血n-3 PUFA与胃潰瘍疾病的因果关联:一个两样本的门德尔随机化研究
Zebin Dai1, Qinjian Wang1, Bingbing He1
1The Second Affiliated Hospital and Yuying Children's Hospital, Wenzhou Medical University, Wenzhou, People's Republic of China.
The British journal of nutrition
|November 11, 2024
概括
饮食中的欧米茄-3多不和脂肪酸 (PUFA) 可能会降低胃潰瘍疾病 (PUD) 的风险. 来自海洋的omega-3PUFA,特别是EPA,DPA和DHA,与PUD显示出显著的反向关联.
科学领域:
- 营养流行病学 营养流行病学
- 胃肠病学 胃肠病学
- 遗传学 是一个遗传学.
背景情况:
- 饮食中的欧米茄-3多不和脂肪酸 (PUFA) 与预防胃潰瘍疾病 (PUD) 的潜在益处有关.
- 关于n-3PUFA和PUD关系的观察流行病学数据有限,需要进一步调查因果关系.
研究的目的:
- 调查饮食中的n-3PUFA对患上胃潰瘍疾病 (PUD) 的风险的因果影响.
- 为了区分植物衍生的与海洋衍生的n-3PUFA对PUD风险的影响.
主要方法:
- 采用孟德尔的随机化分析,利用遗传变异作为用于血n-3PUFA水平的仪器变量.
- 仪器变量包括与总,植物衍生 (α-烯酸) 和海洋衍生 (EPA,DPA,DHA) n-3 PUFA.相关的遗传变异.
- 评估了这些变体与PUD风险的评估效应大小估计,使用来自英国生物银行的数据.
主要成果:
- 总血n-3PUFA的基因预测的一个标准偏差增加与明显降低PUD风险有关 (OR = 0.91;P = 0.020).
- 海洋衍生的n-3PUFA显示出显著的反向关联:EPA (OR = 0.81),DPA (OR = 0.72),和DHA (OR = 0.87).
- 来自植物的α-烯酸与PUD风险没有显著关联 (OR = 5.41).
结论:
- 基因预测的高血水平的n-3PUFA,特别是来自海洋的EPA,DPA和DHA,与胃潰瘍疾病的风险相反相关.
- 这些发现表明,n-3PUFA摄入量可能为PUD的初级预防提供了可行的策略.
- 基于海洋的n-3脂肪酸似乎是对抗PUD的保护作用的关键贡献者.
相关概念视频
01:30Peptic Ulcer Disease I: Introduction
139
Peptic Ulcer Disease (PUD) is characterized by mucosal excavation in the esophagus, stomach, pylorus, or duodenum. It can manifest as acute or chronic based on the extent and duration of mucosal involvement.
An acute ulcer, marked by superficial erosion and minimal inflammation, swiftly resolves upon identifying and addressing the underlying cause. In contrast, a chronic ulcer persists, potentially eroding through the muscular wall and forming fibrous tissue.
Peptic ulcers can also be...
An acute ulcer, marked by superficial erosion and minimal inflammation, swiftly resolves upon identifying and addressing the underlying cause. In contrast, a chronic ulcer persists, potentially eroding through the muscular wall and forming fibrous tissue.
Peptic ulcers can also be...
139
01:24Pathophysiology of Peptic Ulcer Disease: Mucosal Defense Factors
356
Peptic ulcer disease, commonly called PUD, represents a multifaceted condition characterized by disruptions in the lining of the gastrointestinal (GI) tract. Central to the protection of the gastrointestinal lining is the mucosal-bicarbonate barrier. This physiological defense mechanism is a formidable shield against the corrosive effects of gastric acid and pepsin secretion in the stomach. Its role is pivotal in maintaining the structural integrity of the stomach's inner lining.
356
01:22Pathophysiology of Peptic Ulcer Disease: Injurious Factors
542
Peptic ulcers are sores on the stomach's inner lining and the upper small intestine, which are the result of disruptions in the mucosal layer that houses parietal cells which produce gastric acid, and chief cells which secrete pepsinogen.
In the antrum region, G cells secrete the gastrin hormone that binds to gastrin-cholecystokinin-B (CCK2) receptors on parietal and enterochromaffin-like (ECL) cells in the fundic glands. Simultaneously, the vagus nerve releases acetylcholine, which binds...
In the antrum region, G cells secrete the gastrin hormone that binds to gastrin-cholecystokinin-B (CCK2) receptors on parietal and enterochromaffin-like (ECL) cells in the fundic glands. Simultaneously, the vagus nerve releases acetylcholine, which binds...
542
01:28Peptic Ulcer Disease III: Clinical Manifestations and Diagnostic Studies
89
Peptic ulcer disease (PUD) presents with diverse symptoms depending on the location and severity of the ulcer. Clinical manifestations of peptic ulcer include dull pain and a burning sensation in the mid-epigastric region.
Few clinical manifestations differentiate gastric ulcers from duodenal ulcers. Distinctions in the location, timing, and pain relief are crucial for healthcare providers in differentiating between gastric and duodenal ulcers during clinical assessments.
Few clinical manifestations differentiate gastric ulcers from duodenal ulcers. Distinctions in the location, timing, and pain relief are crucial for healthcare providers in differentiating between gastric and duodenal ulcers during clinical assessments.
89
01:20Drugs for Peptic Ulcer Disease: Prostaglandin Analogs as Mucosal Protective Agents
355
The gastric mucosa produces prostaglandins E2 (PGE2) and prostacyclin (PGI2), crucial in maintaining gastric health. They exert cytoprotective effects, including increasing bicarbonate secretion, releasing protective mucin, reducing gastric acid output, and preventing harmful vasoconstriction. These effects are mediated through various receptors, such as EP1, EP2, EP3, and EP4.
Non-steroidal anti-inflammatory drugs (NSAIDs) can induce peptic ulcers by inhibiting cyclooxygenase, decreasing...
Non-steroidal anti-inflammatory drugs (NSAIDs) can induce peptic ulcers by inhibiting cyclooxygenase, decreasing...
355
01:28Peptic Ulcer Disease II: Pathophysiology
289
Peptic Ulcer Disease (PUD) is characterized by the development of ulcers in the stomach or duodenal mucosa. Its pathophysiology is complex, involving a balance between damaging and protective elements.
Damaging agents such as Helicobacter pylori, gastric acid, pepsin, and nonsteroidal anti-inflammatory drugs (NSAIDs) can weaken the mucosal defense, allowing hydrogen ions to infiltrate back and harm epithelial cells.
Damaging agents such as Helicobacter pylori, gastric acid, pepsin, and nonsteroidal anti-inflammatory drugs (NSAIDs) can weaken the mucosal defense, allowing hydrogen ions to infiltrate back and harm epithelial cells.
289