• View in gallery
    Figure 1—

    Results of the dilutional parallelism evaluations of an enzyme-labeled immunometric assay for measurement of serum gastrin concentration in dogs. Serum samples were collected from 3 healthy dogs (designated as dogs A, B, and C). This assay was performed on 3 replicates of dog A serum, 6 replicates of dog B serum, and 3 replicates of dog B serum for each of the following dilutions: 1:2, 1:4, 1:8, 1:16, 1:32, 1:64, and 1:128. Serum from dog A (low gastrin concentration) was used as the diluent.

  • View in gallery
    Figure 2—

    Percentage change in mean serum cTLI concentrations in 10 healthy dogs before (0 hours [baseline]) and at 1 to 2 and 6 hours after consumption of 1 meal of each of 4 diets (1-week interval between diet treatments). Dogs were fed a maintenance commercial dog foodc that had a crude fat content of 16% (diet A [circles]); a low-fat commercial dog foodd that had a crude fat content of 5% (diet B [diamonds]); diet A with supplemental pancreatic enzymes (diet C [triangles]); and diet B with supplemental pancreatic enzymes and MCT oil (diet D [squares]). Food was withheld from the dogs for at least 12 hours prior to the feeding of each diet. Data are reported as mean ± SD percentage change from baseline values.

  • View in gallery
    Figure 3—

    Percentage change in mean serum cPLI concentrations in 10 healthy dogs before (0 hours [baseline]) and at 1 to 2 and 6 hours after consumption of 1 meal of each of 4 diets (1-week interval between diet treatments). Food was withheld from the dogs for at least 12 hours prior to the feeding of each diet. Data are reported as mean ± SD percentage change from baseline values. See Figure 2 for key.

  • View in gallery
    Figure 4—

    Change in mean serum gastrin concentrations in 10 healthy dogs before (0 hours [baseline]) and at 5 to 10 minutes and 1 to 2 hours after consumption of 1 meal of each of 4 diets (1-week interval between diet treatments). Food was withheld from the dogs for at least 12 hours prior to the feeding of each diet. Data are reported as mean ± SD actual change from baseline values. See Figure 2 for key.

  • 1.

    Qin HL, Su ZD, Gao Q, et al.Early intrajejunal nutrition: bacterial translocation and gut barrier function of severe acute pancreatitis in dogs. Hepatobiliary Pancreat Dis Int 2002;1:150154.

    • Search Google Scholar
    • Export Citation
  • 2.

    Weber CK, Adler G. Acute pancreatitis. Curr Opin Gastroenterol 2003;19:447450.

  • 3.

    Meier RF, Beglinger C. Nutrition in pancreatic diseases. Best Pract Res Clin Gastroenterol 2006;20:507529.

  • 4.

    Hess RS, Saunders HM, Van Winkle TJ, et al.Clinical, clinico-pathologic, radiographic, and ultrasonographic abnormalities in dogs with fatal acute pancreatitis: 70 cases (1986–1995). J Am Vet Med Assoc 1998;213:665670.

    • Search Google Scholar
    • Export Citation
  • 5.

    Mansfield CS, Jones BR. Plasma and urinary trypsinogen activation peptide in healthy dogs, dogs with pancreatitis and dogs with other systemic diseases. Aust Vet J 2000;78:416422.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 6.

    Williams DA, Batt RM. Sensitivity and specificity of radioimmunoassay of serum trypsin-like immunoreactivity for the diagnosis of canine exocrine pancreatic insufficiency. J Am Vet Med Assoc 1988;192:195201.

    • Search Google Scholar
    • Export Citation
  • 7.

    Watson P. Pancreatitis in the dog: dealing with a spectrum of disease. In Pract 2004;26:6477.

  • 8.

    Steiner JM. Diagnosis of pancreatitis. Vet Clin North Am Small Anim Pract 2003;33:11811195.

  • 9.

    Steiner JM, Teague SR, Williams DA. Development and analytic validation of an enzyme-linked immunosorbent assay for the measurement of canine pancreatic lipase immunoreactivity in serum. Can J Vet Res 2003;67:175182.

    • Search Google Scholar
    • Export Citation
  • 10.

    Steiner JM, Rutz GM, Williams DA. Serum lipase activities and pancreatic lipase immunoreactivity concentrations in dogs with exocrine pancreatic insufficiency. Am J Vet Res 2006;67:8487.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 11.

    Williams DA. The pancreas. In: Guilford WG, Center S, Strombeck D, et al, eds. Strombeck's small animal gastroenterology. 3rd ed. Philadelphia: WB Saunders Co, 1996;381410.

    • Search Google Scholar
    • Export Citation
  • 12.

    IMMULITE 2000 Gastrin [package insert]. Los Angeles: Diagnostic Products Corp, 2005.

  • 13.

    Williams DA, Steiner JM. Canine exocrine pancreatic disease. In: Ettinger SJ, Feldman EC, eds. Textbook of veterinary internal medicine. St Louis: Elsevier Saunders, 2005;14821488.

    • Search Google Scholar
    • Export Citation
  • 14.

    Shea JC, Bishop MD, Parker EM, et al.An enteral therapy containing medium-chain triglycerides and hydrolyzed peptides reduces postprandial pain associated with chronic pancreatitis. Pancreatology 2003;3:3640.

    • Crossref
    • Search Google Scholar
    • Export Citation

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Pancreatic response in healthy dogs fed diets of various fat compositions

Fleur E. JamesDepartment of Veterinary Clinical Sciences, Murdoch University, Perth, WA, Australia 6150.

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Caroline S. MansfieldDepartment of Veterinary Clinical Sciences, Murdoch University, Perth, WA, Australia 6150.

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Jörg M. SteinerDepartment of Small Animal Clinical Sciences, College of Veterinary Medicine and Biomedical Sciences, Texas A&M University, College Station, TX 77843.

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David A. WilliamsDepartment of Small Animal Clinical Sciences, College of Veterinary Medicine and Biomedical Sciences, Texas A&M University, College Station, TX 77843.

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Ian D. RobertsonDepartment of Veterinary Clinical Sciences, Murdoch University, Perth, WA, Australia 6150.

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Abstract

Objective—To indirectly assess the pancreatic response in healthy dogs that were fed diets of different fat compositions with or without supplemental pancreatic enzymes and medium-chain triglycerides (MCTs).

Animals—10 healthy adult dogs.

Procedures—Dogs were fed 4 diets once in random order at 1-week intervals; food was withheld from the dogs for ≥ 12 hours prior to the feeding of each diet. Diets A and B contained 16% and 5% crude fat, respectively; diet C was composed of diet A with pancreatic enzymes; and diet D was composed of diet B with pancreatic enzymes and MCTs. Serum canine trypsin–like immunoreactivity (cTLI) and canine pancreatic lipase immunoreactivity (cPLI) concentrations were measured before (0 hours) and at 1 to 2 and 6 hours after feeding. Serum gastrin concentration was measured at 0 hours and at 5 to 10 minutes and 1 to 2 hours after feeding. A gastrin assay validation study was performed to confirm accuracy of test results in dogs. Data were analyzed by use of a repeated-measures general ANOVA.

Results—Serum cTLI, cPLI, or gastrin concentrations in the dogs did not differ among the different diets fed, among dogs, or over time. When multiple comparisons were analyzed, diet D caused the least amount of measurable pancreatic response, although this difference was not significant.

Conclusions and Clinical Relevance—Results did not indicate a significant effect of dietary fat content or addition of supplemental MCT oil or pancreatic enzymes in diets on serum cTLI, cPLI, or gastrin concentrations in healthy dogs.

Abstract

Objective—To indirectly assess the pancreatic response in healthy dogs that were fed diets of different fat compositions with or without supplemental pancreatic enzymes and medium-chain triglycerides (MCTs).

Animals—10 healthy adult dogs.

Procedures—Dogs were fed 4 diets once in random order at 1-week intervals; food was withheld from the dogs for ≥ 12 hours prior to the feeding of each diet. Diets A and B contained 16% and 5% crude fat, respectively; diet C was composed of diet A with pancreatic enzymes; and diet D was composed of diet B with pancreatic enzymes and MCTs. Serum canine trypsin–like immunoreactivity (cTLI) and canine pancreatic lipase immunoreactivity (cPLI) concentrations were measured before (0 hours) and at 1 to 2 and 6 hours after feeding. Serum gastrin concentration was measured at 0 hours and at 5 to 10 minutes and 1 to 2 hours after feeding. A gastrin assay validation study was performed to confirm accuracy of test results in dogs. Data were analyzed by use of a repeated-measures general ANOVA.

Results—Serum cTLI, cPLI, or gastrin concentrations in the dogs did not differ among the different diets fed, among dogs, or over time. When multiple comparisons were analyzed, diet D caused the least amount of measurable pancreatic response, although this difference was not significant.

Conclusions and Clinical Relevance—Results did not indicate a significant effect of dietary fat content or addition of supplemental MCT oil or pancreatic enzymes in diets on serum cTLI, cPLI, or gastrin concentrations in healthy dogs.

Acute pancreatitis can be a challenging disease to manage in dogs and may be associated with high morbidity and mortality rates. Part of the traditional treatment recommendation in the management of this disease has been to withhold food from dogs followed by feeding an ultra–low-fat diet. Results of recent studies1–3 in humans and experimental studies in dogs indicate that provision of enteral nutrition early in the course of the disease improves survival and decreases complication rates, but the ideal diet has never been determined.

Serum cTLI concentration is a specific marker of exocrine pancreatic function; assessment of this variable has a relatively low sensitivity for detection of pancreatitis, yet is the most sensitive and specific test for the diagnosis of exocrine pancreatic insufficiency in dogs.4–6 Because measurement of serum cTLI concentration includes all circulating cationic trypsinogen and approximately 80% of cationic trypsin, it may also be used to assess pancreatic adaptation or function.7 Compared with total serum lipase activity, assessment of serum cPLI concentration appears to have improved sensitivity and specificity as a commercially available laboratory test for diagnosis of pancreatitis in dogs; moreover, serum cPLI concentration is unaffected by prednisolone administration or concurrent renal failure.8,9,a Serum cPLI concentration is reduced in dogs with exocrine pancreatic insufficiency and may also be a useful marker for indirect determination of the degree of pancreatic adaptation or response within an individual dog.10

In the gastric antrum, G-type cells secrete gastrin in response to gastric distension and ingestion of protein.11 The main forms of gastrin secreted in dogs are gastrin 34, 17, and 14; collectively, they have a short circulating half-life of 3 to 9 minutes.11 The presence of gastrin, other gastrointestinal hormones such as CCK, and enteric neuropeptides stimulates pancreatic acinar cells to release lysosomes and zymogens in response to food.11 This response occurs both through the anticipation and smell of food (mediated via neural pathways) and as a result of the presence of food in the stomach and small intestine (mediated via hormonal pathways).11 Thus, assessment of serum gastrin concentration may serve as an indirect measure of one aspect of pancreatic stimulation. The purpose of the study reported was to determine whether amounts of dietary fat or addition of pancreatic enzymes and MCTs to diets alters concentrations of cTLI, cPLI, and gastrin in healthy dogs.

Materials and Methods

Analytic validation of an assay for gastrin—An automated chemiluminescent, enzyme-labeled immunometric assayb was used. The assay was based on a ligand-labeled murine monoclonal capture antibody that was specific for gastrin and involved separation by use of an anti–ligand-coated solid phase.12 To analytically validate this assay for use in dogs, the interassay variability was assessed via measurement of the CV and the intra-assay variability was assessed via measurement of the CV and linearity. With owner consent, a blood sample (3 mL) was collected via jugular venipuncture from 3 healthy dogs (designated as dogs A, B, and C; dogs B and C also participated in the analytic part of the study) that each weighed > 9 kg, and serum was obtained. For each dog, serum gastrin concentration was measured. On the basis of our findings, the concentration of gastrin was classified as low (< 8.0 pg/mL) in dog A, medium (8.0 to 13.0 pg/mL) in dog C, and high (> 13.0 pg/mL) in dog B. A second blood sample (20 mL) was collected from dog A after food was withheld for 12 hours. Dogs B and C were each fed one of the experimental diets (diet A that contained 16% crude fat) to stimulate gastrin release, and the second blood sample (12.5 mL) was collected 5 to 10 minutes after feeding. Blood samples were placed on ice and allowed to clot, prior to centrifugation; serum was separated promptly by use of a refrigerated centrifuge at 10°C and immediately divided into aliquots of 100 to 250 μL that were stored at −18°C.

Aliquots of serum were used to prepare 3 batches for analysis (30 samples/batch). Batch 1 consisted of 28 replicates of dog A serum (low-concentration control samples) and 2 replicates of dog B serum (high-concentration control samples). Batch 2 consisted of 2 replicates of dog A serum, 2 replicates of dog B serum, and 26 replicates of dog C serum (medium-concentration control samples). Batch 3 consisted of 3 replicates of dog A serum, 6 replicates of dog B serum, and 3 replicates of dog B serum for each of the following dilutions: 1:2, 1:4, 1:8, 1:16, 1:32, 1:64, and 1:128. Serum from dog A was used as the diluent. Each batch was tested as an entire batch and separate from other batches.

The specificity of the assay for detection of gastrin in human serum had been determined by the manufacturer on the basis of results of assays of samples with high concentrations of mini-gastrin; low, medium, and high concentrations of sulfated gastrin G-17 (type II); low, medium, and high concentrations of both sulfated (type II) and nonsulfated (type I) gastrin G-34; medium and high concentrations of nonsulfated (type I) gastrin G 1-13; low, medium, and high concentrations of pentagastrin; and low, medium, and high concentrations of cerulein.12 The assay antibody interacts predominantly with G-17 and has less interaction with G-34, mini-gastrin, and cerulein.12 Recovery studies were performed by the manufacturer, and results indicated mean recoveries for G-17 type II and G-17 type I of 119% and 116%, respectively.12 Hemolysis did not appear to interfere with the test.12 It was revealed that bilirubin at concentrations > 85.5 μmol/L may interfere with the test and that serum triglyceride concentrations > 11 mmol/L result in degradation of values.12 The assay range was 5 to 1,000 pg/mL, and results < 5 pg/mL were recorded as 0 pg/mL.

Study protocol—The study was approved by the Animal Ethics Committee at Murdoch University, fulfilling requirements of the National Health and Medical Research Council. Healthy staff-owned dogs that weighed > 9 kg were recruited into the study with owner consent. The dogs had no prior history of pancreatitis or clinically important gastrointestinal disease. All dogs were determined to be healthy on the basis of results of physical examination, CBC, serum biochemical analyses, urinalysis, and assessments of serum amylase and lipase activities.

Four experimental diets were used in the study, and each dog was fed all 4 diets once in random order at 1-week intervals. Between dietary treatments, dogs were fed their normal diet. Diet A was a maintenance commercial dog foodc that had a crude fat content of 16% (as stated by the manufacturer). Diet B was a low-fat commercial dog foodd that had a crude fat content of 5% (as stated by the manufacturer). Diet C was composed of diet A with supplemental pancreatic enzymese (lipase, 526 to 1,667 British Pharmacopoeia units/kg; amylase, 421 to 1,200 British Pharmacopoeia units/kg; and protease, 31 to 67 European Pharmacopoeia units/kg). Diet D was composed of diet B with supplemental pancreatic enzymes (as described for diet C) and MCT oilf (0.5 mL/kg; C8 and C10 fatty acids composition > 95%). Food was withheld from the dogs for at least 12 hours prior to the feeding of each diet. For each dog, the amount of each diet fed was based on half of the daily calculated maintenance energy requirement (based on body weight). A blood sample was collected from each dog via jugular venipuncture before (0 hours [baseline]; 6 mL) and at 5 to 10 minutes (3 mL), 1 to 2 hours (6 mL), and 6 hours (3 mL) after feeding each experimental diet. Blood samples were placed on ice and allowed to clot, prior to centrifugation; serum was separated promptly by use of a refrigerated centrifuge at 10°C and stored at −18°C. Serum cTLIg and cPLIh concentrations were measured at 0, 1 to 2, and 6 hours after feeding. Serum gastrin concentration was measuredb,i at 0 hours, 5 to 10 minutes, and 1 to 2 hours after feeding.

Data analysis—The results were analyzed by use of a repeated-measures general ANOVA.j Differences in the dogs’ serum cTLI, cPLI, and gastrin concentrations among diets fed, among dogs, and over time were analyzed, with significance set at a value of P ≤ 0.05. To assess alterations in cTLI and cPLI concentrations from baseline (0 hours) at 1 to 2 and 6 hours after feeding, the percentage change was calculated. To assess alterations in gastrin concentrations from baseline (0 hours) at 5 to 10 minutes and 1 to 2 hours after feeding, the actual change rather than percentage change was calculated to allow for zero values. The interassay CV was determined for serum gastrin concentrations when samples were assayed on different days.

Results

Dogs—Ten healthy dogs were used in the study. The dogs’ ages ranged from 1 to 12 years (mean ± SD age, 5.7 ± 3.68 years) and weights ranged from 9.8 to 40.8 kg (mean weight, 26.5 ± 9.4 kg). There were 2 sexually intact males, 4 castrated males, and 4 spayed females. Among the dogs, there were 2 Labrador Retrievers, 1 Gordon Setter, 1 Miniature Schnauzer, 1 Dalmatian, 1 Australian Cattle Dog, 1 Greyhound, and 3 mixed-breed dogs.

Serum sample quality—The quality of serum samples obtained in the present study was assessed via visual examination. No samples appeared grossly lipemic, hemolyzed, or icteric.

Gastrin assay validation—On the basis of the data obtained by use of the enzyme-labeled immunometric assay on serum samples obtained from 3 healthy dogs, the mean interassay CV was 11.56% and the mean intra-assay CV was 11.41%. Dilutional parallelism evaluations revealed acceptable linearity (Figure 1).

Figure 1—
Figure 1—

Results of the dilutional parallelism evaluations of an enzyme-labeled immunometric assay for measurement of serum gastrin concentration in dogs. Serum samples were collected from 3 healthy dogs (designated as dogs A, B, and C). This assay was performed on 3 replicates of dog A serum, 6 replicates of dog B serum, and 3 replicates of dog B serum for each of the following dilutions: 1:2, 1:4, 1:8, 1:16, 1:32, 1:64, and 1:128. Serum from dog A (low gastrin concentration) was used as the diluent.

Citation: American Journal of Veterinary Research 70, 5; 10.2460/ajvr.70.5.614

Serum cTLI concentration—Among the 10 dogs during the 4 experimental periods, baseline cTLI concentration ranged from 4.4 to 128.5 μg/L (mean ± SD, 13.6 ± 19.5 μg/L). Mean serum concentrations of cTLI at 1 to 2 hours and at 6 hours after feeding were 12.6 and 12.3 μg/L, respectively, in dogs fed diet A; 11.9 and 11.2 μg/L, respectively, in dogs fed diet B; 12.6 and 11.3 μg/L, respectively, in dogs fed diet C; and 12.8 and 11.4 μg/L, respectively, in dogs fed diet D. For each diet, the percentage change (from baseline) in serum cTLI concentration over time was calculated (Figure 2).

Figure 2—
Figure 2—

Percentage change in mean serum cTLI concentrations in 10 healthy dogs before (0 hours [baseline]) and at 1 to 2 and 6 hours after consumption of 1 meal of each of 4 diets (1-week interval between diet treatments). Dogs were fed a maintenance commercial dog foodc that had a crude fat content of 16% (diet A [circles]); a low-fat commercial dog foodd that had a crude fat content of 5% (diet B [diamonds]); diet A with supplemental pancreatic enzymes (diet C [triangles]); and diet B with supplemental pancreatic enzymes and MCT oil (diet D [squares]). Food was withheld from the dogs for at least 12 hours prior to the feeding of each diet. Data are reported as mean ± SD percentage change from baseline values.

Citation: American Journal of Veterinary Research 70, 5; 10.2460/ajvr.70.5.614

Serum cPLI concentration—Among the 10 dogs during the 4 experimental periods, the baseline cPLI concentration ranged from 5.3 to 169.6 μg/L (mean, 29.6 ± 31.6 μg/L). Mean serum concentrations of cPLI at 1 to 2 hours and at 6 hours after feeding were 24.3 and 24.2 μg/L, respectively, in dogs fed diet A; 28.5 and 24.2 μg/L, respectively, in dogs fed diet B; 33.6 and 28.5 μg/L, respectively, in dogs fed diet C; and 59.2 and 42.6 μg/L, respectively, in dogs fed diet D. For each diet, the percentage change (from baseline) in serum cPLI concentration over time was calculated (Figure 3).

Figure 3—
Figure 3—

Percentage change in mean serum cPLI concentrations in 10 healthy dogs before (0 hours [baseline]) and at 1 to 2 and 6 hours after consumption of 1 meal of each of 4 diets (1-week interval between diet treatments). Food was withheld from the dogs for at least 12 hours prior to the feeding of each diet. Data are reported as mean ± SD percentage change from baseline values. See Figure 2 for key.

Citation: American Journal of Veterinary Research 70, 5; 10.2460/ajvr.70.5.614

Serum gastrin concentration—Among the 10 dogs during the 4 experimental periods, the baseline gastrin concentration ranged from < 5 to 16 pg/mL (mean, 2.2 ± 4.3 pg/mL). Mean serum concentrations of gastrin at 5 to 10 minutes and at 1 to 2 hours after feeding were 8.3 and 11.0 pg/mL, respectively, in dogs fed diet A; 10.9 and 8.2 pg/mL, respectively, in dogs fed diet B; 9.1 and 8.9 pg/mL, respectively, in dogs fed diet C; and 8.0 and 12.7 pg/mL, respectively, in dogs fed diet D. For each diet, the actual change (from baseline) in serum gastrin concentration over time was calculated (Figure 4).

Figure 4—
Figure 4—

Change in mean serum gastrin concentrations in 10 healthy dogs before (0 hours [baseline]) and at 5 to 10 minutes and 1 to 2 hours after consumption of 1 meal of each of 4 diets (1-week interval between diet treatments). Food was withheld from the dogs for at least 12 hours prior to the feeding of each diet. Data are reported as mean ± SD actual change from baseline values. See Figure 2 for key.

Citation: American Journal of Veterinary Research 70, 5; 10.2460/ajvr.70.5.614

Data comparisonsIn the study dogs, serum cPLI and cTLI concentrations did not differ significantly among diets fed, among dogs, or over time. Compared with the other diets, diet D was associated with a higher mean baseline serum cPLI concentration, but this difference was not significant (P = 0.2). Serum gastrin concentration at 0 hours was significantly different from values at the 2 later time points after feeding. Serum gastrin concentration did not differ among diets fed; diet D induced the least amount of pancreatic response, compared with the effects of the other diets, although this difference was not significant (P = 0.33). No significant deviation from this finding was apparent in data for any individual dog.

Discussion

Known triggers for pancreatic stimulation include gastric distension, dietary protein and fatty acid intake, emptying of gastric contents into the duodenum, and enteric neuropeptides.11 Results of the present study indicated no significant effect of the content of fat or the presence or absence of supplemental pancreatic enzymes and MCTs on the degree of pancreatic stimulation (assessed by measurement of serum cTLI, cPLI, and gastrin concentrations) in healthy dogs. Serum gastrin concentration was monitored to assess the immediate effects of gastric distension on pancreatic stimulation, and serum cTLI concentration was monitored to assess overall pancreatic function. Assessment of serum cPLI concentration was also undertaken; this variable reflects the pancreatic response in relation to varying dietary fat content because colipase is activated and converted into lipase to enable fat digestion and because cPLI is specific to the pancreas.

The variables measured in our study are considered indirect indices of pancreatic stimulation in dogs. Gastrin, cTLI, and cPLI were chosen as indicators because they remain stable in serum samples and because high-specificity assays for measurement of serum concentrations are commercially available. To determine the degree of pancreatic response in healthy dogs in the study of this report, the percentage changes in serum cTLI and cPLI concentrations and the actual change in serum gastrin concentration were assessed over time and among the 4 diets fed. It is possible that the measurements of these serum markers of pancreatic function were not sufficiently sensitive to accurately assess exocrine pancreatic stimulation, and instead more direct intraduodenal markers should be measured. However, the latter procedures are more technically difficult and invasive to perform. In our opinion, the variables measured in the present study are useful as indirect measures of pancreatic response. It was not possible to calculate the percentage change in serum gastrin concentration from baseline values for all dogs at all time points after feeding of the diets because some concentrations were less than the detection limit of the assay. The assessment of serum gastrin was still considered appropriate because none of the concentrations were less than the detection limit of the assay during the validation process. The fact that some of the study dogs had serum gastrin concentrations that were less than the detection limit of the assay at various time points during the 4 diet treatments is considered to reflect individual variation rather than inaccuracy of the test.

Because of the short half-life of gastrin, serum concentrations were assessed at 5 to 10 minutes after feeding and again at 1 to 2 hours after feeding. Mean serum concentrations of gastrin at these 2 time points after feeding did not differ significantly, which likely represents ongoing secretion because of the persistence of food within the stomach 2 hours after feeding. There was no significant difference in the dogs’ serum gastrin concentration over time, among the 4 diets fed, or among dogs; thus, the preferred sample collection time point cannot be determined.

The specificity of the gastrin assay used in the present study was assessed by the manufacturer. The antibody in the assay reacts predominantly with G-17 and, to lesser extents, with G-34, mini-gastrin, and cerulein. Cerulein is considered an important pancreatic stimulant.12,13 Hemolysis in serum samples does not interfere with the test.12 The validation procedure performed in the present study revealed acceptable intra- and interassay CVs for an enzyme-based assay; therefore, results obtained for the study dogs can be considered reliable. Bilirubin concentrations > 85.5 μmol/L may interfere with the test, and serum triglyceride concentrations > 11 mmol/L have been associated with degradation of values.12 No samples in the present study were grossly lipemic, hemolyzed, or icteric.

In the study of this report, indirect indicators of pancreatic adaptation or response were measured in 10 healthy dogs that had no previous history of pancreatitis or any other intestinal illness. It is unknown whether differences in diet composition, especially the percentage of crude fat, can markedly alter the degree of pancreatic stimulation or outcome in dogs with a history of naturally occurring pancreatitis. Standard enteral diets contain long-chain triglycerides, and consumption of such diets increases CCK secretion and, subsequently, pancreatic stimulation in humans.14 Enteral administration of MCTs is thought to result in minimal CCK secretion, thereby reducing pancreatic stimulation.14 The type of dietary fat may play a more important role than fat content per se, but whether this is of benefit in treatment of pancreatitis is not known. Although there is no evidence that restriction of dietary fat alters pancreatic stimulation, restriction of dietary fat in dogs that have a confirmed history of pancreatitis is an important recommendation. Further studies would be required to adequately challenge the dogma of feeding low-fat diets to all dogs with pancreatitis, rather than feeding such diets only to those with hyperlipidemia after food has been withheld.

Administration of supplemental pancreatic enzymes has been applied in the management of people and dogs with exocrine pancreatic insufficiency that is secondary to chronic pancreatitis.3,7 The provision of pancreatic enzymes appears to decrease postprandial pain in humans with chronic pancreatitis and has been suggested to decrease the risk of reoccurrence of acute pancreatitis via a negative feedback effect on pancreatic enzyme secretion.3 The reduction in the signs of pain may also be attributable to other unknown mechanisms. In the present study, diets C and D included supplemental pancreatic enzymes; the reduced (albeit not significantly) pancreatic response associated with diet D was most likely attributable to the addition of MCTs. The effects of dietary supplements containing pancreatic enzymes, however, may be more appreciable in dogs with acute or chronic pancreatitis rather than in clinically normal dogs. Nevertheless, results of the present study indicated that the fat content of diets or the addition of MCT oil or pancreatic enzymes to diets fed to healthy dogs did not have any significant effect on serum concentrations of cTLI, cPLI, or gastrin, which may have implications for the treatment of pancreatitis (both acute and chronic) in dogs.

Abbreviations

CCK

Cholecystokinin

cPLI

Canine pancreatic lipase immunoreactivity

cTLI

Canine trypsin–like immunoreactivity

CV

Coefficient of variation

MCT

Medium-chain triglyceride

a.

Steiner J M, Lees GE, Willard MD, et al. Serum canine pancreatic lipase immunoreactivity (cPLI) concentration is not altered by oral prednisone administration (abstr). 21st Annu Meet Am Coll Vet Intern Med J Vet Intern Med 2003;17:444.

b.

Immunolite 2000, Diagnostic Products Corp, Los Angeles, Calif.

c.

PurinaONE, adult dog, chicken and rice formula, Nestlé Purina PetCare Co, St Louis, Mo.

d.

Royal Canin, Canine Veterinary Diet, digestive low fat, Royal Canin, Aimargues, France.

e.

CREON 5000, CREON 10000, and CREON FORTE, Solvay Pharmaceuticals, Pymble, NSW, Australia.

f.

SHS international Ltd, Liverpool, England.

g.

Commercial radioimmunoassay, canine TLI assay, Siemens Healthcare Diagnostics, Deerfield, Ill. Testing was performed at the Gastrointestinal Laboratory, Department of Small Animal Clinical Sciences, College of Veterinary Medicine and Biomedical Sciences, Texas A&M University, College Station, Tex.

h.

Enzyme-linked immunosorbent assay, Gastrointestinal Laboratory, Department of Small Animal Clinical Sciences, College of Veterinary Medicine and Biomedical Sciences, Texas A&M University, College Station, Tex.

i.

Testing was performed at Royal Perth Hospital, Perth, WA, Australia.

j.

SPSS, version 14.0, SPSS Inc, Chicago, Ill.

References

  • 1.

    Qin HL, Su ZD, Gao Q, et al.Early intrajejunal nutrition: bacterial translocation and gut barrier function of severe acute pancreatitis in dogs. Hepatobiliary Pancreat Dis Int 2002;1:150154.

    • Search Google Scholar
    • Export Citation
  • 2.

    Weber CK, Adler G. Acute pancreatitis. Curr Opin Gastroenterol 2003;19:447450.

  • 3.

    Meier RF, Beglinger C. Nutrition in pancreatic diseases. Best Pract Res Clin Gastroenterol 2006;20:507529.

  • 4.

    Hess RS, Saunders HM, Van Winkle TJ, et al.Clinical, clinico-pathologic, radiographic, and ultrasonographic abnormalities in dogs with fatal acute pancreatitis: 70 cases (1986–1995). J Am Vet Med Assoc 1998;213:665670.

    • Search Google Scholar
    • Export Citation
  • 5.

    Mansfield CS, Jones BR. Plasma and urinary trypsinogen activation peptide in healthy dogs, dogs with pancreatitis and dogs with other systemic diseases. Aust Vet J 2000;78:416422.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 6.

    Williams DA, Batt RM. Sensitivity and specificity of radioimmunoassay of serum trypsin-like immunoreactivity for the diagnosis of canine exocrine pancreatic insufficiency. J Am Vet Med Assoc 1988;192:195201.

    • Search Google Scholar
    • Export Citation
  • 7.

    Watson P. Pancreatitis in the dog: dealing with a spectrum of disease. In Pract 2004;26:6477.

  • 8.

    Steiner JM. Diagnosis of pancreatitis. Vet Clin North Am Small Anim Pract 2003;33:11811195.

  • 9.

    Steiner JM, Teague SR, Williams DA. Development and analytic validation of an enzyme-linked immunosorbent assay for the measurement of canine pancreatic lipase immunoreactivity in serum. Can J Vet Res 2003;67:175182.

    • Search Google Scholar
    • Export Citation
  • 10.

    Steiner JM, Rutz GM, Williams DA. Serum lipase activities and pancreatic lipase immunoreactivity concentrations in dogs with exocrine pancreatic insufficiency. Am J Vet Res 2006;67:8487.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 11.

    Williams DA. The pancreas. In: Guilford WG, Center S, Strombeck D, et al, eds. Strombeck's small animal gastroenterology. 3rd ed. Philadelphia: WB Saunders Co, 1996;381410.

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Contributor Notes

Dr. Williams' present address is Department of Veterinary Clinical Medicine, College of Veterinary Medicine, University of Illinois, Urbana, IL 61802.

Supported by Nestlé Purina PetCare Company by provision of a residents' research grant. Presented as a poster at the 16th European College of Veterinary Animals-Companion Animals Congress, Amsterdam, September 2006.

Address correspondence to Dr. James.