戒烟后β细胞分泌增加源于碳水化合物的渴求增加？
2012-05-19 12:13:55 来源：
丁香园 作者： 评论：0 点击：
Despite the known health hazards of cigarette smoking, many smokers fail toquit smoking, mainly due to nicotine’s addictiveness, but also because of fearfrom gaining weight. However, the mechanism of weight gain after smokingcessation is not fully elucidated yet.
尽管清楚吸烟对于身体的危害，许多吸烟者仍然戒烟失败，这主要是由于尼古丁的成瘾性，同时也有一部分担心体重增加的原因。然而对于戒烟后体重增加的机制还么有全部阐述清楚。
Healthy long-term smokers (28±2 years, 10F/20M, 23.4±1.3 kg/m2)participating in a smoking cessation programme underwent 3-hour oral glucosetolerance tests (oGTT) and body composition measurements while still smoking(Visit A; n=27) and after a minimum of 3 (3 m; n=14) and 6months (6 m; n=8) of non-smoking. Fasting (QUICKI) and dynamic insulinsensitivity (OGIS) were calculated. First phase beta-cell secretion wascalculated as the ratio of C-peptide and glucose areas under the curve in thefirst 40 min of oGTT (IGI40). Appetite was quantified with afree-choice-buffet. Fasting plasma concentrations of neuropeptide-Y (NPY),peptide-YY (PYY), glucagon-like-peptide-1 (GLP-1), leptin, ghrelin and visfatinwere measured.
身体健康的长期吸烟者(28±2years, 10F/20M, 23.4±1.3 kg/m2)，和那些还在吸烟的受试者(Visit A; n=27)以及戒烟时间在3个月 (3 m; n=14)和6个月(6 m; n=8)的受试者，参与了戒烟项目中，并且接受了3小时的葡萄糖耐量测试以及身体组成成分的测定。空腹(QUICKI)和动态时的胰岛素敏感性也进行了计算。第一相胰岛β细胞的分泌情况的计算是通过计算C肽与前40分钟时的oGTT(IGI40)曲线下的葡萄糖面积。食欲通过自助餐进行量化。并且对空腹时神经肽Y(NPY)的浓度，酪酪肽抗体（PYY），胰高血糖素样多肽（GLP-1），瘦素，生长激素释放肽，以及内脏脂肪素进行了测定。
Body weight and fat mass increased after 3 m (+4% and +22% respectively) andafter 6 m non-smoking (+5% and +35% respectively, P<0.05 vsbaseline). Participants showed significant fasting insulin resistance (QUICKI:3 m:0.37±0.02 vs baseline:0.41±0.2; P<0.05) at 3 m, but not at 6 m,while OGIS remained unchanged throughout. IGI40 increased by 31% after 3 m(baseline:0.299±0.11 vs 3 m:0.391±0.11, P<0.01), but reversed tonormal after 6 m (0.265±5). Accordingly, carbohydrate ingestion wassignificantly increased after 3 m (3 m:500±39 kcal vs baseline:396±45 kcal; P<0.05),but not after 6 m. Fasting NPY was increased at 3 m (3 m: 0.41±0.03 ng/ml vsbaseline:0.26±0.04 ng/ml; P<0.05), but not at 6 m. Interestingly,increased beta-cell-secretion at 3 m was less pronounced in participantsfinally succeeding to quit smoking for at least 6 m, as opposed to thoserelapsing after 3 m (P<0.05).
在戒烟3个月(体重增加4% ，脂肪量增加22%)与6个月后体重与脂肪量(体重增加5% ，脂肪量增加35%)增加。参与研究的受试者在3个月时显示出显著地空腹胰岛素抵抗（戒烟3个月后空腹胰岛素:0.37±0.02vs 基线时0.41±0.2; P<0.05)，但是并没有在6个月时显示出明显的空腹胰岛素抵抗。在戒烟后3个月受试者空腹神经肽NPY显著地升高(戒烟3个月后:0.41±0.03 ng/ml vs 基线时:0.26±0.04 ng/ml; P<0.05)，但是在戒烟后6个月的受试者空腹神经肽NPY并没有显著地升高。有趣的是相对于那些在戒烟3个月后又继续吸烟的受试者，那些成功戒烟至少6个月后的受试者在戒烟3个月时胰岛β细胞分泌功能的增加并不明显。
Smoking cessation leads to a transient increase of first phase beta-cellsecretion in response to glucose, fasting insulin resistance and NPY plasmalevels. These alterations could contribute to increased carbohydrate cravingand consequent body weight gain after smoking cessation (Fig. 1).
戒烟会导致第一相的葡萄糖刺激的胰岛素分泌增加，空腹胰岛素抵抗以及神经肽NPY升高。这些变化会导致对碳水化合物的渴求增加以及戒烟后的体重增加(Fig. 1)。
Figure 1 Glucose plasma concentrations and insulin and C-peptideserum concentrations during the 180 min 75g oral glucose tolerance test insmokers (black) and after 3 (grey) and 6 months (white) of smoking cessation.
图表1 75g口服葡萄糖耐量测试葡萄糖浓度和胰岛素以及C肽浓度，吸烟患者（黑色线），戒烟3个月后（灰色线），戒烟6个月后（白色线）
Declaration of interest: The authors declare that there is no conflict ofinterest that could be perceived as prejudicing the impartiality of theresearch project.
利益关系声明：作者声明该研究没有与研究公正性相关的利益冲突
Funding: This work was supported, however funding details are unavailable.
资金：本研究得到基金支持，然而基金使用的详细信息并没有完全呈现。
尽管清楚吸烟对于身体的危害，许多吸烟者仍然戒烟失败，这主要是由于尼古丁的成瘾性，同时也有一部分担心体重增加的原因。然而对于戒烟后体重增加的机制还么有全部阐述清楚。
Healthy long-term smokers (28±2 years, 10F/20M, 23.4±1.3 kg/m2)participating in a smoking cessation programme underwent 3-hour oral glucosetolerance tests (oGTT) and body composition measurements while still smoking(Visit A; n=27) and after a minimum of 3 (3 m; n=14) and 6months (6 m; n=8) of non-smoking. Fasting (QUICKI) and dynamic insulinsensitivity (OGIS) were calculated. First phase beta-cell secretion wascalculated as the ratio of C-peptide and glucose areas under the curve in thefirst 40 min of oGTT (IGI40). Appetite was quantified with afree-choice-buffet. Fasting plasma concentrations of neuropeptide-Y (NPY),peptide-YY (PYY), glucagon-like-peptide-1 (GLP-1), leptin, ghrelin and visfatinwere measured.
身体健康的长期吸烟者(28±2years, 10F/20M, 23.4±1.3 kg/m2)，和那些还在吸烟的受试者(Visit A; n=27)以及戒烟时间在3个月 (3 m; n=14)和6个月(6 m; n=8)的受试者，参与了戒烟项目中，并且接受了3小时的葡萄糖耐量测试以及身体组成成分的测定。空腹(QUICKI)和动态时的胰岛素敏感性也进行了计算。第一相胰岛β细胞的分泌情况的计算是通过计算C肽与前40分钟时的oGTT(IGI40)曲线下的葡萄糖面积。食欲通过自助餐进行量化。并且对空腹时神经肽Y(NPY)的浓度，酪酪肽抗体（PYY），胰高血糖素样多肽（GLP-1），瘦素，生长激素释放肽，以及内脏脂肪素进行了测定。
Body weight and fat mass increased after 3 m (+4% and +22% respectively) andafter 6 m non-smoking (+5% and +35% respectively, P<0.05 vsbaseline). Participants showed significant fasting insulin resistance (QUICKI:3 m:0.37±0.02 vs baseline:0.41±0.2; P<0.05) at 3 m, but not at 6 m,while OGIS remained unchanged throughout. IGI40 increased by 31% after 3 m(baseline:0.299±0.11 vs 3 m:0.391±0.11, P<0.01), but reversed tonormal after 6 m (0.265±5). Accordingly, carbohydrate ingestion wassignificantly increased after 3 m (3 m:500±39 kcal vs baseline:396±45 kcal; P<0.05),but not after 6 m. Fasting NPY was increased at 3 m (3 m: 0.41±0.03 ng/ml vsbaseline:0.26±0.04 ng/ml; P<0.05), but not at 6 m. Interestingly,increased beta-cell-secretion at 3 m was less pronounced in participantsfinally succeeding to quit smoking for at least 6 m, as opposed to thoserelapsing after 3 m (P<0.05).
在戒烟3个月(体重增加4% ，脂肪量增加22%)与6个月后体重与脂肪量(体重增加5% ，脂肪量增加35%)增加。参与研究的受试者在3个月时显示出显著地空腹胰岛素抵抗（戒烟3个月后空腹胰岛素:0.37±0.02vs 基线时0.41±0.2; P<0.05)，但是并没有在6个月时显示出明显的空腹胰岛素抵抗。在戒烟后3个月受试者空腹神经肽NPY显著地升高(戒烟3个月后:0.41±0.03 ng/ml vs 基线时:0.26±0.04 ng/ml; P<0.05)，但是在戒烟后6个月的受试者空腹神经肽NPY并没有显著地升高。有趣的是相对于那些在戒烟3个月后又继续吸烟的受试者，那些成功戒烟至少6个月后的受试者在戒烟3个月时胰岛β细胞分泌功能的增加并不明显。
Smoking cessation leads to a transient increase of first phase beta-cellsecretion in response to glucose, fasting insulin resistance and NPY plasmalevels. These alterations could contribute to increased carbohydrate cravingand consequent body weight gain after smoking cessation (Fig. 1).
戒烟会导致第一相的葡萄糖刺激的胰岛素分泌增加，空腹胰岛素抵抗以及神经肽NPY升高。这些变化会导致对碳水化合物的渴求增加以及戒烟后的体重增加(Fig. 1)。
Figure 1 Glucose plasma concentrations and insulin and C-peptideserum concentrations during the 180 min 75g oral glucose tolerance test insmokers (black) and after 3 (grey) and 6 months (white) of smoking cessation.
图表1 75g口服葡萄糖耐量测试葡萄糖浓度和胰岛素以及C肽浓度，吸烟患者（黑色线），戒烟3个月后（灰色线），戒烟6个月后（白色线）
Declaration of interest: The authors declare that there is no conflict ofinterest that could be perceived as prejudicing the impartiality of theresearch project.
利益关系声明：作者声明该研究没有与研究公正性相关的利益冲突
Funding: This work was supported, however funding details are unavailable.
资金：本研究得到基金支持，然而基金使用的详细信息并没有完全呈现。
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