INVESTIGATIONS INTO HYPERLIPIDEMIA AND ITS POSSIBLE ...

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115 The biochemical, metabolic, and genetic bases of hypertriglyceridemia in Miniature Schnauzers have not been elucidated. Therefore, definitive recommendations for effective prevention and specific management of this condition are currently unavailable. The most commonly recommended initial approach in the management of primary hypertriglyceridemia in Miniature Schnauzers is the use of a low-fat diet. 131,252 Feeding a low-fat diet is also commonly the recommended approach in the management of dogs suspected of having chronic pancreatitis. 286 There are several commercially available diets marketed as “low-fat”, although their actual lipid content might vary substantially between one another. To our knowledge, none of these diets have been evaluated with regard to their effectiveness in the management of primary hypertriglyceridemia in Miniature Schnauzers. Also, the effect of low-fat diets on serum concentrations of markers for pancreatitis has not been evaluated. Therefore, the aim of the present 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. Materials and methods Dogs Miniature Schnauzers with hypertriglyceridemia of various degrees were included in the study (Group 1). These dogs were selected from a pool of >300 Miniature Schnauzers that were enrolled as part of several ongoing projects related to hypertriglyceridemia in this breed. The requirements for inclusion in the present study
116 were a diagnosis of hypertriglyceridemia and willingness of each dog’s owners to enroll their dog in the study. All dogs included in the study had to have absence of any clinical signs at the time of blood collection and no history of diseases or current use of drugs known to affect lipid metabolism. They also had to have a normal body condition score (BCS; between 4 and 6 on a scale of 1 to 9). In addition, for each dog, serum Spec cPL, glucose, total T4, and free T4 (by equilibrium dialysis) concentrations were measured. Based on the historical information for each dog and the results of the tests performed, all hypertriglyceridemic dogs enrolled in this study were diagnosed as having primary idiopathic hypertriglyceridemia. A group of 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 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. Dogs of Group 2 had to have absence of any clinical signs at the time of blood collection and no history of diseases or current use of drugs known to affect lipid metabolism. They also had to have a normal BCS (between 4 and 6 on a scale of 1 to 9) and be on diets that were not labeled as low-fat diets at the time of blood collection.
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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
Page 77 and 78: 64 gastrointestinal signs or suspec
Page 79 and 80: 66 CHAPTER III SERUM TRIGLYCERIDE C
Page 81 and 82: 68 logical assumption that a defect
Page 83 and 84: 70 pancreatitis. For the same reaso
Page 85 and 86: 72 Spec cPL concentrations were mea
Page 87 and 88: 74 were significantly more likely t
Page 89 and 90: 76 Figure 5. Comparison of serum tr
Page 91 and 92: 78 Figure 7. Comparison of serum tr
Page 93: 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 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 and 176: 162 times (P=0.0343) for a serum cP
Page 177 and 178: 164 peaks than dogs of other breeds
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166 19.3; 95% CI, 2.0-184.0; P=0.00
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168 4) Specific lipoprotein classes
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170 REFERENCES 1949;8:96-97. 1. Lew
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172 17. Whitney MS, Boon GD, Rebar
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174 33. Ford RB. Clinical managemen
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176 50. Nelson RW, Turnwald GH, Wil
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178 66. Williams DA, Steiner JM. Ca
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180 82. Yilmaz Z, Senturk S. Charac
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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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