Absorption Of Linoleic Acid Research Articles

Exploring the potential role of microbiota and metabolites in acute exacerbation of chronic obstructive pulmonary disease.

The acute exacerbation of chronic obstructive pulmonary disease seriously affects the respiratory system function and quality of life of patients. This study employed 16S rRNA sequencing and metabolomics techniques to analyze the respiratory microbiota and serum metabolites of COPD and AECOPD patients. The results showed that the microbial diversity in the respiratory tract of AECOPD patients was significantly lower than that of COPD patients, and the relative abundance of Bacteroidetes, Prevotella and Neisseria in the respiratory tract of AECOPD patients was significantly lower than that of COPD patients. However, the relative abundance of Haemophilus_D, Veillonella_A and Pseudomonas_E, in AECOPD patients was significantly higher than that of COPD patients, and the ability of respiratory microbiota in AECOPD patients to participate in alanine metabolism was significantly lower than that of COPD patients. Metabolome results further revealed that the serum alanine levels in AECOPD patients were significantly lower than those in COPD patients, and these differential metabolites were mainly involved in linoleic acid metabolism, protein digestion and absorption and regulation of lipolysis in adipocytes. In summary, the structural characteristics of respiratory microbiota in COPD and AECOPD patients are different from those in healthy populations, and their microbiota diversity decreases and microbial community structure and function will also undergo changes when acute exacerbations occur. In addition, the predicted microbial community function and metabolomics results indicate that the onset of AECOPD is mainly related to energy and amino acid metabolism disorders, especially alanine metabolism.

Deciphering the molecular signature of selective neuronal vulnerability in the wake‐promoting lateral hypothalamic area in Alzheimer’s disease: A digital multiplexed gene expression study across Braak stages

AbstractBackgroundSleep/wake disturbance is a common and debilitating symptom of Alzheimer’s disease (AD) that precedes cognitive loss. The lateral hypothalamic area (LHA) is critical in orchestrating the sleep/wake cycle through the neuropeptide orexin and melanin‐concentrating hormone. We previously demonstrated that LHA neurons accumulate AD‐tau from Braak stage (BB) 0 and losses ∼72% of neurons by BB6. Little is known about the molecular changes underlying LHA vulnerability during AD progression. We investigated RNA expression changes in LHA across Braak stages to close this gap.MethodWe dissected LHA from 30um‐thick sections of the brain from healthy control (HC) and subjects at progressive AD stages and extracted RNA using conventional techniques. We ran RNA transcriptomic assay using customized and neuropathology nCounter® (Nanostring) panels. The Wald statistical test was used to compare the groups, and the genes were considered differentially expressed when log2 fold‐change was > = |1| and the p‐value was <0.05.ResultWe found an upregulation of HCRTR1, LDHC, NKX6, and SLC11A1 from early stages (BB2‐3), whereas HCRTR2 RNA levels remained stable. Circadian gene PER2 was downregulated from the intermediate stages (BB4). Gene Ontology analyses detected dysregulation of neuropeptide‐ligand interaction pathways from early AD. Linoleic acid metabolism, fat digestion and absorption, and immune pathways became dysregulated at intermediate stages, while glycolysis and gluconeogenesis pathways were in late stages (BB5‐6). Of note, it is critical to consider that the massive LHA neuronal loss during AD progression may confound the interpretation of changes in late stages because of the few remaining neurons.ConclusionnCounter® is suitable for identifying transcriptome changes in LHA, even at early AD stages. Molecular profiling of LHA across the Braak stage revealed that the earliest changes are associated with an imbalance in neurotransmitter receptors, while the decline in metabolism and increased inflammation marked the intermediate stage. The late‐stage AD is characterized by hypoglycemia and energy deficit. Notably, discrepancies in receptor behavior can inform more effective symptomatic treatment for sleep dysfunction in AD.

Using a transcriptomic approach to understand poor growth performance in farmed orange-spotted grouper (Epinephelus coioides) larvae: a case study in a commercial hatchery

ABSTRACT The orange-spotted grouper (Epinephelus coioides) is one of the most popular fish in aquaculture due to its high economic value. However, the random occurrence of slow-growing population has led to profit loss. Therefore, transcriptomic analysis was performed to identify the molecular mechanisms involved in driving slow and fast growth, towards addressing this issue. Results show that low expression of developmental genes such as bone morphogenetic protein 1 (BMP 1) and somatostatin (SST), as well as GH/IGF axis-related genes (IGF-1, IGF2, IGFBP1, IGFBP2) and its downstream signalling pathways are correlated with the metabolism and digestive-system-related pathways in slow-growing groupers. Enrichment analysis further revealed that cellular process and biological regulation, as well as several pathways including glycolysis/gluconeogenesis, linoleic acid metabolism, protein digestion and absorption, and cholesterol metabolism were differentially expressed in slow-growing groups. The findings implied that the genomic architecture of growth between the different families raised and the likely problem of inbreeding have led to significantly reduced growth. It is also suggested that better husbandry practices (optimal dietary requirement) is also vital in supporting the success of a genetic improvement programme. These findings recommend growth improvement of orange-spotted groupers via molecular monitoring and artificial selection, complemented by specific dietary feeding.

Transcriptome Analysis Reveals Increases in Visceral Lipogenesis and Storage and Activation of the Antigen Processing and Presentation Pathway during the Mouth-Opening Stage in Zebrafish Larvae.

The larval phase of the fish life cycle has the highest mortality, particularly during the transition from endogenous to exogenous feeding. However, the transcriptional events underlying these processes have not been fully characterized. To understand the molecular mechanisms underlying mouth-opening acclimation, RNA-seq was used to investigate the transcriptional profiles of the endogenous feeding, mixed feeding and exogenous feeding stages of zebrafish larvae. Differential expression analysis showed 2172 up-regulated and 2313 down-regulated genes during this stage. Genes associated with the assimilation of exogenous nutrients such as the arachidonic acid metabolism, linoleic acid metabolism, fat digestion and absorption, and lipogenesis were activated significantly, whereas dissimilation including the cell cycle, homologous recombination, and fatty acid metabolism were inhibited, indicating a physiological switch for energy storage occurred during the mouth-opening stage. Moreover, the immune recognition involved in the antigen processing and presentation pathway was activated and nutritional supply seemed to be required in this event confirmed by qPCR. These results suggested the energy utilization during the mouth-opening stage is more tended to be reserved or used for some important demands, such as activity regulation, immune defense, and lipid deposition, instead of rapid growth. The findings of this study are important for understanding the physiological switches during the mouth-opening stage.

Plant oils' inclusion in high fish meal-substituted diets: effect on digestion and nutrient absorption in gilthead sea bream (Sparus aurata L.)

Here, we performed an 11-week trial to study the effects of four experimental diets on the digestion, nutrient absorption and intestinal histology of gilthead sea bream. The diets were formulated with a low fish meal content (25%) and were rich (75%) in plant proteins. Fish oil (FO) was replaced at 0%, 33%, 66% and 100% by graded levels of a blend of vegetable oils (VO) (diets FO, 33VO, 66VO and 100VO respectively). Protease activity increased in the pyloric caeca (PC) and decreased in the proximal intestine (PI) of the 66 and 100VO groups, while lipase and α-amylase activities were not modified by VO. The capacity of brush-border membrane vesicles obtained from PC, PI and distal intestine to absorb amino acids was not modified, but d-glucose and linoleic acid absorption diminished when VO was included in the diets. In summary, these results show that when 75% of protein is provided by vegetable sources in the diet of gilthead sea bream, up to 66% of FO can be replaced by a blend of VO without compromising digestive processes. Only the total replacement of VO results in an impaired digestion, with reduced total protease activity and accumulation of lipid droplets in the enterocytes of the PI.

Effect of occlusion on the percutaneous penetration of linoleic acid and glycerol

The effect of occlusion on the in vitro percutaneous absorption of linoleic acid was investigated. A greater skin concentration of linoleic acid from an ethanolic vehicle was observed in non-occluded experiments compared with occluded experiments ( P<0.05). Such changes were not observed as consistently when ethanol was replaced with a less volatile organic solvent (cyclomethicone). These observations were attributed to the increase in the concentration gradient due to the unimpeded evaporation of volatile solvents, which provided a greater driving force and enhanced non-occluded delivery in these systems, compared with occluded systems. Conversely, the percutaneous absorption of a polar material (glycerol) from an aqueous solution did not yield any such differences. While more conclusive comparisons between volatile and non-volatile solvents and penetrants would be required to substantiate fully these comparisons, it is apparent that non-occlusion of volatile solvents may enhance percutaneous absorption. The physicochemical properties of the penetrant, for example its natural state at skin temperature (i.e. solid or liquid) may further determine the degree of enhanced percutaneous absorption compared with occluded environments.

Intestinal absorption and postabsorptive metabolism of linoleic acid in rats with short-term bile duct ligation.

We investigated in bile duct-ligated (BDL) and sham-operated control rats whether the frequent presence of essential fatty acid deficiency in cholestatic liver disease could be related to linoleic acid malabsorption, altered linoleic acid metabolism, or both. In plasma of BDL rats, the triene-to-tetraene ratio, a biochemical marker for essential fatty acid deficiency, was increased compared with controls (0.024 +/- 0.004 vs. 0.013 +/- 0.001; P < 0.05). Net and percentage of dietary linoleic acid absorbed were decreased in BDL rats compared with control rats (1.50 +/- 0.16 mmol/day and 81.3 +/- 3.3% vs. 2.08 +/- 0.07 mmol/day and 99.2 +/- 0.1%, respectively; each P < 0.001). At 24 h after [(13)C]linoleic acid administration, BDL rats had a similar ratio of plasma [(13)C]arachidonic acid to plasma [(13)C]linoleic acid concentration compared with control rats. Delta(6)-Desaturase activity was not significantly different in hepatic microsomes from control or BDL rats. At 3 h after [(13)C]linoleic acid administration, plasma appearance of [(13)C]linoleic acid and cumulative expiration of (13)CO(2) were decreased in BDL rats, compared with controls (by 54% and 80%, respectively). The present data indicate that the impaired linoleic acid status in cholestatic liver disease is mainly due to decreased net absorption and not to quantitative alterations in postabsorptive metabolism.

Effects of different medium-chain fatty acids on intestinal absorption of structured triacylglycerols.

To study the effect of the chain length of medium-chain fatty acids on the intestinal absorption of long-chain fatty acids, we examined the lymphatic transport of fat following administration of five purified structured triacylglycerols (STAG) containing different medium-chain fatty acids in the sn-1,3 positions and long-chain fatty acids in the sn-2 position in a rat model. Significant amounts of medium-chain fatty acids were found in lymph samples after intragastric administration of 1,3-dioctanoyl-2-linoleyl-sn-glycerol (8:0/18:2/8:0), 1,3-didecanoyl-2-linoleyl-sn-glycerol, and 1,3-didodecanoyl-2-linoleyl-sn-glycerol. The accumulated lymphatic transport of medium-chain fatty acids increased with increasing carbon chain length. The recoveries of caprylic acid (8:0), capric acid (10:0), and lauric acid (12:0) were 7.3 +/- 0.9, 26.3 +/- 2.4, and 81.7 +/- 6.9%, respectively. No significant differences were observed for the maximal intestinal absorption of linoleic acid (18:2n-6) when the chain length of medium-chain fatty acids at the primary positions was varied, and the absorption of 18:2 and oleic acid (18:1) from 8:0/18:2/8:0 and 1,3-dioctanoyl-2-oleyl-sn-glycerol was similar. We conclude that the chain length of the medium-chain fatty acids in the primary positions of STAG does not affect the maximal intestinal absorption of long-chain fatty acids in the sn-2 position in the applied rat model, whereas the distribution of fatty acids between the lymphatics and the portal vein reflects the chain length of the fatty acids.

Biliary phospholipid secretion is not required for intestinal absorption and plasma status of linoleic acid in mice

Biliary phospholipids have been hypothesized to be important for essential fatty acid homeostasis. We tested this hypothesis by investigating the intestinal absorption and the status of linoleic acid in mdr2 Pgp-deficient mice which secrete phospholipid-free bile. In mice homozygous (−/−) for disruption of the mdr2 gene and wild-type (+/+) mice, dietary linoleic acid absorption was determined by 72 h balance techniques. After enteral administration, [ 13C]-linoleic acid absorption was determined by measuring [ 13C]-linoleic acid concentrations in feces and in plasma. The status of linoleic acid was determined in plasma and in liver by calculating the molar percentage of linoleic acid and the triene:tetraene ratio. Although plasma concentration of [ 13C]-linoleic acid at 2 h after enteral administration was significantly lower in (−/−) compared to (+/+) mice ( P≤0.05), net intestinal absorption of dietary linoleic acid or of [ 13C]-linoleic acid was similar in (+/+) and (−/−) mice. Molar percentage of linoleic acid and the triene:tetraene ratio were not different in whole plasma or in liver of (−/−) compared to (+/+) mice. Present data indicate that biliary phospholipids are involved in the rate of appearance in plasma of enterally administered linoleic acid, but are not required for net intestinal absorption or plasma status of linoleic acid.

Bile diversion in rats leads to a decreased plasma concentration of linoleic acid which is not due to decreased net intestinal absorption of dietary linoleic acid

Decreased bile secretion into the intestine has been associated with low plasma concentrations of essential fatty acids (EFA) in humans. We studied the mechanism behind this relationship by determining the status and absorption of the major dietary EFA, linoleic acid (LA), in control and 1-week bile-diverted rats. The absorption of LA was quantified by a balance method and by measuring plasma concentrations of [ 13C]LA after its intraduodenal administration. Absolute and relative concentrations of LA in plasma were decreased in bile-diverted rats ( P<0.01 and P<0.001, respectively). Fecal excretion of LA was increased at least 20-fold in bile-diverted rats (0.72±0.11 vs. 0.03±0.00 mmol/day; P<0.0001). Due to increased chow ingestion by bile-diverted rats, net intestinal absorption of LA was similar between bile-diverted and control rats (1.96±0.14 vs. 1.91±0.07 mmol/day, respectively; P>0.05). After intraduodenal administration of [ 13C]LA, plasma concentrations were approximately 3–4-fold lower in bile-diverted rats for at least 6 h ( P<0.001). Plasma concentrations of both [ 12C]arachidonic acid and [ 13C]arachidonic acid were increased in bile-diverted rats ( P<0.05). We conclude that decreased plasma concentrations of LA in 1-week bile-diverted rats are not due to decreased net intestinal absorption of LA, but may be related to increased metabolism of LA.

Absorption of isomeric, palmitic acid‐containing triacylglycerols resembling human milk fat in the adult rat

The effect of the positional distribution of palmitic acid (16:0) in triacylglycerols (TAG) on 16:0 apparent absorption in adult rats was investigated. The rats were fed two diets which contained 30 energy % as fat with identical total fatty acid compositions, both containing 30% 16:0. The Betapol diet contained TAG with 73% of total 16:0 in the sn-2 position, the control diet contained TAG with 6% of total 16:0 in the sn-2 position. After six weeks on these diets, the rats were killed two or six hours after the last meal, and the small intestine was removed, cut into 10-cm segments, and the fatty acid composition of the segment's contents was determined. At both time points the amount of 16:0 in the intestinal segments starting at 40 cm from the stomach was much lower in the animals fed Betapol than in the animals fed the control diet. Overall absorption of 16:0 and stearic acid was significantly greater in the Betapol group. Absorption of oleic and linoleic acid from the small intestine was similar in both groups, although the overall absorption was significantly greater in the animals fed Betapol. Total fat absorption was significantly higher in the Betapol-fed rats than in the control-fed rats. No effect on calcium and nitrogen absorption, on plasma total cholesterol and TAG levels, and on bodyweights (growth) was seen. The data demonstrate that the positional distribution of the fatty acids in the TAG molecule affects the site of absorption in the small intestine and particularly the net absorption of saturated fatty acids.

Intestinal conversion of linoleic acid to arachidonic acid in the rat

The arachidonic acid (C20:4, n-6) appearing in intestinal lymph during linoleic acid (C18:2, n-6) absorption may originate from enterocyte synthesis or from the liver either after secretion in biliary phospholipids at the same time dietary linoleic acid absorption occurs or via plasma. The radioactivity measured in the total bile collected during the 6 hours of linoleic acid absorption is too small to explain hepatic origin of the C20:4 detected by high performance liquid chromatography analysis of labeled fatty acids recovered in the lymph, in the intestinal mucosa, and the intestinal wall at the peak of linoleic acid intestinal absorption. This study confirms the probability that under in vivo conditions, during the absorption processes, rat intestine is able to convert dietary linoleic acid independent of liver desaturases and elongase activities.

Intestinal absorption of linoleic acid in experimental renal failure

Linoleic acid (LA) transport in rats with experimental short-term and long-term renal failure (RF) was compared with that of sham-operated normal animals on liberal food intake and pair-fed animals. The perfusions in vivo and incubations in vitro were conducted using a micellar solution containing a wide range of LA concentrations. Both absorption in vivo and uptake in vitro of LA were significantly reduced in animals with short-term RF. Lipid extraction and separation by thin-layer chromatography revealed a marked LA trapping as trilinolein (TL) in the perfused intestinal tissue in the short-term RF group. The esterification process, as defined by the rate of LA incorporation into TL, was moderately reduced in short-term RF animals. The thickness of the unstirred water layer showed no significant difference among the groups studied. In contrast, animals with long-term RF exhibited normal absorption of LA in vivo at all concentrations tested. In conclusion, LA absorption is reduced in short-term RF and restored in long-term RF. Several steps including LA transport into and TL transport out of the enterocyte and the esterification process were impaired in short-term RF. These changes are not due to alteration in the unstirred water layer, anorexia, weight loss or a rapid effect of uraemic chemical environment or circulatory factors.

Lymphatic absorption of structured glycerolipids containing medium‐chain fatty acids and linoleic acid, and their effect on cholesterol absorption in rats

The effects of various structured triglycerides containing medium-chain (caprylic or capric acids) and long-chain (linoleic acid) fatty acids on fatty acid and cholesterol absorption were studied in lymph-cannulated rats. A considerable portion of capric and caprylic acid was absorbed through the lymph duct, although to a lesser extent than was linoleic acid. Capric and linoleic acid located at the 2-position of 2-decanoyl-1,3-dilinoleoyl-glycerol (18:2/10:0/18:2) and 2-linoleoyl-1,3-didecanoyl-glycerol (10:0/18:2/10:0), respectively, tended to be absorbed more efficiently than those located at the 1- and 3-position or those from tricaprin (10:0/10:0/10:0) or trilinolein (18:2/18:2/18:2). A similar trend was observed when the medium-chain fatty acid was caprylic acid instead of capric acid. Caprylic acid absorption from 2-octanoyl-1,3-dilinoleoyl-glycerol (18:2/8:0/18:2) was significantly greater (p less than 0.05) than from 2-linoleoyl-1,3-dioctanoyl-glycerol (8:0/18:2/8:0) or tricaprylin (8:0/8:0/8:0). Preferential absorption of caprylic and linoleic acid was not observed when the 1 to 2 and the 2 to 1 mixtures of 8:0/8:0/8:0 and 18:2/18:2/18:2, respectively, were administered. The structured lipids did not affect the lymphatic absorption of cholesterol. The results suggest that structured triglycerides composed of medium-chain fatty acids and linoleic acid may be more useful for the treatment of lipid malabsorption than are mixtures of medium-chain triglyceride (MCT) and long-chain triglyceride (LCT).

Caecal and colonic uptake of both linoleic acid and cholesterol in rats following intestinal resection

Caecal and colonic uptake of both linoleic acid and cholesterol were studied in rats after distal small bowel resection (DSBR). The results showed that the surgical operation increased the caecal and colonic uptake of linoleic acid. Supplementation with linolenic acid inhibited caecal and colonic uptake of linoleic acid. Experiments carried out in the presence of rotenone and ouabain suggest that facilitated diffusion is the predominant mechanism of caecal and colonic linoleic acid absorption, at least at low concentrations. An increase in caecal and colonic uptake of cholesterol was observed after the surgical operation. The study showed that facilitated diffusion seems to be the mechanism of linoleic acid absorption in the caecum and colon, and that both organ growth and changes in transport function of the epithelial cells of caecum and colon appear to be involved in the adaptive response of the bowel to intestinal resection.

The Effect of Exercise on Absorption and Clearance of Linoleic Acid

The Effect of Exercise on Absorption and Clearance of Linoleic Acid

Effects of pectin on fatty acid and glucose absorption and on thickness of unstirred water layer in rat and human intestine

Effects of pectin, a soluble dietary fiber, on fatty acid and glucose absorption were studied in vivo in rats and humans by perfusing the intestine with linoleic acid and glucose solutions with and without pectin. Linoleic acid and glucose absorption decreased with increasing concentrations of pectin. The reduction in linoleic acid absorption was not caused by binding of linoleic acids by pectin or impaired micelle formation due to binding of bile acid by pectin. The unstirred water layer expanded with increasing concentrations of pectin. These results suggest that enlargement of the unstirred water layer is closely associated with the reduction of absorption of fatty acid and glucose ingested with pectin.

Malabsorption of long-chain fatty acid in cholera toxin-induced secretory diarrhea.

The effects of cholera toxin-induced diarrhea on the absorption of fatty acids of different chain lengths were investigated using rat small intestine. In the study using isolated jejunal loops, the absorption of the long-chain fatty acid, linoleic acid, into the intestinal mucosa was significantly impaired 90 min after the administration of linoleic acid micelles in the cholera toxin-treated rats. This reduction of linoleic acid absorption in the cholera toxin-treated rats was not found at 180 min. We could not find any mucosal accumulation of labeled linoleic acid or disturbance of triglyceride formation in the intestinal mucosa as compared with that of controls. The amount of linoleic acid transported into the intestinal lymph was delayed and reduced in cholera toxin-treated rats. Furthermore, the absorption of the medium-chain-length fatty acid, octanoic acid, was unchanged in the cholera toxin-treated rats. These results suggest that intestinal secretion induced by cholera toxin may delay the mucosal uptake and lymphatic transport of long-chain fatty acids. Cholera toxin may not affect triglyceride formation in the epithelial cells.

Linoleic acid absorption from lipid supplements in patients with cystic fibrosis with pancreatic insufficiency and in control subjects.

To determine the relative role of malabsorption as the cause of decreased linoleic acid in blood and tissue lipids of patients with cystic fibrosis (CF) and pancreatic insufficiency, the increase in plasma linoleic acid was determined after ingestion of various lipid supplements. CF patients with documented pancreatic insufficiency and normal control subjects were given each of four different lipid supplements on separate days (a minimum of 3 days apart). The supplements were commercial safflower oil, Microlipid, Captex 810D, and Captex 810B. Fasting subjects consumed 36 g of lipid in a milk shake containing 15 g of protein and 45 g of carbohydrate. Plasma samples obtained at 0, 2, 4, 6, and 8 h after the meal showed that CF patients absorbed linoleic acid from all of the lipid preparations tested when administered with their regular dose of pancreatic enzyme supplement. The mean maximal increase in percent plasma linoleic acid in CF patients was not different from controls after ingestion of safflower oil, Microlipid, and Captex 810B. With Captex 810D the CF patients had a significantly higher increase in percent plasma linoleic acid than controls, 6.75% vs. 2.27%, respectively, at 2 h (p less than 0.01), and 11.10% vs. 4.65% at 8 h (p less than 0.01). The CF patients also appeared to absorb the Captex products faster than controls, suggesting that presence of medium chain length fatty acids in these structured lipids facilitated their utilization by CF patients. The results indicate that malabsorption alone cannot account for the inadequate or marginal essential fatty acid status of CF patients.(ABSTRACT TRUNCATED AT 250 WORDS)

Linoleic Acid Absorption from Lipid Supplements in Patients with Cystic Fibrosis with Pancreatic Insufficiency and in Control Subjects

To determine the relative role of malabsorption as the cause of decreased linoleic acid in blood and tissue lipids of patients with cystic fibrosis (CF) and pancreatic insufficiency, the increase in plasma linoleic acid was determined after ingestion of various lipid supplements. CF patients with documented pancreatic insufficiency and normal control subjects were given each of four different lipid supplements on separate days (a minimum of 3 days apart). The supplements were commercial safflower oil, Microlipid, Captex 810D, and Captex 810B. Fasting subjects consumed 36 g of lipid in a milk shake containing 15 g of protein and 45 g of carbohydrate. Plasma samples obtained at 0, 2, 4, 6, and 8 h after the meal showed that CF patients absorbed linoleic acid from all of the lipid preparations tested when administered with their regular dose of pancreatic enzyme supplement. The mean maximal increase in percent plasma linoleic acid in CF patients was not different from controls after ingestion of safflower oil, Microlipid, and Captex 810B. With Captex 810D the CF patients had a significantly higher increase in percent plasma linoleic acid than controls, 6.75% vs. 2.27%, respectively, at 2 h (p &lt; 0.01), and 11.10% vs. 4.65% at 8 h(p &lt; 0.01). The CF patients also appeared to absorb the Captex products faster than controls, suggesting that presence of medium chain length fatty acids in these structured lipids facilitated their utilization by CF patients. The results indicate that malab‐sorption alone cannot account for the inadequate or marginal essential fatty acid status of CF patients. The fact that linoleic acid was absorbed as well by CF patients as controls in the present study suggests that CF patients in many previous supplementation studies either have not been given sufficient linoleic acid or have used the linoleic acid ingested to meet caloric needs. There is increasing evidence that adequate total caloric intake may be a far more important factor in determining the essential fatty acid status of CF patients than previously recognized. Our results suggest that long‐term consumption of supplemental linoleic acid in addition to adequate caloric intake should improve the linoleic acid status of most, if not all, CF patients.