Impact of Cigarette Smoking Cessation on High-Density Lipoprotein Functionality

Takata, Kohei; Imaizumi, Satoshi; Kawachi, Emi; Suematsu, Yasunori; Shimizu, Tomohiko; Abe, Satomi; Matsuo, Yoshino; Tsukahara, Hitomi; Noda, Kohei; Yahiro, Eiji; Zhang, Bo; Uehara, Yoshio; Miura, Shin‐ichiro; Saku, Keijiro

doi:10.1253/circj.cj-14-0638

Cited by 53 publications

(43 citation statements)

References 48 publications

(25 reference statements)

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“…Although former smokers were included in the no smoker group in this study, former smokers showed an almost normal range of HSP 27 levels. The fact that a favorable effect of smoking cessation on oxidative stress is consistent with the previous studies [25][26][27].…”

Section: Plasma Hsp 27 Levels and Smoking Habitssupporting

confidence: 91%

Plasma heat shock protein 27 is increased in renal dysfunction and habitual smoking in a Japanese general population

Nakayoshi

Adachi

Ohbu-Murayama

et al. 2016

Journal of Cardiology

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Section: Plasma Hsp 27 Levels and Smoking Habitssupporting

confidence: 91%

Plasma heat shock protein 27 is increased in renal dysfunction and habitual smoking in a Japanese general population

Nakayoshi

Adachi

Ohbu-Murayama

et al. 2016

Journal of Cardiology

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“…This suggests that lipid metabolism is abnormal in schizophrenic patients before the commencement of antipsychotic drug treatment. It is well-known that smoking alters serum lipid profiles, as characterized by increased total cholesterol (TC), triglycerides (TG), ApoB/ApoA1 ratio, and low-density lipoprotein cholesterol (LDL-c), along with decreased high-density lipoprotein cholesterol (HDL-c) [14][15][16]. However, the mechanisms by which smoking changes serum lipid and lipoprotein levels are still unknown.…”

Section: And Thomas R Kostenmentioning

confidence: 99%

“…Unexpectedly, we found no significant differences in the lipid profiles of smokers versus non-smokers. In the general population, smoking is associated with abnormal profiles, such as elevated TC, TG, LDL-c, and ApoB, and reduced HDL-c and ApoA1 [14][15][16], suggesting that smoking has potentially long-term atherogenic effects on lipid metabolism. The biological mechanisms linking smoking and atherogenesis are complex, but a presumed linkage is that nicotine stimulates the sympathetic adrenal system to secrete catecholamines [26] These catecholamines then increase lipolysis and the concentration of plasma free fatty acids, which in turn increases the synthesis of hepatic TG and VLDL-c in the blood stream [17,18].…”

Section: Symptoms and Lipid Profiles In Smokers Versus Non-smokersmentioning

confidence: 99%

Smoking and Serum Lipid Profiles in Schizophrenia

Tan

et al. 2016

Neurosci. Bull.

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Schizophrenia is associated with a high prevalence of cigarette-smoking and abnormal lipid profiles. The purpose of this study was to determine whether the profiles differ between schizophrenic smokers and non-smokers and whether the lipid profiles are related to psychopathological symptoms. Serum lipid profiles were measured in 130 male inpatients with DSM-IV-defined schizophrenia: 104 smokers and 26 non-smokers. Symptoms were assessed using the Positive and Negative Syndrome Scale (PANSS). Our results showed that positive PANSS symptoms were fewer in smokers than in non-smokers, while the negative symptoms were fewer in those who smoked more cigarettes. Total protein and globulin levels were significantly lower in the smokers than in the non-smokers. However, there was no significant difference in total cholesterol, triglycerides, high-density lipoprotein cholesterol (HDL-c), low-density lipoprotein cholesterol, apolipoprotein A1, or apolipoprotein B between the smokers and non-smokers. However, the PANSS positive subscale had a significant negative correlation with the HDL-c levels (a protective factor) in the smokers but not in the non-smokers. Our findings suggest that schizophrenic patients who smoke have fewer psychotic symptoms, but contrary to expectation, smoking does not alter lipid profile levels.

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“…Nevertheless, a metaanalysis reported that there was no significant change in LDL-C after smoking cessation (165). It was reported that smoking cessation leads to improved HDL functionality (efflux capacity and anti-inflammatory property) (166).…”

Section: Smokingmentioning

confidence: 99%