INVESTIGATIONS INTO HYPERLIPIDEMIA AND ITS POSSIBLE ...

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163 In the third part of the study, the goal was to assess the feasibility and usefulness of a novel, convenient, and economical density gradient ultracentrifugation method as a means for lipoprotein fingerprinting in dogs, and to characterize and compare the lipoprotein profiles of healthy dogs of various breeds, healthy Miniature Schnauzers, and Miniature Schnauzers with primary hypertriglyceridemia using the same method. Thirty-five healthy dogs of various breeds with serum triglyceride and cholesterol concentrations within their respective reference intervals (Group 1), 31 Miniature Schnauzers with serum triglyceride and cholesterol concentrations within their respective reference intervals (Group 2A), and 31 Miniature Schnauzers with hypertriglyceridemia (Group 2B) were included in the study. The most abundant lipoprotein fraction in dogs of Group 1 was HDL, mainly HDL 2 and HDL 3 . LDL fractions were present in very small amounts, with the exception of LDL 4 and LDL 5 . Triglyceride-rich lipoproteins were also found in very small amounts. The lipoprotein profiles of Miniature Schnauzers with serum triglyceride and cholesterol concentrations within the reference interval (Group 2A) were generally similar to the ones seen in dogs of Group 1 with regard to the abundance of major lipoprotein classes. However, most dogs in Group 2A showed some distinct differences in some lipoprotein fractions and subfractions. Using sliced inverse regression analysis, the group to which each dog belonged (i.e., Miniature Schnauzer versus other breeds) could be accurately predicted based on their lipoprotein profiles in 85% of the cases (P=0.00017). The most important lipoprotein fractions that served as predictors were the TRLs and the LDL fraction corresponding to LDL 4 and LDL 5 . Miniature Schnauzers had more prominent TRL
164 peaks than dogs of other breeds, while dogs of other breeds had more prominent LDL 4 and LDL 5 peaks. Sliced inverse regression analysis in Groups 2A and 2B showed that the group to which each dog belonged (i.e., Miniature Schnauzers with normal serum triglyceride concentration versus Miniature Schnauzers with hypertriglyceridemia) could be accurately predicted based on their lipoprotein profiles in 95% of cases (P=0.000002). By far, the most important lipoprotein fraction that served as a predictor was the TRL fraction, which was more prominent in the dogs with hypertriglyceridemia. Fractions corresponding to LDL 2 , LDL 3 , LDL 4 , were more prominent in Miniature Schnauzers with serum triglyceride concentrations within the reference interval. The aim of the fourth part of the study was to evaluate the effect of a commercially available low-fat diet on serum lipid and pancreas-specific lipase (Spec cPL ® ) concentrations and lipoprotein profiles in Miniature Schnauzers with primary hypertriglyceridemia. Sixteen Miniature Schnauzers with hypertriglyceridemia of various degrees were included in the study (Group 1). A group of 28 healthy Miniature Schnauzers with serum triglyceride and cholesterol concentrations within the respective reference intervals (Group 2) was used as a control group for the lipoprotein profile analysis portion of the study. Dogs in Group 2 were used in order to obtain lipoprotein profiles from a group of healthy Miniature Schnauzers that could be used for illustration of whether lipoprotein profiles of hypertriglyceridemic Miniature Schnauzers tended to approach those of the healthy ones after the diet change. Each one of the dogs in Group 1 had a total of 4 blood samples collected. The first sample (sample 1) was used to diagnose primary hypertriglyceridemia. Then, in order to confirm the results of the
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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
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105 Figures 14A and 14B: Representa
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107 Specifically, 97% of non-hypert
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109 The fraction of TRLs was a sign
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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 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: 162 times (P=0.0343) for a serum cP
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
Page 219 and 220: 206 289. Carpentier YA, Scruel O. C
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