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CSIRO Health Sciences & Nutrition, Adelaide, South Australia 5000, Australia and * Department of Physiology, The University of Adelaide, Adelaide, South Australia 5005, Australia
2To whom correspondence should be addressed. E-mail: glen.patten{at}csiro.au.
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ABSTRACT |
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 TOP ABSTRACT INTRODUCTIONMATERIALS AND METHODSRESULTSDISCUSSIONLITERATURE CITED |
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and U-46619 compared with the SF group (P < 0.05). FO feeding increased the incorporation of (n-3) PUFA {eicosapentaenoic [20:5(n-3)], docosapentaenoic [22:5(n-3)] and docosahexaenoic acids [22:6(n-3)]} primarily at the expense of (n-6) PUFA {linoleic [18:2(n-6)] and arachidonic acids [20:4(n-6)]} in the ileum and colon phospholipid fatty acids (P < 0.05). The FO group had a lower cecal digesta pH (P < 0.001) and a greater butyrate concentration than the SF group (P < 0.05). These results suggest that dietary (n-3) PUFA may modulate the contractility of the small intestine.
KEY WORDS: • rats • fish oil • colon • ileal contractility • eicosanoids
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INTRODUCTION |
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TOPABSTRACTINTRODUCTIONMATERIALS AND METHODSRESULTSDISCUSSIONLITERATURE CITED |
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–3
) and aid in gut wound healing (4
,5
). Further, human trials also suggest that high intakes of (n-3) may be beneficial in ulcerative colitis and Crohn’s disease (6
,7
), indicating an important role for these long-chain PUFA in gastrointestinal health. The mechanism(s) by which (n-3) PUFA exert their varied physiologic actions relate initially to changes in membrane fatty acid composition. Such compositional alterations not only modify endogenous mediator profiles such as eicosanoids, but also influence physiologic responses to exogenous agonists. These altered responses arise from functional changes in membrane receptors, ion channels and second messenger systems, as well as from structural changes brought about by specific physicochemical changes in the membrane milieu, and from the modulation of gene expression.
The physiologic effects of fish oil supplementation were evaluated in the present study by feeding young rats 3 synthetic diets containing 170 g/kg fat (
34% of total energy). The first diet contained 170 g/kg Sunola oil (SO), rich in monounsaturated fatty acid. In the second diet, 100 g/kg of the SO was replaced by saturated animal fat (SF), and in the third diet by fish oil (FO) enriched with long-chain (n-3) PUFA. Of particular interest were the dietary lipid effects on the in vitro contractile responses of isolated colon and ileum to various agonists of gastrointestinal contractility including acetylcholine and several eicosanoid classes because the latter compounds have been reported to play important roles in bowel health and disease, particularly in relation to secretion, nutrient uptake and contractility (8
–11
).
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MATERIALS AND METHODS |
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TOPABSTRACTINTRODUCTIONMATERIALS AND METHODSRESULTSDISCUSSIONLITERATURE CITED |
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Male Sprague-Dawley rats were purchased from Adelaide University Central Animal Facility at 4 wk of age and housed in the small animal colony of CSIRO Health Sciences & Nutrition (HS&N). The rats consumed a commercial low -linolenic acid rat diet (Glen Forrest Stockfeeders, Glen Forrest, Western Australia, Australia) based on the AIN 93G diet (12
) containing 7% fat as SO and water ad libitum for 5 wk. They were subjected to a 12-h light:dark cycle at 23°C. The rats were housed and the experiment conducted with the approval of the CSIRO HS&N animal ethics committee.
Diets.
At 9 wk of age the rats were separated into the 3 dietary groups, housed 3–5 per cage and consumed synthetic diets ad libitum. The diets were stored at -20°C and changed daily. The diets were based on the AIN-93M diet (12
) containing 170 g/kg fat as SO {as 850 g/kg oleic acid [18:1(n-9)] and 100g/kg linoleic acid [18:2(n-6)]} (Meadow Lea Foods, Mascot, Sydney, NSW, Australia) designated as the SO group or 100 g/kg of the SO replaced by animal fat (as beef and mutton drippings of mainly saturated fat; Metro Quality Foods, Greenacres, New South Wales, Australia) designated as the SF group or by fish oil {Fishaphos Oral Liquid, 170 g/kg of total fatty acids as eicosapentaenoic acid (EPA) [20:5(n-3)] and 110 g/kg as docosahexaenoic acid (DHA) [22:6(n-3)] (Felton Grimwade & Bickford, Oakleigh South, Victoria, Australia)} designated as the FO group. The diets are as indicated in Table 1
with the fatty acid compositions in Table 2
. The fat represented 34% of the energy supplied by the diet.
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At the completion of the 4-wk experimental feeding period, the rats were weighed and then killed by Nembutal anesthesia (60 mg/kg intraperitoneal) and exsanguination. The small intestine was removed, gently flushed with saline and sections of the ileum 0.1 m from the ileocecal junction were dissected for physiologic recordings. Remaining sections of the ileum were snap-frozen in liquid nitrogen and stored at -80°C for total phospholipid fatty acid analysis. The colon was removed and flushed with saline; a section of the proximal colon was used for physiologic recordings, and the remaining proximal section of colon was snap-frozen for fatty acid analysis. The total cecal digesta was snap-frozen in liquid nitrogen and stored at -80°C for later pH and short-chain fatty acid (SCFA) analysis.
Diet total lipid fatty acid analysis.
Powdered diet (0.5 g) was adjusted to a volume of 3.2 mL in a glass test tube with 0.4 U/L clarase (Enzyme Solutions, Park Orchards, Victoria, Australia) in 0.5 mol/L sodium acetate and incubated for 1 h at 45–50°C to release fat from the plant cell wall. To this mixture were added 8 mL of methanol and 4 mL of chloroform containing 5 mmol/L BHT; the suspension was blended in an Ultra-Turrax (Janke & Kunkel GmbH & Co., Staufen, Germany) at high speed for 2 min. Finally, 4 mL of water was added and blended for 30 s. The mixture was centrifuged at 3000 x g for 15 min. The top methanol/water layer was carefully removed. The chloroform phase containing the lipid was removed by thin glass pipette and dried under N2. The fatty acids were methylated in 0.2 mol/L H2SO4 in dry methanol for 18 h at 50°C. The fatty acid methyl esters (FAME) were dissolved in hexane and cleaned on 20-mm Florisil columns with hexane. FAME were eluted with 0.96 mol/L diethyl ether in hexane and dried under N2. The purified FAME were dissolved in 50 µL isooctane and a 0.1-µL aliquot was injected into a 30 m x 0.5 mm bonded-phase vitreous silica BPX70 column (SGE International, Sydney, NSW, Australia) in a Hewlett-Packard 5711 gas chromatograph (GC; Hewlett-Packard, Alto Palo, CA) fitted with a cold on-column injector (SGE OCI-3) and flame ionization detector (13
). Hydrogen was used as the carrier gas and the oven temperature program was from 130 to 230°C at 4°C/min. Peak identification was based on a comparison of retention times with standard FAME mix 68A (Nu-Chek-Prep, Elysian, MN) to which 20:5(n-3) methyl ester was added.
Total phospholipid fatty acid analysis of colonic and ileal tissues.
Small frozen sections (150 mg) of ileum or colon were ground in a glass homogenizer and total lipids extracted in methanol/chloroform/water (2:4:1) containing 0.2 mmol/L BHT by shaking for 15 min. The homogenate suspension was centrifuged for 2 min at 1000 x g in a Beckman GPR centrifuge (Palo Alto, CA) with a swing-out rotor. The lower organic solvent layer was removed and dried under N2. Lipid was reconstituted into hexane and the phospholipids separated from the other fats by TLC (Kieselgel 60 F254, Merck, Darmstadt, Germany) in acetone/petroleum spirit (1:3) containing BHT. Methanolysis of the phospholipid band was performed at 50°C for 18 h. Water/petroleum spirit (3:5) was then added and shaken. The top phase was transferred to a glass tube and the last step repeated. The solution was dried under N2. The FAME were dissolved in hexane and transferred to 4-mm (i.d) columns containing 20 mm Florisil. After the columns were washed with hexane, FAME were eluted with 0.96 mol/L diethyl ether in hexane and dried under N2. The FAME were dissolved in 50 µL isooctane and separated and measured by GC as described above (13
).
pH and SCFA analysis of cecal digesta.
A standard mixture of acetic, propionic, isobutyric, butyric, isovaleric, valeric, caproic and heptanoic acids was used to calibrate the GC. Cecal digesta samples were added to 5 mmol/L heptanoic acid as internal standard, pH 7.0 with NaOH in centrifuge tubes and homogenized using an Ultra-Turrax. This mixture was centrifuged at 200 x g in a Beckman GRP bench-top centrifuge at 5°C for 10 min. The pH of the sample supernatant was then measured. A 0.1-mL aliquot of the supernatant was placed into a 5-mL round- bottomed Quickfit flask, acidified with 20 µL of 1.0 mol/L phosphoric acid and the shell quickly frozen in ethanol at -70°C. The sample was then freeze-dried. The flask was then sealed from the pump and transferred to a 50°C water bath and the contents distilled into a cooled flask. A 1-µL sample was manually injected into a Hewlett-Packard 5710A GC for SCFA content using a 2 m x 2 mm i.d. column of Tenax TA (Alltech, Baulkham Hills, NSW, Australia) coated with 1% phosphoric acid. The carrier gas was nitrogen with an injector temperature of 150°C. The oven was held at 160°C for 2 min and increased by 16°C/min to 200°C for flame ionization detection.
Physiologic recording of colonic and ileal contractility.
Sections of proximal colon or ileum (0.03–0.04 m) were tied by suture cotton at the proximal end of the tissue to a small plastic plug connected to a glass plug via a plastic sleeve, which was placed into the bottom of the organ chamber. The distal end of the tissue was connected to the free end of a 0.15-m arm of an isotonic transducer (Harvard Bioscience, catalog # 60–3001, South Nattick, MA) by a short length of suture cotton (14
). The transducer was sustaining 0.5 g of tension at the other end. Contractions were measured via an A-D converter (BIOPAC Systems model MP 100, Santa Barbara, CA) and translated and stored using AcqKnowledge version 3.5.7 (Microsoft Corporation, Santa Rosa, CA) for Windows 98. A 15° rotation of the torsion arm was equivalent to 2 V. Results are given as volts per gram of (gut) tissue (V/g).
The tissue was bathed in a modified Krebs-Henseleit bicarbonate buffer containing (in mmol/L): 118 NaCl; 25 NaHCO3; 4.7 KCl; 1.2 MgSO4; 1.2 NaH2PO4; 1.8 CaCl2 and 11 glucose, at pH 7.4 in the water-jacketed organ bath at 37°C. The bathing medium was aerated constantly with 95:5 O2/CO2 via a needle through the buffer inlet at the bottom of the chamber. The contents of the bath could be flushed from the bottom and withdrawn from an overflow near the top using a vacuum source. The tissue was then induced to contract by the accumulative addition of pharmacologic agents to the bath as indicated.
Contraction of quiescent rat colon and ileum.
The gastrointestinally active agonists were added sequentially to the bath containing colonic or ileal tissue. Dose-response curves were generated by cumulative addition of agonists added as a small bolus to the incubating tissue. Each agent was washed out from the bath after maximal contraction had been achieved and the tissue stabilized at baseline for 15 min before the addition of the next agonist. Acetylcholine chloride was added again at the completion of each experiment and only tissue with 100% recovery of contractile activity was used for experimental determinations.
Pharmacologic agents and suppliers.
The following pharmacological agents (concentration range in µmol/L used in organ bath) and the suppliers were as follows: prostaglandin (PG)E2 (1–5000); PGF2 (1–5000); 8-iso-PGE2 (3–5000); 8-iso-PGF2 (3–10000) and U-46619 (1–5000) were from Sapphire Bioscience (Crows Nest, NSW, Australia) and acetylcholine chloride (1–2000); histamine dihydrochloride (10–20000); 5-hydroxytryptamine (5-HT, serotonin; 1–3000); fine chemicals were from Sigma Chemical (Sydney, NSW, Australia).
Data analysis.
Data are shown as means ± SEM. Statistical evaluation was performed by ANOVA, with Bonferroni multiple comparison post test performed when the F-test was significant at P < 0.05. The 50% effective concentration (EC50; nmol/L) and maximal contraction (V/g of tissue) values were determined using graph fits in GraphPad PRISM 3.01 (GraphPad Software, San Diego, CA) with R2 values > 0.99.
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RESULTS |
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TOPABSTRACTINTRODUCTIONMATERIALS AND METHODSRESULTSDISCUSSIONLITERATURE CITED |
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The initial body weights of the 9-wk-old rats were (g): SO group, 345 ± 9; SF group, 340 ± 6; and FO group, 365 ± 5 with the latter two differing significantly (P < 0.05). However, after 4 wk of consuming the diets, the net increases for the SO, SF and FO groups were 127 ± 6, 149 ± 11 and 125 ± 5 g, which did not differ, resulting in final body weights of 472 ± 12, 489 ± 9 and 491 ± 7 g, respectively, which were not significantly different.
Diet fatty acid content.
Replacement of 100 g/kg SO by 100 g/kg animal fat (SF) led to lower proportions of oleic [18:1(n-9)] and linoleic acids [18:2(n-6)] with concomitantly higher proportions of the saturated fats, myristic (14:0), palmitic (16:0) and stearic acids (18:0) (400 g/kg of diet). Similarly, replacement with 100 g/kg fish oil (FO diet) also led to a lower proportion of oleic [18:1(n-9)] and linoleic acids [18:2(n-6)] and higher proportions of saturated fat (230 g/kg) with a total content of 210 g/kg (n-3) fatty acids, mainly as EPA and DHA. The (n-6)/(n-3) ratios of the SO, SF and FO diets were 37.4, 8.3 and 0.3, respectively (Table 2)
.
Fatty acid contents of total phospholipids of colon and ileum.
The major differences in the fatty acid composition of colonic and ileal tissue were the higher proportions of (n-3) PUFA [EPA, docosapentaenoic acid (DPA) and DHA] in the FO group compared with the SO and SF groups (P < 0.001), with concomitantly lower proportions of total monounsaturated and (n-6) PUFA (P < 0.05), mainly as arachidonic acid 20:4(n-6) and 22:5(n-6) (Table 3
). Therefore, the (n-6)/(n-3) ratio of the FO group approximated unity (1.0) and was significantly lower (P < 0.001) in the colon and ileum compared with the SO and SF groups. There were slightly but significantly higher proportions of total saturated and total PUFA in the ileal tissue of the FO group compared with the SO or SF groups (P < 0.05).
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The dose-response curves for acetylcholine and 8-iso-PGE2 for the colon and ileum are compared in Figure 1
. The dose-response curves for PGE2, PGE2 and U-46619 for the ileum are shown in Figure 2
. The calculated EC50 (nmol/L) and maximal contraction (V/g tissue) values for the colonic and ileal tissue are given in Table 4
. The agonists histamine and 5-HT, which were quite active in guinea pig ileum (15
,16
), and 8-iso-PGF2, which has strong vasoconstricting effects in rat aorta (17
), had little effect on rat gut at concentrations up to 10 µmol/L in these preparations (results not shown). For the rat colon, there was no differences in the EC50 or the maximal contraction (V/g) among the 3 dietary groups induced by acetylcholine or 8-iso-PGE2, with the rat colon being relatively insensitive to U-46619. However, for the ileum, the FO group had greater maximal contractions (P < 0.05) induced by acetylcholine and 8-iso-PGE2 than the SO and SF groups (Fig. 1)
. The ileum also had greater maximal contractions induced by PGE2, PGF2 and U-46619 compared with the SF group (Fig. 2)
. Groups did not differ in either colon or ileum in the EC50 values for any of the gastrointestinal agonists used.
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The pH of the cecal digesta from the FO group was lower (P < 0.001) than in the SF group. The concentration of butyrate in the FO group was greater than in the SF group (P < 0.05) (Table 5
).
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DISCUSSION |
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TOPABSTRACTINTRODUCTIONMATERIALS AND METHODSRESULTSDISCUSSIONLITERATURE CITED |
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); however, few data exist concerning the effectiveness of isoprostanes and thromboxanes. We report here a significantly higher maximal contractility of the ileum in the fish oil–supplemented group to all active pharmacological agents studied, i.e., acetylcholine, 8-iso-PGE2, PGE2 and F2, and the thromboxane mimetic, U-46619. Although the colonic tissue demonstrated similar PUFA profiles, particularly the (n-3) PUFA composition, fish oil supplementation did not affect the in vitro contractility variables.
Although the extent of maximal contractility of the colon and ileum was similar for all agonists tested, the sensitivities (EC50) were of a similar order of potency reported for rats (19
). For the ileum, the rank order for the agonists was PGF2 > U-46619 > acetylcholine > 8-iso-PGE2 
PGE2. As shown for guinea pig ileum (17
), U-46619 exhibited very low potency in the rat colon (19
), but in this study, was relatively potent in rat ileum. It has been found that prostanoid effects on gut tissue are site and indeed, species dependent (18
,20
). These results support the concept that there is not a unique isoprostane receptor in these tissues (17
).
Fish oil supplementation has been shown to increase the incorporation of (n-3) PUFA into the small intestine of pigs (21
) and the small and large bowel of rats (22
,23
). In this study we found that feeding rats with a 100 g/kg fish oil–supplemented diet for 4 wk also led to a higher proportion of (n-3) PUFA in the colon and ileum relative to the other supplements used. Specifically, the proportions of EPA, DPA and DHA of the total phospholipid fraction of gut tissue from the fish oil supplemented group (FO) was higher than in rats fed diet containing SO or saturated animal fat (SF), which had concomitantly higher total (n-6) PUFA proportions composed predominantly of linoleic [18:2(n-6)] and arachidonic acids [20:4(n-6)], respectively. The total proportions of saturated fatty acids (mainly 16:0) and total PUFA proportions were higher, with oleic acid [18:1(n-9)] lower, in the ileal tissue of the FO group compared with the SO and SF groups, but this trend was not evident for the colon. It is difficult to explain the greater contractile responses of the ileal tissue from the FO group to gastrointestinally active agonists compared with colonic tissue on the basis of these subtle membrane fatty acid compositional differences alone.
Studies investigating the effects of long chain (n-3) PUFA on contractility have yielded different results depending on the muscle type studied or mode of administration of the particular fatty acid(s). Fish oil supplementation has been shown to alter the contractile activity of isolated adult cardiomyocytes (24
), cardiac papillary muscle (25
), perfused heart (26
) and left ventricular ejection fraction in vivo (27
). In contrast, human bowel transit times were not altered in response to (n-3) PUFA-supplemented diets or acute (n-3) fatty acid administration (28
). However, acute administration of long-chain (n-3) PUFA into the human duodenum did decrease cholecystokinin release and shortened contraction duration of the gallbladder (29
). Although it is not necessarily valid to correlate the increased ileal contraction of the dietary fish oil–supplemented rats with modulation of whole-animal gut transit, it may well relate to isolated contractile patterns of the motor complexes (29
) and to small bowel health in general without changes in intestinal peristalsis.
The mechanism by which fish oil supplementation produces a relatively higher ileal response to gastrointestinal agonists in vitro may involve changes in membrane fluidity (30
–32
) or specific local effects that may modify receptor mechanisms or ion channels that involve calcium handling within the ileal smooth muscle cells linked to electrical coupling and contraction. Reports have shown that acute (n-3) PUFA administration to cardiac tissue can influence various ion channels including sarcolemmal L-type calcium current (33
,34
) as well as direct effects of (n-3) PUFA on the calcium content of the sarcoplasmic reticulum (SR) via SR uptake and SR release processes (35
). Dietary (n-3) PUFA supplementation has also been reported to influence calcium signaling in rat T cells (36
). However, little information of this type is available for smooth muscle such as gut. Acetylcholine, prostaglandins, iso-prostaglandins and thromboxanes are all believed to act via G-protein–coupled receptor systems on the cell membrane that regulate cellular function (37
,38
). Receptor binding studies of gastrointestinal agonist subtypes complemented by reverse transcription-polymerase chain reaction technologies for eicosanoid receptor subtypes may help to explain why dietary fish oil increases the contractility of the ileum but not the colon. However, because the large intestine is primarily for drying and storage of digestive waste material, the contractile properties influenced by (n-3) PUFA in the ileum may not be translated to the distal bowel.
The finding that 8-iso-PGE2 promoted gut contractility may have pathophysiologic importance because 8-iso-PGE2 is formed nonenzymatically in situ due to peroxidation of membrane arachidonic acid (38
). Therefore, it is conceivable that disease conditions that reflect increased oxidative stress, such as inflammatory bowel disease and ulcerative colitis, may be associated with increased isoprostane levels. Because these agents have potent vasoactive properties, isoprostanes may also influence mucosal microcirculation. It was reported recently that (n-3) PUFA and vitamin E supplementation inhibited lipid peroxidation and increased mucosal blood flow in rats with experimental colitis (39
).
Dietary fish oil supplementation in this study decreased the cecal pH compared with saturated fat supplementation, and this was not associated with an increase in the SCFA content. Depending on the diet and animal model employed, a decreased cecal pH has been found to be associated with increased gastrointestinal transit time (40
), whereas a lowering of colonic pH has been associated with reduced large bowel transit time (41
) and reduced incidence of cancer (42
,43
). SCFA have been implicated in the control of gastrointestinal contractility and motility at the level of the rumen (44
) and stomach (45
), the small intestine (46
) and the colon (47
). In this study, the specific effect of fish oil on gastrointestinal transit in rats was not measured. The interplay between intestinal pH and SCFA content and the feedback mechanisms involved in gastrointestinal contractility and motility have not yet been fully elucidated (48
,49
).
In summary, we demonstrated for the first time that dietary fish oil supplementation increases in vitro contractility of the ileum to gastrointestinal modulators of motility. Although both the ileum and colon had similar total phospholipid fatty acid profiles in terms of the type and extent of incorporation of (n-3) PUFA after fish oil supplementation, the colon did not exhibit higher in vitro contractility, possibly due to its limited physiologic role. Fish oil supplementation also decreased the cecal pH and increased butyrate concentration (compared with the SF diet), changes that are important in bowel health. The mechanism whereby (n-3) PUFA substitution in the diet increased ileal contractility is yet to be determined. However, the implications for animals and humans consuming (n-3) PUFA may well be manifest in improved ileal contractility and functioning in inflammatory (1
–3
,6
,50
) conditions such as Crohn’s disease in particular (7
), and wound or surgical healing (5
) in which normal small bowel function has been compromised.
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ACKNOWLEDGMENTS |
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FOOTNOTES |
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3 Abbreviations used: DHA, docosahexaenoic acid; DPA, docosapentaenoic acid; EC50, 50% effective concentration; EPA, eicosapentaenoic acid; FAME, fatty acid methyl esters; FO, fish oil; GC, gas chromatograph; 5-HT, 5-hydroxy tryptamine (serotonin); PG, prostaglandin; PUFA, polyunsaturated fatty acids; SCFA, short-chain fatty acids; SF, saturated animal fat; SO, Sunola oil; SR, sarcoplasmic reticulum.
Manuscript received 10 February 2002. Initial review completed 17 March 2002. Revision accepted 22 May 2002.
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TOPABSTRACTINTRODUCTIONMATERIALS AND METHODSRESULTSDISCUSSIONLITERATURE CITED |
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