AIM: The α1-antitrypsin-low-density lipoprotein complex (AT-LDL) and serum amyloid A-LDL complex (SAA-LDL) are oxidatively modified LDL complexes that promote atherosclerosis. The serum levels of AT-LDL and SAA-LDL are suggested to be increased by obesity and smoking. We have previously demonstrated that larger weight gain after smoking cessation (SC) perturbs a decrease in the serum level of AT-LDL at 3 months after SC. However, changes of these atherosclerotic makers ＞3 months after SC are unknown. This study investigated post-SC time-dependent changes in two atherogenic lipoproteins, AT-LDL and SAA-LDL, and in the extent of abdominal obesity. METHODS: In 50 outpatients who had continued SC for 1 year, we measured serum AT-LDL and SAA-LDL levels by the enzyme-linked immunosorbent assay before SC, and at 3 months and 1 year after SC. RESULTS: Both body mass index and waist circumstance significantly increased from pre-SC to 3 months after SC and from 3 months after SC to 1 year after SC. Although the serum levels of AT-LDL and SAA-LDL were unchanged from pre-SC to 3 months after SC, these levels decreased significantly from 3 months after SC to 1 year after SC. CONCLUSIONS: The extent of abdominal obesity and levels of two atherogenic lipoproteins time-dependently change after SC. Although abdominal obesity progressively worsened after SC, the beneficial effect of non-smoking overcomes the potential vascular risks by cessation-associated obesity at 1 year after SC.
AIM: The α1-antitrypsin-low-density lipoprotein complex (AT-LDL) and serum amyloid A-LDL complex (SAA-LDL) are oxidatively modified LDL complexes that promote atherosclerosis. The serum levels of AT-LDL and SAA-LDL are suggested to be increased by obesity and smoking. We have previously demonstrated that larger weight gain after smoking cessation (SC) perturbs a decrease in the serum level of AT-LDL at 3 months after SC. However, changes of these atherosclerotic makers ＞3 months after SC are unknown. This study investigated post-SC time-dependent changes in two atherogenic lipoproteins, AT-LDL and SAA-LDL, and in the extent of abdominal obesity. METHODS: In 50 outpatients who had continued SC for 1 year, we measured serum AT-LDL and SAA-LDL levels by the enzyme-linked immunosorbent assay before SC, and at 3 months and 1 year after SC. RESULTS: Both body mass index and waist circumstance significantly increased from pre-SC to 3 months after SC and from 3 months after SC to 1 year after SC. Although the serum levels of AT-LDL and SAA-LDL were unchanged from pre-SC to 3 months after SC, these levels decreased significantly from 3 months after SC to 1 year after SC. CONCLUSIONS: The extent of abdominal obesity and levels of two atherogenic lipoproteins time-dependently change after SC. Although abdominal obesity progressively worsened after SC, the beneficial effect of non-smoking overcomes the potential vascular risks by cessation-associated obesity at 1 year after SC.
Authors: K Kotani; N Satoh-Asahara; Y Kato; R Araki; A Himeno; H Yamakage; K Koyama; M Tanabe; M Oishi; T Okajima; A Shimatsu Journal: J Int Med Res Date: 2011 Impact factor: 1.671
Authors: S Goya Wannamethee; Gordon D O Lowe; A Gerald Shaper; Ann Rumley; Lucy Lennon; Peter H Whincup Journal: Eur Heart J Date: 2005-04-07 Impact factor: 29.983
Authors: Carole Clair; Nancy A Rigotti; Bianca Porneala; Caroline S Fox; Ralph B D'Agostino; Michael J Pencina; James B Meigs Journal: JAMA Date: 2013-03-13 Impact factor: 56.272