INVESTIGATIONS INTO HYPERLIPIDEMIA AND ITS POSSIBLE ...

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133 Hypertriglyceridemia has been linked to several conditions in dogs (especially Miniature Schnauzers), including pancreatitis, insulin resistance, hepatobiliary disease, and ocular disease. 252 The degree of hypertriglyceridemia seems to play an important role in most conditions. 252,279 Therefore, management of hypertriglyceridemia with a goal to reduce serum triglyceride concentrations below 500 mg/dL is usually recommended even when clinical sings are not present. 252 The results of the preset study suggest that the study diet is effective in lowering serum triglyceride concentrations to values below the ones considered to be associated with risk for disease (a recommended cut-off of 500 mg/dL was used in the present study), and in some cases it even led to normalization of serum triglyceride concentrations. From each dog in Group 1, 2 samples were collected before the diet change and 2 after the diet change. This was done to ensure that dogs had persistent hyperlipidemia before the diet change and that some dogs would not spontaneously have serum and triglyceride concentrations within the reference range. For samples collected after the diet change, this was done to ensure that any reduction in serum and cholesterol concentration was not temporary or random. Therefore, each dog served as its own control. There was no significant difference in serum triglyceride or cholesterol concentrations between samples 1 and 2 (i.e., before the diet change) or between samples 3 and 4 (i.e., after the diet change). The fact that significant differences were detected only when serum triglyceride and cholesterol concentrations were compared between time-points before and after the diet change strongly suggests that this was due to an effect of the diet.
134 It is interesting to note that there was great variation in serum triglyceride concentrations between samples 1 and 2 (i.e., sample before the diet change). There also was variation between samples 3 and 4 (i.e., after the diet change) but it was not as prominent as compared to before the diet change. As mentioned above, there was no statistically significant difference between these time-points overall, but there was considerable variation within individual dogs. This was despite the fact that the dogs had been fasted for >15 hours. A plausible explanation is that, because the diet was not controlled during the first 2 sample collections, food of a different fat content might have been consumed before each of the blood collections. Alternatively, this variation might be normal for this condition as no long-term studies have evaluated the fluctuation of serum triglyceride concentration over time in Miniature Schnauzers with hyperlipidemia. A similar observation of such variation has also been described in another study with Miniature Schnauzers with pancreatitis. 280 This might suggest that at least 2 samples should be collected and evaluated during the diagnostic evaluation Miniature Schnauzers for hyperlipidemia to ensure that an accurate estimate of the severity of hyperlipidemia is obtained. Another observation was that, although >50% of the dogs were classified as normal after the diet change based on their lipoprotein profiles, a considerable percentage (44%) of dogs was still classified as hyperlipidemic based on their lipoprotein profiles. This is in agreement with the observation that serum triglyceride concentrations were significantly reduced but not normalized in some of the dogs (Figure 22). It is not known why the dogs responded to the diet change to different
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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
Page 96 and 97: 83 Although serum cholesterol conce
Page 98 and 99: 85 Footnotes a Spec cPL ® , IDEXX
Page 100 and 101: 87 several subfractions, with diffe
Page 102 and 103: 89 Miniature Schnauzers (Group 2) T
Page 104 and 105: 91 Assays Serum triglyceride (refer
Page 106 and 107: 93 Figure 8. Custom-built fluoresce
Page 108 and 109: 95 range HDL 1 has not been accurat
Page 110 and 111: 97 mg/dL) were significantly higher
Page 112 and 113: 99 Figure 10: Serum cholesterol con
Page 114 and 115: 101 (Eigenvalues=0.5455; P=0.00017;
Page 116 and 117: 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 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 and 168: 154 fraction of these dogs (about 3
Page 169 and 170: 156 of lipoproteins might also have
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
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184 111. Lam CW, Yuen YP, Cheng WF,
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186 127. Crispin SM. Ocular manifes
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188 144. Lindsay S, Entenmann C, Ch
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190 161. Steiner JM. Canine pancrea
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192 176. Steiner JM, Teague SR, Wil
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194 191. Steiner JM. Diagnosis of p
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196 208. Talukdar R, Vege S. Recent
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198 224. Koch K, Drewelow B, Liebe
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200 241. Petrov MS, van Santvoort H
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202 258. Ewald N, Hardt PD, Kloer H
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204 274. Otvos JD, Jeyarajah EJ, Be
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206 289. Carpentier YA, Scruel O. C
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