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Stomach pH Regulation01:21

Stomach pH Regulation

The human body carefully regulates the internal pH of different organs to maintain homeostasis. For example, while the blood plasma maintains a neutral pH of 7, the stomach lumen has an acidic pH of 1.5 - 3.5. The low pH of stomach lumen helps kill pathogens in the food and break down complex food molecules.
The acid-secreting gastric mucosal epithelial cells (parietal cells) lining the stomach lumen maintain the low pH in the lumen. Numerous ion transporters and channels on these parietal...
Pathophysiology of Peptic Ulcer Disease: Injurious Factors01:22

Pathophysiology of Peptic Ulcer Disease: Injurious Factors

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 to M3...
Pathophysiology of Peptic Ulcer Disease: Mucosal Defense Factors01:24

Pathophysiology of Peptic Ulcer Disease: Mucosal Defense Factors

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. Bicarbonate,...
Acid Suppressive Drugs for Peptic Ulcer Disease: Proton Pump Inhibitors01:13

Acid Suppressive Drugs for Peptic Ulcer Disease: Proton Pump Inhibitors

Peptic ulcers, often induced by H. pylori infections or NSAID usage, arise from disruptions in the delicate balance of gastric acid production. Peptic ulcers stem from heightened gastric acid levels due to H. pylori infections or NSAID use. The protective mucus layer diminishes in the presence of these factors, allowing gastric acid to erode the stomach lining and form ulcers.
Gastric acid, a potent cocktail of hydrogen and chloride ions, is produced in specialized parietal cells within the...
Acid Suppressive Drugs for Peptic Ulcer Disease: Histamine H2-Receptor Antagonists01:28

Acid Suppressive Drugs for Peptic Ulcer Disease: Histamine H2-Receptor Antagonists

Histamine H2 receptors, which are intricately located on the basolateral membrane of parietal cells, play a crucial role in modulating gastric acid secretion. When released from enterochromaffin-like cells, histamine engages H2 receptors, initiating the cyclic AMP (cAMP) pathway. In this pathway, adenylyl cyclase converts ATP into cAMP, elevating intracellular cAMP levels. The activation of protein kinase A follows, stimulating the proton pump. This stimulation prompts the secretion of hydrogen...
Acid Suppressive Drugs for Peptic Ulcer Disease: Antacids01:31

Acid Suppressive Drugs for Peptic Ulcer Disease: Antacids

In the complex environment of the gastric lumen, excessive acid secretion can lead to the formation or worsening of ulcers within the delicate mucosal layer. Antacids, such as sodium bicarbonate and calcium carbonate, provide relief by neutralizing this acid, transforming it into harmless salt and water. This neutralization process raises the gastric pH from a highly acidic level of 1 to a more basic 3-4, reducing the acidity within the stomach.
However, this neutralization reaction between...

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Updated: Jul 18, 2026

Evaluation of Amino Acid Consumption in Cultured Bone Cells and Isolated Bone Shafts
06:32

Evaluation of Amino Acid Consumption in Cultured Bone Cells and Isolated Bone Shafts

Published on: April 13, 2022

饮食中酸盐对甲状腺功能的影响

R A BLOOMFIELD, C W WELSCH, G B GARNER

    Science (New York, N.Y.)
    |November 24, 1961
    PubMed
    概括

    饮食中酸盐的摄入会影响甲状腺在老鼠和绵羊中的代谢. 水平对于减轻酸盐的作用至关重要.

    科学领域:

    • 内分泌学 在内分泌学.
    • 动物营养 动物营养
    • 毒理学 毒理学 毒理学

    背景情况:

    • 甲状腺激素对于调节新陈代谢至关重要.
    • 是甲状腺激素的一个关键成分.
    • 食中酸盐是一种常见的环境污染物.

    研究的目的:

    • 研究食中酸盐对大鼠和绵羊中代谢的影响.
    • 为了确定饮食中含量在调节酸盐对甲状腺影响中的作用.

    主要方法:

    • 鼠和绵羊被食含有特定度酸盐的饮食.
    • 评估了甲状腺功能和代谢.
    • 饮食中的含量各不相同.

    主要成果:

    • 在老鼠中,0.31%的酸盐和在绵羊中,0.92%的酸盐改变了正常的代谢.
    • 酸盐对代谢的影响取决于饮食中的度.

    结论:

    • 饮食中酸盐可以干扰哺乳动物的甲状腺代谢.
    • 充足的饮食对于在酸盐暴露的情况下维持甲状腺功能很重要.
    关键词:
    亚酸盐/营养和饮食甲状腺/生理学

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