INVESTIGATIONS INTO HYPERLIPIDEMIA AND ITS POSSIBLE ...

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155 Both LDL and HDL fractions contain mainly cholesterol. 252 The fact that the overall serum cholesterol concentration was normal in the majority of dogs with pancreatitis might be explained by the fact that increases in LDL fractions were balanced by a concurrent decrease in the HDL fractions. It is possible that during pancreatitis lipoprotein metabolism is altered in a way that facilitates redistribution of lipid components (mainly cholesterol) between LDL and HDL fractions. Further studies are needed to elucidate the mechanism of lipoprotein metabolism alterations in dogs with pancreatitis. The changes in lipoprotein profiles in dogs with pancreatitis described in the present study are in agreement with the findings of studies on experimentally induced pancreatitis in dogs. 18-20 Those studies have all reported similar findings, including increases in LDL and decreases in HDL fractions. Based on these findings, serum alterations in the major lipoprotein fractions are similar between naturally occurring and experimentally induced pancreatitis. However, changes in lipoprotein subfractions as a result of experimental pancreatitis have not been reported in other studies and differences might be present. TRLs were overall decreased in dogs with pancreatitis in the present study. To the authors’ knowledge, this has not been described before in dogs with pancreatitis without concurrent diseases affecting the lipoprotein metabolism. Since TRL are the main lipoprotein fractions containing triglycerides, this finding contradicts another finding of the present study, which showed that serum triglyceride concentrations were significantly higher in dogs with pancreatitis. This finding might suggest that the content
156 of lipoproteins might also have changed in dogs with pancreatitis, and that TRL, LDL, and/or HDL contained higher concentrations of triglycerides than those in healthy dogs. Further studies are needed to describe the lipid content of the lipoprotein fractions of dogs with pancreatitis. Overall, some of the changes observed in the present study with regard to serum lipid concentrations and lipoprotein profiles are similar to the changes reported in humans or animal models with various types of inflammation or infection. 287-289 Similar to the changes in acute phase proteins that occur during inflammation, major changes take place in lipoprotein metabolism in response to inflammation. These changes affect both the concentration and composition of serum lipoproteins and are mainly mediated by hormones and cytokines. 287-289 Typical lipoprotein changes in response to inflammation in humans include an increase in serum triglyceride concentration (due to an increased production of triglycerides and VLDL by the liver), and a decrease in HDL cholesterol. 287-289 Similar changes were observed in the present study. Changes in LDL molecules are more difficult to compare between humans and dogs because these 2 species differ substantially in their LDL metabolism. Nevertheless, inflammation in humans appears to induce a shift in LDL profiles leading to the appearance of small dense LDL molecules that correspond to fractions LDL 4 and LDL 5 , a finding that was also observed in the dogs of Group 1 in the present study. It seems likely that, as in humans, changes in serum lipid concentrations and lipoprotein profiles in dogs with pancreatitis might be the result of a general inflammatory response rather than a
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INVESTIGATIONS INTO HYPERLIPIDEMIA
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INVESTIGATIONS INTO HYPERLIPIDEMIA
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iv was found to be useful for the s
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vi ACKNOWLEDGEMENTS I would like to
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viii TABLE OF CONTENTS Page ABSTRAC
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x LIST OF FIGURES FIGURE Page 1 Cor
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xii FIGURE Page 20 1-dimensional sl
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2 the results of these initial stud
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4 and HDL 1 concentrations and a de
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6 and, in smaller concentrations, L
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8 HDL molecules can be further subd
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10 reach the vasculature, they acqu
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12 Endocrine disease Most commonly,
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14 with varying frequencies in dogs
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16 hypercholesterolemia was found o
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18 Primary hyperlipidemia with hype
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20 Atherosclerosis Although dogs ap
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22 Dietary management Typically, th
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24 therapy when the latter fails to
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26 followed from the 1970s until to
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28 this theory, zymogen granules th
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30 be quite different, especially i
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32 Drugs As in humans, drug-induced
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34 Signalment Dogs of any age, bree
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36 erroneously direct the clinician
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38 of changes over time in serum Sp
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40 they have been shown to have a l
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42 revealed either a normal pancrea
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44 At present, a definitive diagnos
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46 factors should always be investi
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48 associated pancreatitis is much
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50 clear whether hyperlipidemia was
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52 hepatobiliary disease in both Mi
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54 the reference range, while Group
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56 ROC analysis and calculation of
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58 Figure 3. Serum cPLI concentrati
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60 There was no significant differe
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62 severe (typically ≥1,000 mg/dl
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64 gastrointestinal signs or suspec
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66 CHAPTER III SERUM TRIGLYCERIDE C
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68 logical assumption that a defect
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70 pancreatitis. For the same reaso
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72 Spec cPL concentrations were mea
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74 were significantly more likely t
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76 Figure 5. Comparison of serum tr
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78 Figure 7. Comparison of serum tr
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80 pancreatitis as it cannot be pre
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83 Although serum cholesterol conce
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85 Footnotes a Spec cPL ® , IDEXX
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87 several subfractions, with diffe
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89 Miniature Schnauzers (Group 2) T
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91 Assays Serum triglyceride (refer
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93 Figure 8. Custom-built fluoresce
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95 range HDL 1 has not been accurat
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97 mg/dL) were significantly higher
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99 Figure 10: Serum cholesterol con
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101 (Eigenvalues=0.5455; P=0.00017;
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103 Figure 12: Representative lipop
Page 118 and 119: 105 Figures 14A and 14B: Representa
Page 120 and 121: 107 Specifically, 97% of non-hypert
Page 122 and 123: 109 The fraction of TRLs was a sign
Page 124 and 125: 111 Schnauzers without hyperlipidem
Page 126 and 127: 113 Footnotes a Roche/Hitachi MODUL
Page 128 and 129: 115 The biochemical, metabolic, and
Page 130 and 131: 117 Study design Each one of the do
Page 132 and 133: 119 Questionnaires and consent form
Page 134 and 135: 121 a target intensity of 30%, and
Page 136 and 137: 123 might affect lipid metabolism (
Page 138 and 139: 125 Figure 16. Serum triglyceride c
Page 140 and 141: 127 Figure 18. Serum Spec cPL conce
Page 142 and 143: 129 Figure 19. 1-dimensional sliced
Page 144 and 145: 131 Dogs that did not respond to th
Page 146 and 147: 133 Hypertriglyceridemia has been l
Page 148 and 149: 135 degrees. One possible explanati
Page 150 and 151: 137 Footnotes a Royal Canin Gastroi
Page 152 and 153: 139 concentrations and lipoprotein
Page 154 and 155: 141 inclusion criteria for the stud
Page 156 and 157: 143 light source j , located in a d
Page 159 and 160: 146 Serum triglyceride and choleste
Page 161 and 162: 148 Figure 22. Serum triglyceride c
Page 163 and 164: 150 Figure 24. 1-dimensional sliced
Page 165 and 166: 152 Discussion The purpose of the p
Page 167: 154 fraction of these dogs (about 3
Page 171 and 172: 158 Footnotes a Roche/Hitachi MODUL
Page 173 and 174: 160 the etiology of pancreatitis, b
Page 175 and 176: 162 times (P=0.0343) for a serum cP
Page 177 and 178: 164 peaks than dogs of other breeds
Page 179 and 180: 166 19.3; 95% CI, 2.0-184.0; P=0.00
Page 181 and 182: 168 4) Specific lipoprotein classes
Page 183 and 184: 170 REFERENCES 1949;8:96-97. 1. Lew
Page 185 and 186: 172 17. Whitney MS, Boon GD, Rebar
Page 187 and 188: 174 33. Ford RB. Clinical managemen
Page 189 and 190: 176 50. Nelson RW, Turnwald GH, Wil
Page 191 and 192: 178 66. Williams DA, Steiner JM. Ca
Page 193 and 194: 180 82. Yilmaz Z, Senturk S. Charac
Page 195 and 196: 182 97. Fojo SS, Stalenhoef AF, Mar
Page 197 and 198: 184 111. Lam CW, Yuen YP, Cheng WF,
Page 199 and 200: 186 127. Crispin SM. Ocular manifes
Page 201 and 202: 188 144. Lindsay S, Entenmann C, Ch
Page 203 and 204: 190 161. Steiner JM. Canine pancrea
Page 205 and 206: 192 176. Steiner JM, Teague SR, Wil
Page 207 and 208: 194 191. Steiner JM. Diagnosis of p
Page 209 and 210: 196 208. Talukdar R, Vege S. Recent
Page 211 and 212: 198 224. Koch K, Drewelow B, Liebe
Page 213 and 214: 200 241. Petrov MS, van Santvoort H
Page 215 and 216: 202 258. Ewald N, Hardt PD, Kloer H
Page 217 and 218: 204 274. Otvos JD, Jeyarajah EJ, Be
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206 289. Carpentier YA, Scruel O. C
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