Alper Sonmez1, Dragana Nikolic2, Teoman Dogru3, Cemal Nuri Ercin3, Halil Genc3, Mustafa Cesur4, Serkan Tapan5, Yildirim Karslioğlu6, Giuseppe Montalto2, Maciej Banach7, Peter P Toth8, Sait Bagci3, Manfredi Rizzo9. 1. Department of Endocrinology and Metabolic Diseases, Gulhane School of Medicine, Ankara, Turkey. 2. BioMedical Department of Internal Medicine and Medical Specialties, University of Palermo, Italy. 3. Department of Gastroenterology, Gulhane School of Medicine, Ankara, Turkey. 4. Department of Endocrinology, Ankara Guven Hospital, Ankara, Turkey. 5. Department of Medical Biochemistry, Gulhane School of Medicine, Ankara, Turkey. 6. Department of Pathology, Gulhane School of Medicine, Ankara, Turkey. 7. Department of Nephrology and Hypertension, Medical University of Lodz, Poland. 8. Department of Preventive Cardiology, CGH Medical Center, Sterling, IL, USA; Department of Family and Community Medicine, University of Illinois, School of Medicine, Peoria, IL, USA; Ciccarone Center for Cardiovascular Disease Prevention, Johns Hopkins University School of Medicine, Baltimore, MD, USA. Electronic address: peter.toth@cghmc.com. 9. BioMedical Department of Internal Medicine and Medical Specialties, University of Palermo, Italy; Euro-Mediterranean Institute of Science and Technology, Italy.
Abstract
BACKGROUND: Nonalcoholic fatty liver disease (NAFLD) is associated with increased cardiometabolic risk. Although dyslipidemia represents a key factor in this disease, its impact on serum levels of distinct lipoprotein subfractions is largely unknown. OBJECTIVE: To assess the full low-density lipoprotein (LDL) and high-density lipoprotein (HDL) profiles in patients with NAFLD. METHODS: Seven LDL and 10 HDL subfractions were assessed by gel electrophoresis (Lipoprint, Quantimetrix Corporation, USA) in men with biopsy proven NAFLD (simple steatosis [n = 17, age, 34 ± 7 years] and nonalcoholic steatohepatitis [NASH; n = 24, age, 32 ± 6 years]). Exclusion criteria included robust alcohol consumption, infection with hepatitis B or C virus, body mass index ≥ 40 kg/m(2), diabetes mellitus, and hypertension. RESULTS: Compared with simple steatosis, NASH patients had similar body mass index, homeostasis model assessment of insulin resistance index and plasma lipids, with increased levels of both aspartate aminotransferase and alanine transaminase. NASH subjects had lower levels of larger LDL1 (10 ± 4 vs 13 ± 4%, P = .010) and increased smaller LDL3 and LDL4 particles (9 ± 5 vs 5 ± 5%, P = .017 and 3 ± 3 vs 1 ± 2%, P = .012, respectively). No changes were found in the HDL subclass profile. By multiple regression analysis, we found that NASH was associated only with increased levels of LDL3 (P = .0470). CONCLUSIONS: The increased levels of small, dense LDL3 and LDL4 in NASH may help to at least partly explain the increased risk for atherosclerosis and cardiovascular diseases in these patients.
BACKGROUND:Nonalcoholic fatty liver disease (NAFLD) is associated with increased cardiometabolic risk. Although dyslipidemia represents a key factor in this disease, its impact on serum levels of distinct lipoprotein subfractions is largely unknown. OBJECTIVE: To assess the full low-density lipoprotein (LDL) and high-density lipoprotein (HDL) profiles in patients with NAFLD. METHODS: Seven LDL and 10 HDL subfractions were assessed by gel electrophoresis (Lipoprint, Quantimetrix Corporation, USA) in men with biopsy proven NAFLD (simple steatosis [n = 17, age, 34 ± 7 years] and nonalcoholic steatohepatitis [NASH; n = 24, age, 32 ± 6 years]). Exclusion criteria included robust alcohol consumption, infection with hepatitis B or C virus, body mass index ≥ 40 kg/m(2), diabetes mellitus, and hypertension. RESULTS: Compared with simple steatosis, NASH patients had similar body mass index, homeostasis model assessment of insulin resistance index and plasma lipids, with increased levels of both aspartate aminotransferase and alanine transaminase. NASH subjects had lower levels of larger LDL1 (10 ± 4 vs 13 ± 4%, P = .010) and increased smaller LDL3 and LDL4 particles (9 ± 5 vs 5 ± 5%, P = .017 and 3 ± 3 vs 1 ± 2%, P = .012, respectively). No changes were found in the HDL subclass profile. By multiple regression analysis, we found that NASH was associated only with increased levels of LDL3 (P = .0470). CONCLUSIONS: The increased levels of small, dense LDL3 and LDL4 in NASH may help to at least partly explain the increased risk for atherosclerosis and cardiovascular diseases in these patients.
Authors: David E Stec; Darren M Gordon; Jennifer A Hipp; Stephen Hong; Zachary L Mitchell; Natalia R Franco; J Walker Robison; Christopher D Anderson; Donald F Stec; Terry D Hinds Journal: Am J Physiol Regul Integr Comp Physiol Date: 2019-09-04 Impact factor: 3.619
Authors: Kathleen E Corey; Laura A Wilson; Akif Altinbas; Katherine P Yates; David E Kleiner; Raymond T Chung; Ronald M Krauss; Naga Chalasani Journal: Aliment Pharmacol Ther Date: 2019-03-10 Impact factor: 8.171
Authors: Xiongfeng Pan; Atipatsa C Kaminga; Jihua Chen; Miyang Luo; Jiayou Luo Journal: Int J Environ Res Public Health Date: 2020-04-15 Impact factor: 3.390