膳食糖摄入量与成年人群中胆石症患病风险的关联性分析
Association between Dietary Sugar Intake and the Risk of Gallstone Disease in Adults
DOI: 10.12677/acm.2026.162457, PDF, HTML, XML,    科研立项经费支持
作者: 李雅楠, 杨乃龙*：青岛大学附属医院内分泌与代谢性疾病科，山东 青岛；姜良华：海阳市人民医院老年医学科，山东 海阳
关键词: 胆石症；膳食糖；膳食疗法；横断面研究；Gallstone Disease； Dietary Sugars； Diet Therapy； Cross-Sectional Study
摘要: 目的：基于美国国家健康与营养检查调查(NHANES)数据库，探讨成年人群胆石症患病风险与膳食糖摄入量的关系。方法：采用NHANES 2017~2020年的数据进行横断面研究。通过24小时饮食回顾评估膳食糖摄入量，胆石症则依据自我报告判定。运用加权Logistic回归模型调整混杂因素分析关联强度，并使用广义相加模型(GAM)探索非线性关系，通过两步递归法计算拐点。结果：共纳入7087名参与者，膳食糖摄入量的中位数为88.00克(IQR：54.45~131.59克)，胆石症的报告率为11.10%。校正混杂因素后，膳食总糖摄入量每增加10克，胆石症患病风险升高4.5% [OR: 1.045 (95% CI: 1.013~1.078), P = 0.011]。GAM提示存在非线性关联，然而对数似然比检验未检测到统计学上显著的阈值效应(P = 0.067)。结论：成年人群中胆石症患病风险与膳食糖摄入量呈连续、非线性的正相关关系，提示较高的膳食糖摄入量与胆石病患病率上升有关。
Abstract: Objective: To investigate the association between total dietary sugar intake and the risk of gallstone disease in adults based on the National Health and Nutrition Examination Survey (NHANES). Methods: A cross-sectional study was conducted using NHANES 2017~2020 data. Total dietary sugar intake was assessed by 24-hour dietary recall, and gallstone disease was defined by self-report. Weighted Logistic regression models were used to adjust for potential confounders, and generalized additive models (GAM) were applied to examine non-linear relationships, with the inflection point calculated by a two-step recursive method. Results: Among 7087 participants, the median total sugar intake was 88.00 g (IQR: 54.45~131.59 g), and 11.10% reported gallstone disease. After adjusting for confounders, each 10 g increase in total dietary sugar intake was associated with a 4.5% increase in gallstone disease prevalence [OR = 1.045 (95% CI: 1.013~1.078), P = 0.011]. GAM indicated a non-linear relationship. However, the log-likelihood ratio test did not detect a statistically significant threshold effect (P = 0.067). Conclusion: There is a continuous, non-linear positive correlation between the risk of gallstone disease and total dietary sugar intake in adults, suggesting that higher levels of sugar consumption are associated with increased gallstone disease prevalence.
文章引用：李雅楠, 姜良华, 杨乃龙. 膳食糖摄入量与成年人群中胆石症患病风险的关联性分析[J]. 临床医学进展, 2026, 16(2): 829-836. https://doi.org/10.12677/acm.2026.162457

1. 引言

胆石症以胆道系统内形成结石为特征，全球约10%~20%的成年人受累[1] [2]。近年来，随着生活水平和饮食结构的改变，其患病率呈显著上升趋势。胆结石的存在与多种共病风险升高相关，其中包括心血管疾病和胆囊癌[3] [4]。胆结石主要分为胆固醇结石与胆色素结石[5]，其中胆固醇结石最为常见，其形成主要与胆汁中胆固醇过饱和、胆囊动力障碍等因素相关，而胆色素结石则源于胆红素代谢异常[1]。多项研究已阐明，代谢综合征、饮食因素、胆囊运动功能减退、胆红素肠肝循环增强，以及各类药物等均是胆结石明确的危险因素[6]-[8]。其中，饮食是胆结石发病机制中一个关键且可干预的因素[9]-[11]。多项流行病学研究表明，某些特定的饮食模式会增加胆结石的患病风险[9] [12] [13]。这些饮食模式通常表现为富含精制碳水化合物、甜食及脂肪，膳食纤维摄入不足、快餐消费频繁等[9]。过量糖摄入是这些高风险饮食模式的一个显著共同特征。然而，关于膳食糖摄入量与胆结石风险之间关系的定量研究仍然有限，二者之间的确切关联亟待深入探究。因此，本研究旨在利用美国国家健康与营养检查调查(NHANES)的全国代表性样本，探究成年人群膳食糖摄入量与胆结石患病率之间的量化关系，阐明膳食糖在胆结石形成过程中的潜在作用，以期为日后制定降低胆结石患病风险的预防策略和饮食建议提供依据。

2. 资料与方法

2.1. 研究资料

本研究数据来自2017~2020年NHANES，最初纳入15,560名受试者。其中，6328例因年龄在20岁以下被排除，88例因妊娠数据缺失被排除，21例因缺乏胆结石疾病信息被排除，1506例因缺少饮食总糖摄入量的数据被排除，530例因相关协变量值缺失被排除，最终7087名受试者被纳入分析。该项目获得了美国国家卫生统计中心伦理审查委员会的批准，所有参与者均提供了书面知情同意书。

2.2. 调查内容

收集人口学特征、生活方式和合并症等数据。我们采用NHANES的24小时饮食回顾数据[14] [15]，通过与美国农业部(USDA)的食物与营养素数据库系统(FNDDS)和食物模式等效数据库(FPED)进行匹配，以计算总能量和糖摄入量[16]。24小时饮食回顾数据的收集分两次进行：首次回顾在移动体检中心进行面对面访谈，第二次回顾在3~10天后通过电话完成，两次评估均采用相同评估方法以保证数据一致性[17]。本研究采用首次24小时回顾数据，并以克/天为单位对膳食糖摄入量进行量化。膳食糖摄入量定义为六种特定单糖与双糖的总和，包括：葡萄糖、果糖、半乳糖、蔗糖、乳糖和麦芽糖[18] [19]。胆结石疾病通过NHANES访谈过程中自我报告数据进行评估[20] [21]。人口学特征包括年龄、性别、种族(非西班牙裔白人、非西班牙裔黑人、西班牙裔和其他)和贫困收入比(PIR，衡量社会经济地位的指标)。生活方式因素包括吸烟状况(当前、既往或从不吸烟)和饮酒状况(根据摄入的频率和量分类)。身体质量指数(BMI)根据测量的身高和体重计算，并根据世卫组织指南进行分类。我们还评估了三种主要合并症：高血压、高脂血症和糖尿病。高血压的定义依据2017年美国心脏病学会和美国心脏协会指南，综合考虑降压药使用情况和血压读书[22]。高脂血症依据血脂谱异常或降脂药物使用情况判定[23]。糖尿病是通过自我报告的医师诊断、药物使用情况和实验室指标(包括空腹血糖、口服葡萄糖耐量试验结果和糖化血红蛋白水平)相结合来确定的。

2.3. 统计学方法

本研究基于NHANES的复杂抽样设计，应用调查权重、分层和聚类变量进行统计分析。连续变量以均数 ± 标准差表示，分类变量以例数(百分比)描述。应用加权逻辑回归模型探讨膳食糖摄入量与胆石病的关系；使用广义相加模型探讨二者之间的非线性关联，并通过递归算法确定拐点。所有分析使用R软件(4.2.0版)和EmpowerStats完成，P < 0.05视为差异有统计学意义。

3. 结果

不同膳食糖摄入组临床特征比较各组间年龄、性别、种族分布差异均有统计学意义(均P < 0.001)。生活方式方面，吸烟与饮酒状况在不同分组间亦存在显著差异(P < 0.001, P = 0.004)。值得注意的是，糖尿病患病率随糖摄入增加呈下降趋势(Q1组25.11%至Q4组16.42%，P < 0.001)，而胆结石患病率在各组间差异无统计学意义(10.50%~12.48%, P = 0.197)。见表1。

Table 1. Baseline characteristics of study participants by quartiles of dietary sugar intake

表1. 按膳食糖摄入量四等分组的研究对象基线特征

膳食糖摄入量(g/d)

Q1

(0~54.83)

Q2

(54.85~88.18)

Q3

(88.21~131.42)

Q4

(131.54~600.79)

P值

年龄(岁)

51.59 ± 17.56

52.49 ± 17.23

51.33 ± 17.37

49.82 ± 17.04

<0.001

贫困收入比

2.65 ± 1.64

2.69 ± 1.66

2.70 ± 1.63

2.55 ± 1.59

0.027

总能量摄入量(kcal/d)

1496.41 ± 598.94

1798.25 ± 609.86

2136.34 ± 646.48

2637.20 ± 683.08

<0.001

性别[例(%)]

<0.001

女性

1053 (59.42%)

1020 (57.59%)

895 (50.51%)

734 (41.42%)

男性

719 (40.58%)

751 (42.41%)

877 (49.49%)

1038 (58.58%)

种族[例(%)]

<0.001

非西班牙裔白人

602 (33.97%)

618 (34.90%)

645 (36.40%)

694 (39.16%)

非西班牙裔黑人

553 (31.21%)

479 (27.05%)

443 (25.00%)

378 (21.33%)

墨西哥裔美国人

194 (10.95%)

213 (12.03%)

211 (11.91%)

191 (10.78%)

其他

423 (23.87%)

461 (26.03%)

473 (26.69%)

509 (28.72%)

BMI [kg/m2，例(%)]

0.270

≤25

467 (26.81%)

419 (23.92%)

450 (25.70%)

449 (25.55%)

>25

1275 (73.19%)

1333 (76.08%)

1301 (74.30%)

1308 (74.45%)

饮酒状况[例(%)]

0.004

从不

164 (9.26%)

173 (9.77%)

153 (8.63%)

129 (7.28%)

低

603 (34.03%)

656 (37.04%)

670 (37.81%)

600 (33.86%)

中

302 (17.04%)

279 (15.75%)

299 (16.87%)

286 (16.14%)

高

326 (18.40%)

277 (15.64%)

267 (15.07%)

322 (18.17%)

不明

377 (21.28%)

386 (21.80%)

383 (21.61%)

435 (24.55%)

吸烟状况[例(%)]

<0.001

从不

1050 (59.26%)

1072 (60.53%)

1063 (59.99%)

935 (52.77%)

既往

430 (24.27%)

450 (25.41%)

424 (23.93%)

423 (23.87%)

当前

292 (16.48%)

249 (14.06%)

285 (16.08%)

414 (23.36%)

糖尿病[例(%)]

<0.001

否

1327 (74.89%)

1358 (76.68%)

1438 (81.15%)

1481 (83.58%)

是

445 (25.11%)

413 (23.32%)

334 (18.85%)

291 (16.42%)

高脂血症[例(%)]

0.561

否

576 (32.51%)

588 (33.20%)

581 (32.79%)

613 (34.59%)

是

1196 (67.49%)

1183 (66.80%)

1191 (67.21%)

1159 (65.41%)

高血压[例(%)]

0.293

否

915 (51.64%)

937 (52.91%)

964 (54.40%)

963 (54.35%)

是

857 (48.36%)

834 (47.09%)

808 (45.60%)

809 (45.65%)

胆结石[例(%)]

0.197

否

1579 (89.11%)

1550 (87.52%)

1585 (89.45%)

1586 (89.50%)

是

193 (10.89%)

221 (12.48%)

187 (10.55%)

186 (10.50%)

注：BMI为体重指数；数据以均数 ± 标准差或例数(百分比)表示。

表2显示了不同调整模型下膳食糖摄入量与胆石病的关联。将膳食糖作为连续变量分析时，其在所有调整模型中均与胆结石风险显著相关。在完全调整模型(模型3)中，糖摄入每增加10 g，胆结石患病风险增加4.5% (OR = 1.045, 95% CI: 1.013~1.078, P = 0.011)。然而，当以四分位数分组进行分析时，与最低分位组(Q1)相比，中等至较高糖摄入组(Q2~Q4)的胆结石患病风险均无统计学差异(均P > 0.05)。

Table 2. Weighted Logistic regression analysis of the association between dietary sugar intake and the risk of gallstone disease

表2. 膳食糖摄入量与胆结石风险关系的加权Logistic回归分析

未调整模型

模型1

模型2

模型3

膳食糖摄入量 (每10 g)

1.004 (0.988, 1.020) 0.637

1.029 (1.010, 1.049) 0.007

1.027 (1.006, 1.048) 0.026

1.045 (1.013, 1.078) 0.011

膳食糖摄入量分类

Q1

1.0

1.0

1.0

1.0

Q2

0.892 (0.648, 1.228) 0.492

0.903 (0.646, 1.262) 0.558

0.862 (0.632, 1.176) 0.373

0.909 (0.588, 1.405) 0.570

Q3

0.954 (0.670, 1.357) 0.794

1.132 (0.744, 1.724) 0.570

1.100 (0.701, 1.728) 0.686

1.202 (0.668, 2.164) 0.425

Q4

0.823 (0.626, 1.082) 0.176

1.128 (0.845, 1.506) 0.425

1.043(0.768, 1.418) 0.793

1.164 (0.713, 1.901) 0.429

注：未调整模型未调整任何变量；模型1调整了年龄、性别、种族；模型2在模型1的基础上调整了贫困收入比、吸烟状况、饮酒状况；模型3在模型2的基础上调整了总能量摄入量、高血压、糖尿病、高脂血症。

膳食糖摄入量与胆石病的非线性关系：为进一步探讨膳食糖摄入量与胆结石风险的关系，本研究采用广义相加模型进行拟合，发现膳食糖摄入量与胆结石风险呈非线性关联，高风险主要集中于摄入量较高区间(图1)。然而，进一步的阈值效应分析未发现统计学上显著的拐点(P = 0.066) (表3)。

Figure 1. Non-linear relationship diagram between dietary sugar intake and the risk of gallstone disease

图1. 膳食糖摄入量与胆结石患病风险的非线性关系图

Table 3. Piecewise linear regression analysis of the association between dietary sugar intake and the risk of gallstone disease

表3. 膳食糖摄入量与胆结石风险的分段线性回归分析

OR值(95% CI)

P值

标准线性模型

1.029 (1.012, 1.046)

<0.001

两段式线性模型

拐点(g/d)

189

<189

1.015 (0.993, 1.037)

0.176

>189

1.061 (1.024, 1.098)

<0.001

对数似然比检验

0.066

注：暴露因素为膳食糖摄入量(每升高10 g)；结局因素为胆结石风险；OR为比值比；CI为置信区间；调整的协变量有年龄、性别、种族、贫困收入比、吸烟状况、饮酒状况、总能量摄入量、高血压、糖尿病、高脂血症。

4. 讨论

本横断面研究显示，在美国成年人群中，膳食糖摄入量与胆结石患病率之间存在显著的正向关联，且该关联呈现非线性特征。随着每日膳食糖摄入量水平的升高，胆结石患病风险会逐渐增加。

本研究的结果补充并拓展了饮食因素与胆结石风险的现有证据。以往研究多聚焦于宏观膳食模式或特定宏量营养素的作用。例如，Tsai等[24]报告了高碳水化合物摄入与胆囊切除风险增加相关。而近期研究则强调了超加工食品对胆结石风险的潜在影响[25]。在此基础上，本研究通过聚焦膳食糖摄入量，为该领域提供了新的视角。膳食糖作为碳水化合物和超加工食品中的关键组分，有效衔接了宏观饮食模式与微观营养素研究，为今后制定更具针对性的胆结石饮食预防策略提供了理论依据。

关于膳食糖影响胆结石形成的分子机制，目前尚未完全阐明。我们推测，高糖摄入可刺激胰岛素分泌增加并诱发胰岛素抵抗[26] [27]，而后者已被证实可通过多种途径参与胆结石形成[21] [28]。此外，高糖摄入也可能导致肝脏脂代谢紊乱，增加胆固醇合成与分泌[29] [30]，从而提升胆汁中胆固醇饱和度——此为胆固醇性结石形成的关键环节[31]-[33]。

本研究也存在一定的局限性。首先，作为一项横断面研究，本研究无法推断糖摄入与胆结石之间的因果关系。其次，膳食数据的收集采用24小时饮食回顾法，可能引入回忆偏倚及报告误差。此外，尽管已对多种潜在混杂因素进行校正，但仍无法完全排除残余混杂的影响。未来研究可进一步纳入遗传背景、体力活动等变量，并借助前瞻性研究设计或膳食生物标志物以增强因果推断力度。

基金项目

本研究获得青岛大学附属医院院内科研基金(计划编号：4156)支持。

利益冲突

所有作者声明无利益冲突。

NOTES

*通讯作者。

参考文献

[1] Lammert, F., Gurusamy, K., Ko, C.W., Miquel, J., Méndez-Sánchez, N., Portincasa, P., et al. (2016) Gallstones. Nature Reviews Disease Primers, 2, Article No. 16024. [Google Scholar] [CrossRef] [PubMed]
[2] Peery, A.F., Crockett, S.D., Murphy, C.C., Jensen, E.T., Kim, H.P., Egberg, M.D., et al. (2022) Burden and Cost of Gastrointestinal, Liver, and Pancreatic Diseases in the United States: Update 2021. Gastroenterology, 162, 621-644. [Google Scholar] [CrossRef] [PubMed]
[3] Bai, R., Wang, J., Yang, J., Cheng, X., Zhang, S., Zhang, H., et al. (2023) Gallbladder Disease Is Associated with the Risk of Cardiovascular Disease among Uyghurs in Xinjiang: A Prospective Cohort Study. BMC Public Health, 23, Article No. 242. [Google Scholar] [CrossRef] [PubMed]
[4] Stinton, L.M. and Shaffer, E.A. (2012) Epidemiology of Gallbladder Disease: Cholelithiasis and Cancer. Gut and Liver, 6, 172-187. [Google Scholar] [CrossRef] [PubMed]
[5] Chen, L., Yang, H., Li, H., He, C., Yang, L. and Lv, G. (2021) Insights into Modifiable Risk Factors of Cholelithiasis: A Mendelian Randomization Study. Hepatology, 75, 785-796. [Google Scholar] [CrossRef] [PubMed]
[6] Stender, S., Nordestgaard, B.G. and Tybjaerg-Hansen, A. (2013) Elevated Body Mass Index as a Causal Risk Factor for Symptomatic Gallstone Disease: A Mendelian Randomization Study. Hepatology, 58, 2133-2141. [Google Scholar] [CrossRef] [PubMed]
[7] Di Ciaula, A., Wang, D.Q. and Portincasa, P. (2018) Cholesterol Cholelithiasis: Part of a Systemic Metabolic Disease, Prone to Primary Prevention. Expert Review of Gastroenterology & Hepatology, 13, 157-171. [Google Scholar] [CrossRef] [PubMed]
[8] Yuan, S., Gill, D., Giovannucci, E.L. and Larsson, S.C. (2022) Obesity, Type 2 Diabetes, Lifestyle Factors, and Risk of Gallstone Disease: A Mendelian Randomization Investigation. Clinical Gastroenterology and Hepatology, 20, e529-e537. [Google Scholar] [CrossRef] [PubMed]
[9] Di Ciaula, A., Garruti, G., Frühbeck, G., De Angelis, M., de Bari, O., Wang, D.Q., et al. (2019) The Role of Diet in the Pathogenesis of Cholesterol Gallstones. Current Medicinal Chemistry, 26, 3620-3638. [Google Scholar] [CrossRef] [PubMed]
[10] Luo, Y., Gao, X., Xiao, M., Yang, F., Zhu, X., Qiao, G., et al. (2024) Association between Dietary Inflammatory Index and Gallstones in US Adults. Frontiers in Nutrition, 11, Article 1403438. [Google Scholar] [CrossRef] [PubMed]
[11] Chang, C., Chiu, T.H.T., Chang, C., Lin, M. and Lin, C. (2019) Plant-Based Diet, Cholesterol, and Risk of Gallstone Disease: A Prospective Study. Nutrients, 11, Article No. 335. [Google Scholar] [CrossRef] [PubMed]
[12] (1989) Dietary Beans: A Risk Factor for Cholesterol Gallstones? Nutrition Reviews, 47, 369-371.
[13] Ortega, R.M., Fernández-Azuela, M., Encinas-Sotillos, A., Andrés, P. and López-Sobaler, A.M. (1997) Differences in Diet and Food Habits between Patients with Gallstones and Controls. Journal of the American College of Nutrition, 16, 88-95. [Google Scholar] [CrossRef] [PubMed]
[14] Akbar, Z. and Shi, Z. (2023) Dietary Patterns and Circadian Syndrome among Adults Attending NHANES 2005-2016. Nutrients, 15, Article No. 3396. [Google Scholar] [CrossRef] [PubMed]
[15] Ahluwalia, N., Dwyer, J., Terry, A., Moshfegh, A. and Johnson, C. (2016) Update on NHANES Dietary Data: Focus on Collection, Release, Analytical Considerations, and Uses to Inform Public Policy. Advances in Nutrition, 7, 121-134. [Google Scholar] [CrossRef] [PubMed]
[16] Hoy, M.K., Goldman, J.D. and Sebastian, R.S. (2016) Fruit and Vegetable Intake of US Adults Estimated by Two Methods: What We Eat in America, National Health and Nutrition Examination Survey 2009-2012. Public Health Nutrition, 19, 2508-2512. [Google Scholar] [CrossRef] [PubMed]
[17] Kase, B.E., Liese, A.D., Zhang, J., Murphy, E.A., Zhao, L. and Steck, S.E. (2024) The Development and Evaluation of a Literature-Based Dietary Index for Gut Microbiota. Nutrients, 16, Article No. 1045. [Google Scholar] [CrossRef] [PubMed]
[18] Chun, O.K., Chung, C.E., Wang, Y., Padgitt, A. and Song, W.O. (2010) Changes in Intakes of Total and Added Sugar and Their Contribution to Energy Intake in the U.S. Nutrients, 2, 834-854. [Google Scholar] [CrossRef] [PubMed]
[19] Zhang, J., Tang, Z., Lu, Z., Lin, X., Liao, H., Li, Z., et al. (2023) The Association between Dietary Sugar Intake and Nephrolithiasis: Results from National Health and Nutrition Examination Survey 2007-2018. The Journal of Nutrition, 153, 2968-2978. [Google Scholar] [CrossRef] [PubMed]
[20] Cheng, J., Zhuang, Q., Wang, W., Li, J., Zhou, L., Xu, Y., et al. (2024) Association of Pro-Inflammatory Diet with Increased Risk of Gallstone Disease: A Cross-Sectional Study of NHANES January 2017-March 2020. Frontiers in Nutrition, 11, Article 1344699. [Google Scholar] [CrossRef] [PubMed]
[21] Fu, C., Li, X., Wang, Y., Chen, J., Yang, Y. and Liu, K. (2024) Association between Triglyceride Glucose Index-Related Indices with Gallstone Disease among US Adults. Lipids in Health and Disease, 23, Article No. 203. [Google Scholar] [CrossRef] [PubMed]
[22] Whelton, P.K., Carey, R.M., Aronow, W.S., Casey, D.E., Collins, K.J., Dennison Himmelfarb, C., et al. (2018) 2017 ACC/AHA/AAPA/ABC/ACPM/AGS/APhA/ASH/ASPC/NMA/PCNA Guideline for the Prevention, Detection, Evaluation, and Management of High Blood Pressure in Adults: Executive Summary: A Report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines. Circulation, 138, e426-e483. [Google Scholar] [CrossRef] [PubMed]
[23] Aggarwal, R., Bhatt, D.L., Rodriguez, F., Yeh, R.W. and Wadhera, R.K. (2022) Trends in Lipid Concentrations and Lipid Control among US Adults, 2007-2018. JAMA, 328, 737-745. [Google Scholar] [CrossRef] [PubMed]
[24] Tsai, C., Leitzmann, M.F., Willett, W.C. and Giovannucci, E.L. (2005) Glycemic Load, Glycemic Index, and Carbohydrate Intake in Relation to Risk of Cholecystectomy in Women. Gastroenterology, 129, 105-112. [Google Scholar] [CrossRef] [PubMed]
[25] Uche-Anya, E., Ha, J., Khandpur, N., Rossato, S.L., Wang, Y., Nguyen, L.H., et al. (2024) Ultraprocessed Food Consumption and Risk of Gallstone Disease: Analysis of 3 Prospective Cohorts. The American Journal of Clinical Nutrition, 120, 499-506. [Google Scholar] [CrossRef] [PubMed]
[26] Astley, C.M., Todd, J.N., Salem, R.M., Vedantam, S., Ebbeling, C.B., Huang, P.L., et al. (2018) Genetic Evidence That Carbohydrate-Stimulated Insulin Secretion Leads to Obesity. Clinical Chemistry, 64, 192-200. [Google Scholar] [CrossRef] [PubMed]
[27] Hurwitz, B.E., Schneiderman, N., Marks, J.B., Mendez, A.J., Gonzalez, A., Llabre, M.M., et al. (2015) Adaptation of β-Cell and Endothelial Function to Carbohydrate Loading: Influence of Insulin Resistance. Diabetes, 64, 2550-2559. [Google Scholar] [CrossRef] [PubMed]
[28] Cortés, V.A., Barrera, F. and Nervi, F. (2019) Pathophysiological Connections between Gallstone Disease, Insulin Resistance, and Obesity. Obesity Reviews, 21, e12983. [Google Scholar] [CrossRef] [PubMed]
[29] Geidl-Flueck, B., Hochuli, M., Németh, Á., Eberl, A., Derron, N., Köfeler, H.C., et al. (2021) Fructose-and Sucrose-But Not Glucose-Sweetened Beverages Promote Hepatic De Novo Lipogenesis: A Randomized Controlled Trial. Journal of Hepatology, 75, 46-54. [Google Scholar] [CrossRef] [PubMed]
[30] Wu, X., Cui, L., Wang, H., Xu, J., Zhong, Z., Jia, X., et al. (2022) Impact of Dietary Sucralose and Sucrose-Sweetened Water Intake on Lipid and Glucose Metabolism in Male Mice. European Journal of Nutrition, 62, 199-211. [Google Scholar] [CrossRef] [PubMed]
[31] Sun, H., Warren, J., Yip, J., Ji, Y., Hao, S., Han, W., et al. (2022) Factors Influencing Gallstone Formation: A Review of the Literature. Biomolecules, 12, Article No. 550. [Google Scholar] [CrossRef] [PubMed]
[32] Wang, J., Shen, S., Wang, B., Ni, X., Liu, H., Ni, X., et al. (2020) Serum Lipid Levels Are the Risk Factors of Gallbladder Stones: A Population-Based Study in China. Lipids in Health and Disease, 19, Article No. 50. [Google Scholar] [CrossRef] [PubMed]
[33] Zhang, X., Guan, L., Tian, H. and Li, Y. (2022) Prevalence and Risk Factors of Gallbladder Stones and Polyps in Liaoning, China. Frontiers in Medicine, 9, Article 865458. [Google Scholar] [CrossRef] [PubMed]

为你推荐