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Nutrient Metabolism

Intestinal Adaptation Occurs Independently of Parenteral Long-Chain Triacylglycerol and with No Change in Intestinal Eicosanoids after Mid-Small Bowel Resection in Rats¹

Department of Nutritional Sciences, University of Wisconsin-Madison, Madison, WI 53706

² To whom correspondence and reprint requests should be addressed. E-mail: ney{at}nutrisci.wisc.edu.

	ABSTRACT

TOP ABSTRACT MATERIALS AND METHODS RESULTS DISCUSSION LITERATURE CITED

 
The role of enteral or parenteral long-chain triacylglycerol (LCT) in the complex process of intestinal adaptation is poorly defined and may involve alterations in eicosanoid synthesis. Our objective was to determine whether provision of parenteral LCT stimulates eicosanoid synthesis and resection-induced intestinal adaptation. We assessed small bowel structural adaptation, the fatty acid profiles of liver, plasma and jejunal mucosa, and the profile of 11 eicosanoids derived from (n-6) PUFA of the jejunal mucosa in rats maintained with total parenteral nutrition (TPN) with 0 or 32% of nonprotein energy from Intralipid for 7 d after mid-small bowel resection or transection control surgery. There was no evidence of biochemical essential fatty acid (EFA) deficiency in the absence of parenteral fat. Resection-induced gut growth occurred independently of parenteral LCT based on significant mucosal hyperplasia in the jejunum and ileum. The mucosal profile of linoleic acid in the total lipid extract of jejunum increased with the presence of parenteral LCT, but decreased with resection without differences in arachidonic acid. There were no differences in the jejunal profile of 11 (n-6)–derived eicosanoids among the four TPN groups as determined by tandem MS. In summary, small bowel resection–induced adaptation occurs independently of parenteral LCT, and fat-free TPN without EFA deficiency does not alter the profile of jejunal (n-6)–derived eicosanoids. Thus, parenteral administration of LCT does not appear to alter jejunal eicosanoid synthesis nor is it beneficial in stimulating intestinal adaptation.

KEY WORDS: • intestinal adaptation • long-chain triacylglycerol • eicosanoids • parenteral nutrition • bowel resection

Intestinal adaptation to bowel resection is a poorly understood process that involves structural and functional alterations in the remnant gut that aim to enhance nutrient, electrolyte and fluid absorption. Luminal nutrients, hormones, pancreaticobiliary secretions and neural pathways in the gastrointestinal tract are thought to mediate this adaptive response (1). Defining the nutritional components that modulate intestinal adaptation may lead to improved treatments for short bowel syndrome, a form of intestinal failure that often requires parenteral nutrition to maintain nutritional status ater bowel resection in humans.

Several studies suggested that enteral long-chain triacylglycerol (LCT)² and/or its metabolites such as eicosanoids stimulate intestinal adaptation (2–7). In orally fed, mid-small bowel resected rats, a diet enriched in LCT improved adaptive intestinal structure and function better than a diet enriched in medium-chain triglycerides (4). In resected rats given 85% of energy intravenously and 15% intragastrically as fat, carbohydrate or protein, the group that received the fat as LCT had the greatest adaptation (3). Furthermore, resection-induced adaptation in rats is enhanced by the administration of prostaglandins (PG) (5) and diminished by inhibiting PG synthesis via feeding essential fatty acid (EFA)-deficient diets (7) or the administration of aspirin (6). Thus, these studies suggest that enterally administered lipid, primarily as LCT, and/or lipid-derived eicosanoid metabolites stimulate intestinal growth.

It is not clear whether lipid present in total parenteral nutrition (TPN) solutions, primarily (n-6) PUFA derived from soybean oil, has intestinotrophic properties similar to those of enteral LCT. Systemically administered LCT, whether as a component in the TPN solution (8) or as a radiolabeled free fatty acid (FA) (9,10), is rapidly taken up by the small intestine. This implies a role for the systemic uptake of lipid in the intestinal mucosa and the potential for parenteral LCT to affect gut growth. However, there are no reports that directly assessed whether parenteral LCT alters both intestinal FA composition and intestinal growth. Moreover, the role of parenteral LCT in resection-induced intestinal adaptation has not been tested directly. In nonresected piglets, the presence of LCT in the TPN solution did not stimulate greater jejunal and ileal growth compared with a solution containing only glucose and amino acids (11,12), although it did significantly increase duodenal villous area and mucosal height (11). Thus, it is not known whether parenteral LCT stimulates intestinal adaptation after bowel resection, regardless of its ability to alter the intestinal FA composition (8).

Speculations regarding the mechanisms by which long-chain PUFA stimulate intestinal adaptation include LCT acting as structural components of cell membranes, altering membrane composition and membrane-associated enzymes, influencing phospholipid content and composition, and, in particular, being precursors of eicosanoids (7). Of the eicosanoids, PG (derived from the cyclooxygenase pathway) as opposed to leukotrienes or thromboxanes (TX; derived from the lipoxygenase pathway) enhance adaptive growth to a greater degree (13). The PG derived from (n-6) PUFA act in regulating intestinal blood flow, altering motility, influencing fluid secretion, modulating inflammation and transporting ions across membranes (5). These responses are considered components of the adaptive growth process. Furthermore, enteral lipid may exert its intestinotrophic effects via gut hormones. In particular, enteral lipid stimulates the release of glucagon-like peptide-2 (GLP-2) (14), a hormone that is consistently associated with resection-induced intestinal adaptation (15,16).

We reported previously that significant adaptive growth after bowel resection occurred in the entire residual small intestine in the absence of exogenous luminal nutrients due to TPN (15). It is possible that a specific nutritional component of the TPN solution, such as parenteral LCT, mediated the intestinal adaptive response in the parenterally fed rats. Thus, our objective was to determine the intestinal adaptive response to mid-small bowel resection in the presence or absence of parenteral LCT and its association with the jejunal profile of FA and (n-6)–derived eicosanoids in growing, parenterally fed rats.

	MATERIALS AND METHODS

TOP ABSTRACT MATERIALS AND METHODS RESULTS DISCUSSION LITERATURE CITED

 
    Animals and experimental design. The University of Wisconsin-Madison Institutional Animal Care and Use Committee approved the animal facilities and protocols. Male Sprague-Dawley rats (Harlan, Madison, WI) initially weighing 200–225 g were housed in individual stainless steel, wire-bottomed cages with free access to water in a room maintained at 22°C on a 12-h light:dark cycle. The experimental design included six treatment groups, four of which were nourished parenterally and two were nourished orally.

    Parenterally fed treatment groups. The four parenterally fed treatment groups were arranged in a 2 x 2 factorial design as follows: gut resection and parenteral lipid, R+FAT (n = 8), gut resection and no lipid, R+NO FAT (n = 8), gut transection and parenteral lipid, T+FAT (n = 7), or gut transection and no lipid, T+NO FAT (n = 7). The survival rate was 97%; one rat was unable to complete the study due to loss of catheter patency. The parenterally fed rats were adapted to the facility for 3–4 d while consuming a semipurified, powdered diet ad libitum (17). Three days before surgery, rats consumed a semielemental, residue-free, liquid diet ad libitum to minimize intestinal contents at the time of operation (Vital, donated by Ross Laboratories, Columbus, OH).

The 70% mid-jejunoileum surgical procedure and animal care were previously described in detail (15). Briefly, resected rats had bowel from 15 cm distal to the ligament of Treitz until 15 cm proximal to the cecum removed, continuity restored with an end-to-end jejunoileal anastomosis, and saline placed into the peritoneal cavity for fluid resuscitation. Transected rats received a transection cut in the ileum (15 cm proximal to the cecum) and suturing to reestablish continuity. The TPN catheter was placed in the superior vena cava via the external jugular vein after the abdomen was closed (18). Immediately after surgery (d 0), infusion of TPN solution was initiated as previously detailed (15,18,19) and water was freely available.

    Orally fed treatment groups. The two orally fed, nonsurgical treatment groups served as a baseline for the effects of typical enteral lipid metabolism on intestinal growth, fatty acid (FA) profiles and eicosanoid biosynthesis. The groups included were: FAT (n = 5) and NO FAT (n = 5). All rats were adapted to the facility for 7 d while consuming a semipurified, powdered diet ad libitum (17). Rats continued ad libitum consumption of the powdered diet for the 7-d experimental period. All orally fed rats completed the study.

    Composition of TPN and oral diets. TPN rats were given isonitrogenous TPN solutions,³ which provided either 32% of nonprotein energy as fat (32% fat TPN) or with 0% of nonprotein energy as fat (0% fat TPN). The infusion rate of the TPN solution was gradually increased from 20 mL on d 0, to 36 mL on d 1 and 56 mL on d 2–6, providing the sole source of nutrition until the end of the experiment. Mean energy intake over 7 d was 837 kJ/(kg · d). Daily and cumulative energy intakes did not differ between R and T rats given either 32% fat TPN or fat-free TPN.

Orally fed rats consumed ad libitum a semipurified, powdered diet⁴ that provided either 33% of nonprotein energy as fat (33% fat ORAL) or 0% of nonprotein energy as fat (0% fat ORAL) and had a macronutrient composition comparable to the 32% fat and 0% fat TPN solutions, respectively (17). Rats ate 26 g of either diet daily. Mean energy intake over 7 d was 1780 kJ/(kg · d) in the 33% fat ORAL group and 1465 kJ/(kg · d) in the 0% fat ORAL group (P = 0.017). Food cups were weighed daily to calculate the amount of food consumed.

    Small intestine composition and histology. After 7 d of either exclusive TPN or oral feeding, rats were anesthetized by inhalation of isoflurane and killed by exsanguination from the portal vein. The remaining jejunum (the 15 cm distal to the ligament of Treitz) and ileum (anastomosis to ileocecal junction) were removed. The segments were flushed with ice-cold saline (9 g NaCl/L) and placed onto an ice-cold glass plate where tissue sections were cut into defined lengths. To start with, tissue (2 cm) on either side of the jejunoileal anastomosis was discarded. Then, the first centimeter of each remaining segment from the proximal end of the jejunum and ileum was fixed in HistoChoice (Amresco, Solon, OH), embedded in paraffin, cut in 5-µm sections, and stained with hematoxylin and eosin so that villous height and crypt depth could be measured as previously described (20). A 2-cm section, derived from the second and third centimeters of each small bowel segment, was used to determine mucosal mass; the groups did not differ in water content of the intestine. The next 3-cm segment in the small intestine segments was used for the analysis of protein and DNA contents (15). The next 5-cm section in the jejunum was used for quantification of eicosanoids, as detailed below. The last 3- to 4-cm segment in the jejunum was snap-frozen in liquid nitrogen and used for determination of the FA profile as described below. Mucosa (15) was used in the analyses for mucosal mass, concentrations of protein and DNA, eicosanoid contents and FA composition.

    Fatty acid analysis of total lipid extracts. FA composition in the total lipid extract of plasma, liver, and jejunal mucosa, in addition to the Intralipid and oral diet, was determined by GC using previously published methods (21,22). Briefly, after total lipids were extracted from the samples, the FA were transesterified using methanol/benzene (4:1, v/v; 2 mL) and acetyl chloride (200 µL) and the FAME were analyzed on a Varian 3400 GC (Varian, Harbor City, CA). FA were identified by comparing the retention times with those of known standards (Nu-Chek-Prep, Elysian, MN) and expressed as the weight percentage distribution of FAME. The Holman index (i.e., triene:tetraene ratio) was determined by dividing the percentage of eicosatrienoic acid [20:3(n-9)] by the percentage of arachidonic acid [20:4(n-6)] (23). A ratio > 0.2–0.4 is considered to be indicative of biochemical EFA deficiency (24). None of the samples indicated a biochemical EFA deficiency.

    Jejunal eicosanoid profile. Eicosanoids were quantified by HPLC coupled with negative ion electrospray tandem MS (LC/MS/MS), as described previously (25,26). We modified the previously published methods to quantify eicosanoids in the intestine as follows. Briefly, a weighed amount of jejunal mucosa obtained by scraping was homogenized in physiologic saline solution, pH 7.4, similar to previous eicosanoid analyses in the intestine (6). The homogenate was spiked with an internal standard (PGB₂, #11210, Cayman Chemical, Ann Arbor, MI) and applied to preconditioned C18 Bond Elut cartridges (Varian). The cartridges were subsequently washed, and the eicosanoids were then eluted in 12 mL methyl formate. The methyl formate was evaporated to completion under a dry N₂ stream. Samples were then resuspended in 1 mL ethanol, transferred to autosampler vials and quantified by LC/MS/MS within 12 h of collection. This method was successfully used to profile 11 eicosanoids derived from (n-6) FA, including TXB₂, 6-keto-PGF₁, PGF₂, PGE₂, PGD₂, 13-hydroxyoctadecadienoic acid (HODE), 9-HODE, 15-hydroxyeicosatetraenoic acid (HETE), 12-HETE, 8-HETE, and 5-HETE. TX and PG standards (Cayman Chemical) were linear over a range of 5 to 2000 µg/L; HODE and HETE standards (Cayman Chemical) were linear over a range of 5–200 µg/L. Recovery of the PGB₂ internal standard from all samples was 99.4 ± 5.6%.

    Statistical analysis. Parenterally fed treatment groups were compared using two-way ANOVA that determined the significance of main effects and interaction between resection and presence of parenteral lipid (SAS Institute, Cary, NC). Individual differences between groups were determined by one-way ANOVA (P < 0.05) on the four treatment combinations followed by the protected least significant differences technique. Group means of orally fed treatment groups were considered to be significantly different at P < 0.05, as determined by a two-tailed t test (SAS). TPN and ORAL groups were not compared statistically. Data are presented as means ± SEM. Means with different superscripts are significantly different. Differences between groups with 0.05 P < 0.15 are referred to as trends.

	RESULTS

TOP ABSTRACT MATERIALS AND METHODS RESULTS DISCUSSION LITERATURE CITED

 
Body weight and nitrogen balance

    Parenterally fed rats. Body weight gains in resected and transected rats administered TPN with or without parenteral lipid did not differ after 7 d of TPN (R+FAT, 5 ± 3; T+FAT, 1 ± 2, R+NO FAT, 6 ± 5; T+ NO FAT, 5 ± 2 g body weight gain/7 d). Similarly, there were no significant differences in nitrogen intake or nitrogen excretion between the four parenterally fed treatment groups (data not shown). Thus, short-term parenteral nutrition regimens with or without lipid in the form of Intralipid promoted similar whole-body anabolism.

    Orally fed rats. Body weight gains in nonsurgical orally fed rats did not differ after 7 d of oral diets with or without lipid (FAT, 37 ± 3; NO FAT, 31 ± 3 g body weight gain/7 d). Thus, in the short term, enteral nutrition regimens with or without lipid promoted similar whole-body growth.

Jejunal and ileal mucosal composition and histology

    Parenterally fed rats. Resection, independent of parenteral LCT, induced jejunal and ileal mucosal hyperplasia as shown by the significantly greater jejunal and ileal mucosal dry mass and concentrations of protein and DNA (Fig. 1). Morphology mirrored the mucosal concentrations of protein and DNA because resection increased villous height in the ileum (R+FAT, 325 ± 40; T+FAT, 243 ± 10, R+NO FAT, 330 ± 15; T+ NO FAT, 273 ± 15 µm; main effects, resection, two-way ANOVA, P = 0.0012) and tended to increase villous height in the jejunum (R+FAT, 297 ± 7; T+FAT, 251 ± 28, R+NO FAT, 307 ± 19; T+ NO FAT, 263 ± 7 µm; main effects, resection, two-way ANOVA, P = 0.062). Moreover, in nonresected rats, the presence of parenteral LCT did not affect jejunal mass or cellularity, which is in agreement with the report by Shulman and Burrin (11) in nonresected pigs nourished via TPN with or without lipid for 7 d.

View larger version (14K): [in this window] [in a new window]   FIGURE 1 Mucosal dry mass, protein content and DNA content in the jejunum (A) and ileum (B) in 4 groups of rats maintained exclusively with TPN with (FAT) or without (NO FAT) parenteral lipid for 7 d after ileal transection (T) or 70% mid-jejunoileal resection (R) and 2 groups of orally fed, nonsurgical, age-matched rats maintained with (FAT) or without (NO FAT) enteral lipid. Resection showed significant main effects (P < 0.0015) to increase jejunal and ileal mucosal dry mass, protein and DNA based on two-way ANOVA among TPN groups. Values are expressed as means + SEM; n = 6–8 rats per TPN group and n = 5 per ORAL group. Means without a common letter differ based on one-way ANOVA and protected least significant differences.

Liver, plasma, and jejunal mucosal fatty acids of total lipid extracts

    Relationship of the hepatic fatty acid profile to EFA status. There was no evidence of biochemical EFA deficiency in either the orally or parenterally fed groups given the fat-free diets (Table 1). Changes in the hepatic FA profile are a sensitive indicator of EFA deficiency in rats (27). The abnormal FA, eicosatrienoic acid, appears in liver with EFA deficiency and in conjunction with arachidonic acid is used for the calculation of the triene:tetraene ratio [20:3(n-9)/20:4(n-6)] which is an indicator of EFA deficiency (23). A triene:tetraene ratio of >0.2–0.4 indicates biochemical EFA deficiency (24). Parenterally fed rats that did not receive LCT had a significant increase in the hepatic triene:tetraene ratio; however, the value of the ratio was only 0.048 (Table 1). Moreover, both orally and parenterally fed rats given the fat-free diets had the expected decreases in hepatic linoleic [18:2(n-6)] and linolenic [18:3(n-3)] acids and increases in hepatic oleic [18:1(n-9)] and palmitoleic [16:1(n-9)] acids that characterize early depletion of EFA in rats (23). There were no differences in the proportion of arachidonic acid in liver (Table 1) due to the absence of dietary fat.

Jejunal mucosal eicosanoid content

    Parenterally fed rats. There were no significant differences between the TPN groups in the content of any of the 11 eicosanoids in the jejunal mucosa (Tables 5, and 6). The eicosanoid profile can be directly correlated with the FA profile only when the eicosanoid precursor pool, i.e., FA phospholipids, is measured. We were unable to measure the FA profiles of the phospholipid fraction because of limited tissue. The alterations we observed in the FA profile in the total lipid extract of jejunal mucosa are consistent with those of Van Aerde et al. (8) in FA phospholipids of nonresected piglets nourished by TPN, suggesting that we can make an association between our FA and eicosanoid profiles. Thus, the lack of a significant difference in the relative percentage of arachidonic acid, the precursor to the (n-6)–derived eicosanoids, in the jejunal mucosal is consistent with no significant differences in jejunal eicosanoid contents between TPN groups.

2

	DISCUSSION

TOP ABSTRACT MATERIALS AND METHODS RESULTS DISCUSSION LITERATURE CITED

 
The intestinal adaptive response to bowel resection is multifactorial, involving luminal nutrients, hormones and other factors. Although previous studies have shown that resection-induced intestinal adaptation was associated with administration of enteral LCT and eicosanoid biosynthesis (3,4,6,7), the ability of parenteral LCT to stimulate resection-induced intestinal growth has not been directly tested and reported. In this study, we demonstrated in growing, parenterally fed rats free of EFA deficiency that adaptation to mid-small bowel resection occurs independently of parenteral LCT. We observed nearly identical mucosal hyperplasia in the jejunum and ileum of rats administered TPN that was fat-free or provided 32% of nonprotein energy from LCT. Moreover, the profile of 11 eicosanoids derived from (n-6) FA in the jejunal mucosa did not differ among any of the TPN groups.

It is clear that parenteral LCT did not stimulate resection-induced intestinal adaptation. If we were to see such an effect, it would have occurred by 7 d after resection. This is based on our previous report showing that increases in jejunal mucosal mass and concentrations of protein and DNA can occur as early as 8 h after resection in TPN rats (15).

There is one TPN gut resection study that is particularly relevant to the interpretation of our report (30). In that study, Al-Jurf et al. observed no significant resection-induced adaptation when lipid was inadvertently omitted from the TPN solution. However, this resection model was different from ours in that it contained only 2 cm of residual ileum, a segment of bowel critical in resection-induced growth (15,20,31). In contrast, our mid-small bowel resection model retained 15 cm of ileum. Moreover, they did not assess EFA deficiency. It is crucial to consider the nutritional state of the animals because EFA deficiency has been shown to inhibit the adaptive response (7). Specifically, our rats were not EFA deficient and there was no effect of parenteral LCT on intestinal growth. In contrast, refeeding linoleic acid enterally to resected rats with biochemical EFA deficiency stimulated intestinal growth, possibly due to the provision of constituents, i.e., EFA, that were limiting in the growth response (7).

The EFA state of the animal is important because EFA give rise to eicosanoids, which play a role in gut growth. In particular, Vanderhoof et al. (6) administered aspirin and Hart et al. (7) induced EFA deficiency by diet alteration to inhibit eicosanoid synthesis and diminish resection-induced adaptation. However, we used diet modification without induction of EFA deficiency to modulate the intestinal eicosanoid content.

The alterations in intestinal eicosanoids in orally fed rats detected by our novel use of tandem MS are in agreement with diet-induced changes. Specifically, the decreased production of the (n-6)–derived PG, especially PGF₂, in the presence of enteral LCT is consistent with the ability of linolenic acid supplied by the soybean oil to competitively inhibit the production of the PG derived from linoleic acid; this thereby favors the production of a different set of PG derived from linolenic acid (32). In contrast to enteral LCT, parenteral LCT did not significantly modify jejunal eicosanoids.

One explanation for the ability of enteral but not parenteral LCT to improve intestinal growth after resection (3,4) is that the metabolic fate of FA appears to differ if they are derived from the intestinal lumen rather than the systemic circulation. Specifically, it was demonstrated in food-deprived rats that enteral lipid is esterified primarily to triglyceride in the enterocyte, whereas parenteral LCT is preferentially oxidized (10). Given that eicosanoid biosynthesis was not completely inhibited in the current study, it is possible that the basal level of eicosanoids produced by TPN-nourished rats given fat-free nutrition was sufficient to stimulate resection-induced intestinal growth.

Our results do confirm that parenteral LCT can modify the FA profile in the total lipid extract of the intestinal mucosa. This is consistent with the report of alterations in FA of intestinal phospholipids in TPN-nourished piglets by Van Aerde et al. (8). Specifically, we observed a significant decrease in the relative percentage of linoleic acid and a tendency for increases in the relative percentages of palmitoleic acid and oleic acid in the total lipid extract of jejunal mucosa when lipid was omitted from the TPN solution. Van Aerde et al. reported similar decreases in linoleic acid and increases in oleic acid in phospholipids of brush border and enterocyte microsomal membranes in the jejunum and ileum of piglets receiving 3 wk of fat-free TPN compared with TPN providing 40% of nonprotein energy derived from a soybean oil emulsion.

The ability of the intestine to take up parenteral LCT is rapid, as evidenced by two studies that administered radiolabeled free FA systemically (9,10). Rapid uptake of LCT by the small bowel further substantiates a direct role for the systemic uptake of lipid into the intestinal mucosa, as opposed to the endogenous release of FA into the intestinal lumen via biliary secretion. This also indicates that systemic free FA may be an integral source for supplying PUFA to the small intestinal mucosa. For example, in the current study, resection decreased the relative percentage of linoleic acid in the jejunal mucosa, possibly due to increased oxidation to provide energy for the increased synthesis and rapid turnover of the enterocytes (9). This suggests that the growth state of the intestinal epithelium determines the fate of parenteral LCT, specifically linoleic acid.

In summary, these data demonstrate that small bowel resection–induced adaptation occurs independently of parenteral LCT, and fat-free TPN without EFA deficiency does not alter the profile of (n-6)–derived eicosanoids in the jejunal mucosa. Thus, parenteral administration of LCT does not appear to alter eicosanoid synthesis nor is it beneficial in stimulating intestinal adaptation. The effect of LCT on intestinal adaptation appears to depend on whether the lipid is provided parenterally or enterally; enteral administration of LCT may be required to alter intestinal synthesis of eicosanoids.

Our study is consistent with the hypothesis that regulation of intestinal adaptation is a complex process through which a variety of enteral and parenteral nutrients act to alter gut hormone secretion and neurostimulation. One such candidate hormone is GLP-2, an intestinotrophic peptide produced primarily in the ileum and colon. We showed previously that plasma bioactive GLP-2 is significantly increased early after resection in this model (15). Thus, these data support the notion that intestinal adaptation to mid-small bowel resection is associated with the intestinotrophic hormone GLP-2 (15) and occurs independently of parenteral LCT.

	ACKNOWLEDGMENTS

 
We thank Karen Kritsch for assistance with animal care, Alan Higbee for assistance in modifying the eicosanoid profiling method for the intestinal mucosa, and Amy Harms and James Brown at the University of Wisconsin Biotechnology Center for assistance with LC/MS/MS analysis. We also thank Mark E. Cook for advice on the development of the intestinal eicosanoid profiling method and interpretation of the eicosanoid data.

	FOOTNOTES

 
¹ Supported by the National Institute of Diabetes and Digestive and Kidney Diseases Grant RO1-DK-42835, a USDA National Needs Graduate Fellowship and funds from the College of Agriculture and Life Sciences, University of Wisconsin-Madison.

³ Abbreviations used: EFA, essential fatty acid; FA, fatty acid; GLP-2, glucagon-like peptide-2; HETE, hydroxyeicosatetraenoic acid; HODE, hydroxyoctadecadienoic acid; LCT, long-chain triacylglycerol; PG, prostaglandin; R, resection; T, transection; TPN, total parenteral nutrition; TX, thromboxane.

⁴ The 32% fat TPN solution contained (in g/L): 45 amino acids (Travasol 8.5% with electrolytes; Baxter Healthcare, Deerfield, IL), 180 dextrose (Baxter Healthcare) and 28 lipid (142 mL Intralipid; Kabi Pharmacia, Clayton, NC), providing 32% nonprotein energy from fat and 68% nonprotein energy from dextrose (17). The 0% fat TPN solution contained (in g/L): 45 amino acids and 270 dextrose, providing 0% nonprotein energy from fat and 100% nonprotein energy from dextrose. Micronutrient intakes in both 32 and 0% fat TPN are as previously reported (17).

⁵ The 33% fat ORAL diet contained (in g/kg): 163 casein, 3 DL-methionine, 635 dextrose, 70 soybean oil, 70 safflower oil, 12 cellulose, 35 AIN-76 mineral mix, 10 AIN-76A vitamin mix, 2 choline bitartrate, providing 33% nonprotein energy from fat and 67% nonprotein energy from dextrose (17). The 0% fat ORAL diet contained (in g/kg): 163 casein, 3 DL-methionine, 775 dextrose, 12 cellulose, 35 AIN-76 mineral mix, 10 AIN-76A vitamin mix, 2 choline bitartrate, providing 0% nonprotein energy from fat and 100% nonprotein energy from dextrose. All diet ingredients were obtained from Teklad (Madison, WI). Micronutrient intakes in both the 33 and 0% fat ORAL diets are as previously reported (17).

Manuscript received 2 July 2003. Initial review completed 18 September 2003. Revision accepted 9 October 2003.

	LITERATURE CITED

TOP ABSTRACT MATERIALS AND METHODS RESULTS DISCUSSION LITERATURE CITED

 

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