摘要目的 了解糖尿病前期人群中血浆脂联素、内脂素、瘦素、抵抗素水平与结肠息肉发病的相关关系.方法 选择468例接受全结肠镜检查的糖尿病前期患者,其中有结肠息肉248例(糖尿病前期息肉组),无结肠黏膜病变220例(糖尿病前期无息肉组).根据结肠息肉的临床特点,再将其分为单发息肉组与多发息肉组,低危息肉组与高危息肉组.同时选择性别、年龄与糖尿病前期患者匹配的108名糖耐量正常者作为对照组,其中有息肉46例(糖耐量正常息肉组),无息肉62名(糖耐量正常无息肉组).测定所有受试者血浆脂联素、内脂素、瘦素、抵抗素水平,并对糖尿病前期人群中结肠息肉的相关影响因素进行分析.结果 无论是在糖耐量正常人群中,还是在糖尿病前期患者中,与各自的无息肉组相比,息肉组患者血浆内脂素水平显著升高(P＜0.05),脂联素水平显著降低[糖耐量正常者(9.8±4.8对13.3±3.9)mg/L, P＜0.05;糖尿病前期者(5.6±3.7对9.2±4.4)mg/L,P＜0.01],而瘦素、抵抗素水平在2组间差异无统计学意义(均P＞0.05).在糖尿病前期患者中,多发息肉组血浆内脂素水平显著高于单发息肉组(P＜0.05),而血浆脂联素水平显著低于单发息肉组[(4.3±2.6对6.7±3.9)mg/L,P＜0.05],2组间血浆瘦素、抵抗素水平差异无统计学意义(均P＞0.05).此外,糖尿病前期高危息肉组患者血浆脂联素水平也显著低于低危息肉组[(3.7±2.9对7.4±3.5)mg/L, P＜0.05],2组间血浆内脂素、瘦素、抵抗素水平的差异无统计学意义(均P＞0.05).多因素logistic回归分析发现,脂联素为结肠息肉、结肠多发息肉以及结肠高危息肉的独立保护因素.结论 糖尿病前期人群中血浆脂联素水平改变与结肠息肉发病相关.

abstractsObjective To explore the relationship between plasma adiponectin, visfatin, leptin, and resistin levels, and the onset of colonic polyps in prediabetes subjects. Methods A total of 468 prediabetes subjects, who received colonoscopy examination, were enrolled in this study, including 248 cases of colon polyps (polyps group with prediabetes) and 220 cases without colonic mucosal lesions ( polyps-free group with prediabetes). According to the clinical characteristics of colonic polyps, colonic polyps patients with prediabetes were subdivided into single polyp group, multiple polyps group, low-risk polyps group, and high-risk polyps group, respectively. In addition, 108 subjects with normal glucose tolerance, who were matched with prediabetes subjects on gender and age, were selected as control group, and 46 cases of them were refered to polyps group with normal glucose tolerance and 62 cases were refered to polyps-free group with normal glucose. Plasma adiponectin, visfatin, leptin, and resistin levels were measured in all subjects, and related risk factors of colonic polyps in prediabetes patients were analyzed. Results Not only in normal glucose tolerance subjects, but also in prediabetes subjects, plasma visfatin levels in polyps group were significantly higher than those in polyps-free group (P＜0.05), and plasma adiponectin levels were significantly lower than those in polyps-free group [normal glucose tolerance (9.8±4.8 vs 13.3±3.9)mg/L, P＜0.05; prediabetes (5.6 ± 3.7 vs 9.2 ± 4.4)mg/L, P＜0.01], respectively. However, no significant difference in the plasma leptin and resistin levels were observed between polyps-free group and polyps group ( both P＞0. 05), respectively. In addition, in prediabetes subjects, plasma visfatin levels increased (P＜0.05) and adiponectin levels decreased significantly [(4.3 ± 2.6 vs 6.7 ± 3.9) mg/L, P＜0.05] in multiple polyps group than in single polyp group. Nevertheless, there were no significant differences in plasma leptin and resistin levels between two groups (both P＞0.05). Moreover, plasma adiponectin levels decreased significantly in high-risk polyps group with prediabetes than in low-risk polyps group with prediabetes[(3.7±2.9vs7.4±3.5)mg/L,P＜0.05].Meanwhile,noneofplasmavisfatin,leptin,andresistinlevels had shown significant difference between two groups (all P＞0.05). The multivariate logistic regression analysis found that adiponectin was an independent protective factor for colon polyps, multiple colon polyps and high-risk colon polyps. Conclusion The changes of plasma adiponectin levels might be associated with onset of colonic polyps in prediabetes.