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Regulatory effects of HMG CoA reductase inhibitor and fish oils on apolipoprotein B-100 kinetics in insulin-resistant obese male subjects with dyslipidemia.
Diabetes 2002; 51(8):2377-86D

Abstract

Hepatic accumulation of lipid substrates perturbs apolipoproteinB-100 (apoB) metabolism in insulin-resistant, obese subjects and may account for increased risk of cardiovascular disease. In a placebo-controlled trial, we examined the independent and combined effects of decreasing cholesterol synthesis with atorvastatin (40 mg/day) and triglyceride synthesis with fish oils (4 g/day) on apoB kinetics. The subjects were 48 viscerally obese, insulin-resistant men with dyslipidemia who were studied in a fasted state. We found that atorvastatin significantly decreased plasma apoB-containing lipoproteins (P < 0.001, main effect) through increases in the fractional catabolic rate (FCR) of VLDL-, IDL-, and LDL-apoB (P < 0.01). Fish oils significantly decreased plasma levels of triglycerides and VLDL-apoB (P < 0.001), decreased the VLDL-apoB secretion rate (P < 0.01), but increased the conversion of VLDL to LDL (P < 0.001). Compared with placebo, combined treatment with atorvastatin and fish oils decreased VLDL-apoB secretion (P < 0.03) and increased the FCR of apoB in each lipoprotein fraction (P < 0.03) and the percent conversion of VLDL to LDL (P < 0.05). None of the treatments altered insulin resistance. In conclusion, in visceral obesity, atorvastatin increased hepatic clearance of all apoB-containing lipoproteins, whereas fish oils decreased hepatic secretion of VLDL-apoB. The differential effects of atorvastatin and fish oils on apoB kinetics support their combined use in correcting defective apoB metabolism in obese, insulin-resistant subjects.

Authors+Show Affiliations

Department of Medicine, University of Western Australia and the Western Australian Institute for Medical Research, Crawley, Western Australia.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Clinical Trial
Comparative Study
Journal Article
Randomized Controlled Trial
Research Support, Non-U.S. Gov't
Research Support, U.S. Gov't, P.H.S.

Language

eng

PubMed ID

12145148

Citation

Chan, Dick C., et al. "Regulatory Effects of HMG CoA Reductase Inhibitor and Fish Oils On Apolipoprotein B-100 Kinetics in Insulin-resistant Obese Male Subjects With Dyslipidemia." Diabetes, vol. 51, no. 8, 2002, pp. 2377-86.
Chan DC, Watts GF, Barrett PH, et al. Regulatory effects of HMG CoA reductase inhibitor and fish oils on apolipoprotein B-100 kinetics in insulin-resistant obese male subjects with dyslipidemia. Diabetes. 2002;51(8):2377-86.
Chan, D. C., Watts, G. F., Barrett, P. H., Beilin, L. J., Redgrave, T. G., & Mori, T. A. (2002). Regulatory effects of HMG CoA reductase inhibitor and fish oils on apolipoprotein B-100 kinetics in insulin-resistant obese male subjects with dyslipidemia. Diabetes, 51(8), pp. 2377-86.
Chan DC, et al. Regulatory Effects of HMG CoA Reductase Inhibitor and Fish Oils On Apolipoprotein B-100 Kinetics in Insulin-resistant Obese Male Subjects With Dyslipidemia. Diabetes. 2002;51(8):2377-86. PubMed PMID: 12145148.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Regulatory effects of HMG CoA reductase inhibitor and fish oils on apolipoprotein B-100 kinetics in insulin-resistant obese male subjects with dyslipidemia. AU - Chan,Dick C, AU - Watts,Gerald F, AU - Barrett,P Hugh R, AU - Beilin,Lawrence J, AU - Redgrave,Trevor G, AU - Mori,Trevor A, PY - 2002/7/30/pubmed PY - 2002/8/22/medline PY - 2002/7/30/entrez SP - 2377 EP - 86 JF - Diabetes JO - Diabetes VL - 51 IS - 8 N2 - Hepatic accumulation of lipid substrates perturbs apolipoproteinB-100 (apoB) metabolism in insulin-resistant, obese subjects and may account for increased risk of cardiovascular disease. In a placebo-controlled trial, we examined the independent and combined effects of decreasing cholesterol synthesis with atorvastatin (40 mg/day) and triglyceride synthesis with fish oils (4 g/day) on apoB kinetics. The subjects were 48 viscerally obese, insulin-resistant men with dyslipidemia who were studied in a fasted state. We found that atorvastatin significantly decreased plasma apoB-containing lipoproteins (P < 0.001, main effect) through increases in the fractional catabolic rate (FCR) of VLDL-, IDL-, and LDL-apoB (P < 0.01). Fish oils significantly decreased plasma levels of triglycerides and VLDL-apoB (P < 0.001), decreased the VLDL-apoB secretion rate (P < 0.01), but increased the conversion of VLDL to LDL (P < 0.001). Compared with placebo, combined treatment with atorvastatin and fish oils decreased VLDL-apoB secretion (P < 0.03) and increased the FCR of apoB in each lipoprotein fraction (P < 0.03) and the percent conversion of VLDL to LDL (P < 0.05). None of the treatments altered insulin resistance. In conclusion, in visceral obesity, atorvastatin increased hepatic clearance of all apoB-containing lipoproteins, whereas fish oils decreased hepatic secretion of VLDL-apoB. The differential effects of atorvastatin and fish oils on apoB kinetics support their combined use in correcting defective apoB metabolism in obese, insulin-resistant subjects. SN - 0012-1797 UR - https://www.unboundmedicine.com/medline/citation/12145148/Regulatory_effects_of_HMG_CoA_reductase_inhibitor_and_fish_oils_on_apolipoprotein_B_100_kinetics_in_insulin_resistant_obese_male_subjects_with_dyslipidemia_ L2 - http://diabetes.diabetesjournals.org/cgi/pmidlookup?view=long&amp;pmid=12145148 DB - PRIME DP - Unbound Medicine ER -