Site of bile acid absorption in the rat

Bile acid absorption was measured in the small intestine of the rat using⁹¹Y as a nonabsorbed reference substance. Some 50% of the secreted bile acids were absorbed in the proximal half of the small intestine. In situ incubations of ligated intestinal segments into which tauro(¹⁴C-carbonyl)cholic acid was introduced confirmed the considerable uptake of bile acids in the jejunum. The in situ experiments indicated that serosal transport is the limiting stage of bile acid absorption in the jejunum but not in the ileum. Increasing bile acid concentrations in the in situ experiments did not affect the percentage disappearance of dose from the jejunum but reduced the percentage mucosal uptake in the ileum. It is concluded that, in the rat, the proximal small intestine is as important in the absorption of bile acids as the distal small intestine.     

In vitro and in vivo effects of exogenous lipids on the enzymatic hydrolysis of rat bile phospholipids

The addition of total phospholipids, phosphatidylcholines, triglycerides, cholesterol or glycerol to incubation media containing rat pancreatic juice and bile labeled with [9,10³H₂] oleic acid (90% of the radioactivity present as phospholipids) had no effect on the hydrolysis of bile endogenous phospholipids. The introduction of 2 or 10 mg of phosphatidylcholines and 0.5 ml of bile (≈ 1.5 mg of phospholipids)into the rat upper duodenum decreased the rate of absorption of rative bile phospholipids. It was not followed by an increase of free fatty acids released from biliary phospholipids in the intestinal lumen. The introduction of bile (0.5 ml) and small amounts of triolein (1.4–3.5 mg) into the duodenum had little effect on the rate of hydrolysis and absorption of native bile phospholipids, but caused a reduced absorption of the free fatty acids released or those coming from initial nonphosphorus biliary lipids. The introduction of bile (0.5 ml) and large amounts of triolein (30 mg) into the duodenum increased the rates of hydrolysis and absorption of endogenous bile phospholipids. These observations suggest that luminal lipid components can modify the organization of luminal micelles and, consequently, the action of the pancreatic phospholipase A₂ and the absorption of bile lipids.     

Intestinal absorption of unconjugated dihydroxy bile acids: Non-mediation by the carrier system involved in long chain fatty acid absorption

Experiments were performed using isolated mucosal cells from the rat jejunum or using the perfused jejunum in the anesthetized rat to test whether lipophilic unconjugated dihydroxy bile acids are absorbed from the proximal small intestine via the same carrier mechanism involved in the uptake of long chain fatty acids. With isolated jejunal mucosal cells, the cellular uptake rate of deoxycholic acid or chenodeoxycholic acid increased linearly with time, showed no evidence of saturation, and was not decreased by the presence of a monospecific antibody to the membrane fatty acid binding protein. In contrast, oleate uptake was saturable, was inhibited by the same antibody, but was not affected by the presence of chenodeoxycholic acid or deoxycholic acid. Bile acid uptake by isolated enterocytes occurred at one-eighth the rate of fatty acid uptake if expressed in relation to total solute concentration; if expressed in relation to monomeric concentration, initial bile acid uptake was four orders of magnitude slower than fatty acid uptake. In the isolated perfused jejunal segment, chenodeoxycholic acid and deoxycholic acid uptake was not influenced by the presence of the antibody to membrane fatty acid binding protein, whereas absorption of oleate was inhibited by more than 70%. These experiments indicate that absorption of unconjugated lipophilic dihydroxy bile acids in the rodent jejunum does not involve the carrier mediated uptake mechanism involved in the absorption of long chain fatty acids—the mechanism is likely to be passive nonionic diffusion.     

Preferential metabolism of linoleic acid by five-day-old barley shoots

The degradation of exogenous radioactively labeled fatty acids by 5-day-old barley shoots was examined. [1-¹⁴C] Linoleic acid was observed to be degraded 7 times faster than [1-¹⁴C] oleic acid and 5 times faster than [1-¹⁴C] palmitic acid. The pathway of degradation was determined by identifying the water-soluble products and determined to be β-oxidation. During a 15 min incubation, the barley shoots took up 0.91 nmol/g fresh wt of linoleic acid, of which 0.16 nmol/g fresh wt was incorporated into glutamic acid, 0.07 nmol/g fresh wt into succinic acid and 0.002 nmol/g fresh wt into carbohydrates. By 30 min, additional TCA cycle intermediates, especially malic acid, were detected. Palmitic acid and oleic acid were broken down to the same products. The rates of uptake and the distribution of label into lipids were determined. The uptake of label by the tissue was similar for all 3 fatty acid substrates. Label from linoleic, oleic and palmitic acids was found to be incorporated into similar lipids, primarily phosphatidylcholine (PC), and the extent of incorporation was comparable. Although all 3 fatty acid substrates were broken down by β-oxidation, the reason for the more rapid degradation of linoleic acid was not established. It does not appear to be related to uptake of substrate or incorporation of label into lipids.     

Is there an entero-hepatic circulation of the bile phospholipids?

Bile previously labeled with tritiated oleic acid (the main radioactivity was on bile phospholipids) was mixed with pure isolated phospholipids previously labeled with¹⁴C oleic acid; this mixture was perfused during 6 or 23 hr into the duodenum of test rats bearing a bile fistula. At the time of decapitation, in the small intestine a large hydrolysis of the¹⁴C phospholipids was found. In contrast no bile phospholipid hydrolysis was observed. In the collected bile samples of the test rats, no¹⁴C could be detected (this means a very large decrease of the¹⁴C fatty acids specific activities by the body fatty acids), and the tritiated fatty acids specific activities were only 2.5–12 times lower than in the perfused bile. These results can be explained, assuming that the bile phospholipids enter in an entero-hepatic circulation and are preserved from the dilution in a large pool of lipids.     

Lecithin inhibits fatty acid and bile salt absorption from rat small intestine in vivo

During digestion of a fatty meal, long chain free fatty acids (FFA) and lecithin are among the lipids solubilized in intestinal contents as mixed micelles with bile salts. We hypothesized that if lecithin were not hydrolyzed, the mixed micelles would be abnormal, and absorption of FFA and bile salts would be depressed. To test this hypothesis, isolated segments of rat small intestine were infused in vivo with micellar solutions of 2 mMolar linoleic acid and 10 mMolar taurocholate to which was added 3 mMolar 1-palmitoyl, 2-oleoyl lecithin (a common lecithin in bile and food), or 1-palmitoyl lysolecithin (the hydrolytic product of lecithin). Absorption of FFA and bile salt was measured under steady state conditions using a single-pass technique. Lecithin depressed the rate of FFA absorption by 40% (p<0.025) in jejunal and ileal segments whereas lysolecithin was associated with normal rates of FFA absorption. Lecithin also reduced taurocholate absorption from the ileum by 30% (p<0.05). These data support the idea that lecithin may depress FFA and bile salt absorption from the small intestine in pancreatic insufficiency. The following trivial names are used: lecithin (1,2-diacyl-sn-glycero-3-phosphorylcholine); lysolecithin (1-acyl-sn-glycero-3-phosphorylcholine).     

Hydrolysis of biliary phospholipids in the upper small intestine of the chick

Chick endogenous phospholipids were doubly labeled by an intravenous injection of [³²P] phosphate and [1-¹⁴C] oleic acid, and the free fatty acid and phospholipid fraction of gall bladder bile and in contents of upper small intestine were analyzed 4 days later. There was evidence of hydrolysis of biliary phosphatidylcholine to lysophosphatidylcholine in the duodenum and jejunum, but this did not account for the pronounced increase in the¹⁴C radioactivity of the free fatty acids relative to the³²P phospholipid radioactivity between bile and upper intestinal segments. It is suggested that phosphatidylcholine is largely absorbed in the duodenum of the chick while the remainder is progressively hydrolyzed and absorbed.     

Effect of lecithin on jejunal absorption of micellar lipids in man and on their monomer activity in vitro

The effect of lecithin on jejunal absorption of fatty acids and octadecenoylglycerol was studied in healthy volunteers with a jejunal perfusion system which excluded pancreatic and biliary secretions from the test segment. Lecithin significantly reduced the absorption of oleic acid (P<0.05) and octadecenoylglycerol (P<0.01), while it had no effect on the absorption of ricinoleic acid. In vitro, lecithin reduced monomer activities of all three lipids; the changes were greater for oleic acid and octadecenoylglycerol than for ricinoleic acid (P<0.02). From these data it is concluded that lecithin reduces monomer activity of fatty acids in mixed micellar solutions and that it can thereby reduce the absorption rates of micellar lipids. Intact lecithin is not absorbed under these conditions. Maldigestion of lecithin in pancreatic insufficiency may, therefore, aggravate the steatorrhea observed in this condition.     

Influence of fatty alcohol and other fatty acid derivatives on fatty acid uptake into rat intestinal epithelial cells

We investigated the influence of various substrates on the uptake of long-chain fatty acid into IEC-6, rat intestinal epithelial cell line. The uptake of [³H]oleic acid into IEC-6 cells was a saturable function of the oleic acid concentration. Long-chain fatty acids significantly inhibited the oleic acid uptake into IEC-6 cells and shorter-chain fatty acids had little or no effect. Various fatty acid esters suppressed the oleic acid uptake into IEC-6. Fatty alcohols also inhibited oleic acid uptake into IEC-6 and the length of the carbon chain played an important role. These results suggest that long-chain fatty acid uptake was inhibited by the substrates which had a structure similar to long-chain fatty acids, especially those with a long carbon chain. At least two molecules, fatty acid translocase and fatty acid transport protein type 4, which are considered to be involved in the long-chain fatty acid transport into the cell, were expressed on IEC-6 cells, supporting the existence of the carrier-mediated system of long-chain fatty acid transport on IEC-6 cells.     

Reduced secretion of triacylglycerol in CaCo-2 cells transfected with intestinal fatty acid-binding protein

The fatty acid-binding proteins are hypothesized to be involved in cellular fatty acid transport and trafficking. We established CaCo-2 cells stably transfected with intestinal fatty acid-binding protein (I-FABP) and examined how the expression of this protein may influence fatty acid metabolism. I-FABP expression was detectable in I-FABP-transfected cells, whereas parent CaCo-2 cells as well as mock-transfected cells failed to express detectable levels of I-FABP mRNA or protein at any stage of differentiation. For studies of lipid metabolism, cells were incubated with [¹⁴C]oleic acid in taurocholate micelles containing monoolein, and distribution of labeled fatty acid in cellular and secreted lipids was examined. In one transfected cell clone, expressing the highest level of I-FABP, labeled cellular triacylglycerol increased approximately twofold as compared to control cells. The level of intracellular triacylglycerol in two other I-FABP-transfected clones resembled that of control cells. However, secretion of triacylglycerol was markedly reduced in all the I-FABP-expressing cell lines. Our data suggest that increased expression of I-FABP leads to reduced triacylglycerol secretion in intestinal cells.     

Tissue culture of cocoa bean (Theobroma cacao L.): Incorporation of fatty acids into lipids of cultured cells

Suspension cell cultures of cocoa bean rapidly incorporated palmitic, stearic, oleic and linoleic acids into cellular lipids. Thus, 75 and 20% of [1-¹⁴C] palmitic acid was incorporated into polar lipids and triglycerides, respectively, after 48 hr. When [1-¹⁴C] oleic and [1-¹⁴C] linoleic acid were added separately, polar lipids consistently contained most of the radioactive fatty acids. Ca. 60% of the stearic acid accumulated as unesterified fatty acid in the cells. Palmitic and stearic acid were not desaturated, but oleic acid and linoleic acid were further desaturated. The kinetics of conversion of oleic acid and linoleic acid suggested a sequential desaturation pathway of 18∶1→18∶2→18∶3 in cocoa bean cell suspensions.     

Different metabolism of saturated and unsaturated long chain plasma free fatty acids by intestinal mucosa of rats

During fat absorption, unsaturated long chain fatty acids are esterified at a higher rate than saturated fatty acids of similar chain length. This phenomenon has been attributed to differences in the binding affinity of fatty acids to a cytosolic fatty acid-binding protein. As intestinal mucosa utilizes plasma free fatty acids as well, we investigated whether long chainplasma free fatty acids of different degree of saturation are metabolized also at different rates.³H-Palmitic and¹⁴C-linoleic acid complexed to rat serum were injected rapidly into a tail vein of fasting rats. One, 2 and 4 min later there was no difference between³H and¹⁴C-radioactivity in intestinal mucosa, suggesting equal initial uptake of the two labeled fatty acids from plasma. Despite their equal uptake, the incorporation of the isotopes into ester lipids was significantly different, however: at 2 min, 53.1±3.9% of³H and 73.8±4.6% of¹⁴C were recovered in ester lipids. Phospholipids and triglycerides accounted for most of the mucosal³H and¹⁴C. At 4 min, a similar distribution of isotopes in intestinal mucosal metabolites was found. These data show that despite equal initial uptake by intestinal mucosa unsaturated long chain fatty acids taken up from plasma are esterified to a higher and oxidized to a lower extent than saturated plasma free fatty acids. Unsaturated plasma free fatty acids, therefore, may provide a more important source of fatty acids for endogenous intestinal lipoprotein lipids than saturated plasma free fatty acids. It is speculated that the fatty acid binding protein might be operative not only in the intracellular transport and metabolism of luminal fatty acids but of plasma free fatty acids as well.     

Fatty acid and sterol specificity of cholesterol esterifying enzyme in developing rat brain

The properties and fatty acid and sterol specificity of cholesterol-esterifying enzyme (EC 3.1.1.13) in rat brain were studied. The enzyme utilized free fatty acid for esterification, and activity was maximal at pH 5.6. Exogenous ATP and CoA did not stimulate the incorporation of free fatty acids into sterol esters. Substrates dispersed in Tween 20 or Triton X-100 were just as effective as the substrates dissolved in acetone solution, while dispersion in propylene glycol or sodium taurocholate was not as effective. Snake venom phospholipase A₂ (EC 3.1.1.4) increased the esterification of cholesterol in the absence of added fatty acid. The fatty acid specificity data indicated that oleic and palmitic acids were the preferred fatty acids. Little or no esterification occurred in the presence of long chain fatty acids (C₂₀–C₂₄). Esterification of cholesterol with palmitate or stearate was not affected by the presence of oleic acid in the mixture. Thus, the nonrequirement of the brain-esterifying enzyme for a bile acid or for an amphiphile such as an unsaturated fatty acid suggests that micellar solubilization of the substrate is not essential for activity. Although the brain enzyme catalyzed the esterification of desmosterol, cholesterol was the preferred substrate. Neither lanosterol (C₂₉ sterols) nor Δ7-dehydrocholesterol was esterified to any significant extent. The presence of low concentrations of desmosterol increased cholesterol esterification slightly, while there was a concentration-dependent inhibition of demosterol esterification by cholesterol. These data on fatty acid and sterol specificity of the esterifying enzyme correlate well with the composition of sterol esters present in developing rat brain.     

Dietary linoleic, α-linolenic and oleic acids are oxidized at similar rates in rats fed a diet containing these acids in equal proportions

The objective of this study was to examine whether whole body oxidation rates of dietary linoleic, α-linolenic and oleic acids differ when the acids are provided in identical quantities. Male rats were fed for 10 wk a 15% fat (w/w) diet containing equal amounts of linoleic, α-linolenic and oleic acids (22.7, 23.0 and 23.2% of total fatty acids, respectively). At week 10, after overnight fasting, rats were intragastrically administered 20 μCi of either [1-¹⁴C]-labelled linoleic, α-linolenic or oleic acid in a 200-μL bolus of oil containing equal quantities of each fatty acid. The appearance of¹⁴CO₂ in expired air was then monitored hourly for 12h for each animal. A preliminary study had shown that growth and food consumption patterns in animals consuming the oil containing equal quantities of each of the fatty acids paralleled the patterns of animals that were self-selecting among separate diets, each of which contained one of the component oils. The appearance of¹⁴C, expressed as percent dose administered, peaked at 2–3 h post-dose for¹⁴C-labelled linoleic (5.28±0.37%/h), α-linolenic (6.92±0.51%/h) and oleic (5.98±0.44%/h) acids. Statistically these values were not significantly different. Cumulative¹⁴CO₂ excretion rates over 12 h were also similar for linoleic (27.2±0.9%), α-linolenic (26.8±1.2%) and oleic (25.9±1.2%) acids. The results suggest that the rat's capacity to oxidize 18-carbon unsaturated fatty acids is not affected by fatty acid unsaturation when these fatty acids are provided at equal dietary levels.     

Effects of a single ingestion of sodium taurocholate on esterified cholesterol concentration in liver and cholesterol turnover in the rat

The overall response of the rat’s cholesterol metabolism to a single ingestion of taurocholate (80 mg) was studied with the isotopic equilibrium method. The bile acid production, measured by the daily¹⁴CO₂ output of rats in isotopic equilibrium of [26-¹⁴C]-cholesterol, initially decreased and then increased. Conversely, the hepatic concentration of esterified cholesterol first increased and then decreased. Moreover, the ingestion of taurocholate increasing the intestinal absorption coefficient of dietary cholesterol increased the abosprtion and decreased the fecal excretion and the intestinal biosynthesis of cholesterol. The balance of these last effects is an excess cholesterol inflow. The classical hypothesis of negative feedback regulation of bile acid production fails to explain the observed biphasic effect of taurocholate. This compound, when its origin is exogenous, appears to stimulate the storage of esterified cholesterol in the liver, at the expense of bile acid synthesis. This accumulation rate takes into account not only the decrease in cholesterol transformation into bile acids but also the excess inflow of cholesterol. As the exogenous taurocholate was eliminated from the body, cholesteryl ester hydrolysis occurred and provided a supplementary source of free cholesterol for bile acid synthesis.     

Differential and interactive effects of calcium channel blockers and cholesterol content of the diet on jejunal uptake of lipids in rabbits

The present study was undertaken to determine the effects of two classes of calcium channel blockers (CCB), nisoldipine (N) and verapamil (V), on the jejunal uptake of lipids in rabbits. The uptake of cholesterol and long-chain fatty acids into rabbit jejunum was examined after 6 and 36 min of exposure to N or Vin vitro (“acute” studies), and after 3-wk feeding of N or V (“chronic” studies). Animals were fed either a low (0.08%) cholesterol diet (LCD) or a high (2.8%) cholesterol diet (HCD), with or without N or V added. Acutein vitro exposure of the jejunum to N or V did not affect the uptake of cholesterol or palmitic acid in rabbits fed LCD or HCD. The effect of N or V feeding depended upon the cholesterol content of the diet; adding N or V to LCD increased cholesterol uptake while adding N or V to HCD enhanced or lowered cholesterol uptake, respectively. Both N and V increased the uptake of stearic acid in LCD. N in HCD had no effect on fatty acid uptake, whereas V lowered the uptake of stearic and linoleic acids and increased the uptake of oleic acid. These changes in lipid uptake were not due to variation in the animals' food intake, body weight gain, or intestinal mucosal surface area. The chronic administration of N or V results in an intestinal adaptive process that alters the jejunal uptake of lipids, the direction of which is influenced by the class of CCB, and by the cholesterol content of the diet. The serum lipid-lowering effect of administering N to rabbits fed HCD demonstrated previously is unlikely to be the result of a decrease in intestinal lipid uptake.     

Variablity of the intestinal uptake of lipids is genetically determined in mice

The response of the plasma cholesterol concentration to changes in dietary lipids varies widely in humans and animals. There are variations in the in vivo absorption of cholesterol between different strains of mice. This study was undertaken in three strains of inbred mice to test the hypotheses that: (i) there are strain differences in the in vitro uptake of fatty acids and cholesterol and (ii) the adaptability of the intestine to respond to variations in dietary lipids is genetically determined. An in vitro intestinal ring technique was used to assess the uptake of medium- and long-chain fatty acids and cholesterol into jejunum and ileum of adult DBA/2, C57BL6, and C57L/J mice. The jejunal uptake of cholesterol was similar in C57L/J, DBA/2, or C57BL6 fed ad libitum a low-fat (5.7% fat, no cholesterol) chow diet. This is in contrast to a previous demonstration that in vivo cholesterol absorption was lower in C57L/J than in the other murine strains. The jejunal uptake of several long-chain fatty acids was greater in DBA/2 fed for 4 wk the high-fat (15.8% fat and 1.25% cholesterol) as compared with the low-fat diet. Furthermore, on the high-fat diet, the uptake of many long-chain fatty acids was higher in DBA/2 than in C57BL6 or C57L/J. The differences in cholesterol and fatty acid uptake were not explained by variations in food uptake, body weight gain, or the weight of the intestine. In summary: (i) there are strain differences in the in vitro intestinal uptake of fatty acids but not of cholesterol; (ii) a high-fat diet enhances the uptake of long-chain fatty acids in only one of the three strains examined in this study; and (iii) the pattern of strain- and diet-associated alterations in the in vivo absorption of cholesterol differs from the pattern of changes observed in vitro. We speculate that genetic differences in cholesterol and fatty acid uptake are explained by variations in the expression of protein-mediated components of lipid uptake.     

Dietary fibers: V. Binding of bile salts,phospholipids and cholesterol from mixed micelles by bile acid sequestrants and dietary fibers

Mixed micelles were prepared containing combinations of either taurocholate or taurochenodeoxycholate, monoolein, oleic acid, dioleylphosphatidylcholine (lecithin) and cholesterol. These were incubated with commercial bile-acid-sequestering resins, cholestyramine and DEAE-Sephadex, or various dietary fibers and fiber components including wheat bran, cellulose, alfalfa, lignin and 2 viscosity grades of guar gum. Binding was determined as the difference between the radioactivity of each micellar component added and that recovered in the centrifugal supernatant after incubation. In general, the extent of bile salt sequestration was characteristic and reproducible for each bile salt, and was largely unaffected by the presence of one or more additional components of the micellar mixture, including the other bile salt. Cholestyramine bound 81–92% of the bile salts and 86–99% of the phospholipid and cholesterol present in micelles. DEAE-Sephadex sequestered only 49% of the taurocholate and 84% of the taurochenodeoxycholate, but completely removed all of the phospholipid and cholesterol from micelles containing either bile salt. Among the dietary fibers, guar gum of either viscosity bound between 20–38% of each micellar component, whereas lignin, alfalfa, wheat bran and cellulose were progressively less effective in sequestratin of individual components of mixed micelles. The extent of sequestration of micellar components by these resins and fibers is reasonably correlated with the effects of these same materials on lymphatic absorption of lipids and to their suggested hypocholesteremic properties.     

Onset and persistence of changes in intestinal transport following dietary fat manipulation

In this study we determined the time-course for the onset and the loss of the effect of short-term feeding rats isocaloric semisynthetic diets containing a high content of saturated (HS) or polyunsaturated (HP) fatty acids on the jejunal and ileal uptake of medium- and long chain fatty acids, cholesterol and glucose. Animals were fed HP or HS for 3, 7 or 14 days; then the diet was switched to standard Purina^® rat chow for a further 3, 7 or 14 days. The uptake of medium chain fatty acids was unchanged. The differences between HP and HS in glucose uptake occurred within 3 days, but persisted for 14 days, whereas there were qualitative as well as quantitative changes in the pattern of lipid uptake: differences in uptake of stearic, oleic, linoleic and linolenic acids and cholesterol occurred after 7 days of feeding HP or HS. Jejunal uptake of linoleic acid was greater in HP than HS on day 7, but HS was greater than HP on day 14. The effect of diet on lipid uptake was similar in the jejunum and ileum. The altered uptake of stearic and oleic acids persisted after the rats were switched back to chow, whereas the uptake of the other nutrients became similar. Thus, (i) changes in dietary content of saturated and polyunsaturated fatty acids have early effects on intestinal transport function; (ii) some of these changes persist even when animals are returned to feeding on chow; and (iii) glucose transport is rapidly altered by dietary changes, whereas lipid uptake changes only after 7 days. We conclude that the transport function of the intestine is responsive to changes in dietary fatty acids.     

Effect of calcium on absorption of fatty acid by rat jejunum in vitro

The effect of Ca⁺⁺ on jejunal osmiophilic particles was studied in a recirculating system which was not contaminated with plasma lipoproteins. An isolated, infused segment of rat jejunum was suspended in a bath of liquid paraffin. Transudate, containing osmiophilic particles, appeared like beads of sweat on the serosal surface, and fell to the bottom of the bath. In the range of 25–38 C, 30 C proved to be optimal for histological preservation of villous architecture. Production of transudate, 20 mg/min/g of jejunum, and transport of [¹⁴C] oleate proceeded nearly linearly after the first 30 min. Necrosis of mid-villus and crypt cells became obvious by light microscopy after one hour. Therefore, transudate was collected between the period of 30–60 min. Shadow casting of transudates, produced when saline was infused, revealed that 86±9 (SD) % of osmiophilic particles was <800 Å in diameter; 13±8% was 800–1000 Å; 0.4±0.5% was 1000–2000 Å. Corresponding values were 58±10, 25±5, and 16±5% when 5 mM [¹⁴C] oleate+2.5 mM monoolein was infused; 75% of the transported [¹⁴C] appeared in triglyceride. Adding 2 mM Ca⁺⁺ to the infusion doubled the transport of [¹⁴C] triglyceride without increasing particle size further. We conclude that luminal Ca⁺⁺ increases the absorption of luminal fatty acid by rat jejunum in vitro.