedly in −Zn rats. The rates of ³H-ROH absorption in −Zn−EFA and −Zn+EFA groups were 0.44 and 0.58 nmol/hr, respectively, compared with 0.78 nmol/hr in +Zn−EFA and 0.98 nmol/hr in +Zn+EFA rats. Dietary EFA alone produced only a mild effect on ³H-ROH absorption. Similarly, the effect of dietary Zn on the lymphatic output of PL was more pronounced than that of EFA. The output of PL was correlated closely with the absorption of ³H-ROH (r = 0.90). No interaction between dietary Zn and EFA was noted in the lymphatic ³H-ROH absorption or PL output. The lymphatic output of linoleic acid (LA) or arachidonic acid (AA) in −Zn rats was approximately 50% of that in their respective Zn adequate controls. However, the PL output in −Zn rats was not related to the amount of EFAs released in the lymph. Dietary Zn had no effect on the rate of intestinal PL synthesis, as determined by incubating a micellar solution of lysophosphatidylcholine (LPC) and ³H-palmitic (³H-PA) or ³H-arachidonic acid (³H-AA) in a jejunal loop in situ. Dietary EFA also did not affect the rate of ³H-PA incorporation into PL. However, the rate of ³H-AA incorporation into PL was significantly lower in −EFA rats than in +EFA rats. In −EFA rats, more ³H-AA was distributed in phosphatidylethanolamine and less in phosphatidylcholine, compared with +EFA groups. The findings indicate that Zn deficiency has a pronounced adverse effect on the lymphatic absorption of retinol, with no interactive effect with dietary EFA. The lowering of ³H-retinol absorption in −Zn rats is correlated highly with a decrease in lymphatic PL output. The decreased PL output is not due to a defect in the intestinal acylation of LPC but probably to impaired biliary secretion of PL into the intestine.
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The intestinal absorption and metabolism of micellar solutions of lipids

Abstract

J. Biol. Chem.

Biochim. Biophys. Acta

J. Biol. Chem.

Biochim. Biophys. Acta

Acta Chem. Scand.

Anal. Biochem.

Arch. Biochem. Biophys.

J. Clin. Invest.

J. Biol. Chem.

Arch. Ges. Physiol.

Biochim. Biophys. Acta

Nature

J. Clin. Invest.

J. Physiol. London