title: Treatment of hypertriglyceridemia by two diets rich either in unsaturated fatty acids or in carbohydrates: effects on lipoprotein subclasses, lipolytic enzymes, lipid transfer proteins, insulin and leptin.
abstract: BACKGROUND
  There is lack of agreement on which dietary regimen is most suitable for treatment of hypertriglyceridemia, especially if high triglyceride concentrations are not due to obesity or alcohol abuse. We compared the effects on blood lipids of a diet high in total and unsaturated fat with a low-fat diet in patients with triglyceride concentrations of > 2.3 mmol/l.
  
  
  METHODS
  Nineteen non-obese male outpatients with triglycerides ranging from 2.30 to 9.94 mmol/l received two consecutive diets for 3 weeks each: first a modified high-fat diet (39% total fat, 8% SFA, 15% monounsaturated fatty acids, 1.6% marine n-3 polyunsaturated fatty acids), and then a low-fat diet (total fat 28%, carbohydrates 54%).
  
  
  RESULTS
  The high-fat diet significantly decreased triglycerides (-63%), total cholesterol (-22%), VLDL cholesterol (-54%), LDL cholesterol ( 16%), total apoC-III (-27%), apoC-III in apoB containing lipoproteins (apoC-III LpB; -31%) and in HDL (apoC-III nonLpB; -29%), apoE in serum (-33%) and apoB-containing lipoproteins (nonHDL-E; -42%), LpA-I (-16%), insulin (-36%), and leptin (-26%) and significantly increased the means of HDL cholesterol (+8%), LDL size (+6%), lipoprotein lipase (LPL, +11%), hepatic lipase (+13%), and lecithin: cholesterol acyltransferase (LCAT, +2%). The subsequent low-fat diet increased triglycerides (+63%), VLDL cholesterol (+19%), apoC-III (+23%), apoC-III LpB (+44%) apoC-III nonLpB (+17%), apoE (+29%) and nonHDL-E (+43%), and decreased HDL cholesterol (-12%), LPL (-3%), and LCAT (-3%). Changes in triglycerides correlated with changes in LPL activity and insulin levels.
  
  
  CONCLUSIONS
  In hypertriglyceridemic patients, a modified diet rich in mono- and n-3 polyunsaturated fatty acids is more effective than a carbohydrate-rich low-fat diet in correcting the atherogenic lipoprotein phenotype.
authors.affiliation: Institute of Arteriosclerosis Research at the University of Münster, Germany.
authors.forename: B
authors.initials: B
authors.lastname: Pieke
authors.forename: A
authors.initials: A
authors.lastname: von Eckardstein
authors.forename: E
authors.initials: E
authors.lastname: Gülbahçe
authors.forename: A
authors.initials: A
authors.lastname: Chirazi
authors.forename: H
authors.initials: H
authors.lastname: Schulte
authors.forename: G
authors.initials: G
authors.lastname: Assmann
authors.forename: U
authors.initials: U
authors.lastname: Wahrburg
mesh_terms: D000328:Adult; D015415:Biomarkers; D002352:Carrier Proteins / Q000097:blood; D004040:Dietary Carbohydrates / Q000008:administration & dosage*; D004042:Dietary Fats, Unsaturated / Q000008:administration & dosage*; D005231:Fatty Acids, Unsaturated / Q000008:administration & dosage*; D006801:Humans; D015228:Hypertriglyceridemia / Q000178:diet therapy*; D007328:Insulin / Q000097:blood; D020738:Leptin / Q000097:blood; D008049:Lipase / Q000097:blood; D008055:Lipids / Q000097:blood*; D008071:Lipoprotein Lipase / Q000097:blood; D008074:Lipoproteins / Q000097:blood*; D008297:Male; D008875:Middle Aged; D013997:Time Factors; D016896:Treatment Outcome; D014280:Triglycerides / Q000097:blood
chemical_list: D015415:Biomarkers; D002352:Carrier Proteins; D004040:Dietary Carbohydrates; D004042:Dietary Fats, Unsaturated; D005231:Fatty Acids, Unsaturated; D007328:Insulin; D020738:Leptin; D008055:Lipids; D008074:Lipoproteins; D014280:Triglycerides; C030363:lipid transfer protein; D008049:Lipase; D008071:Lipoprotein Lipase