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Related Concept Videos

Hormonal Regulation01:40

Hormonal Regulation

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Hormones regulate a significant portion of digestion through activation of the neuroendocrine system. The neuroendocrine system of digestion contains many different hormones all with multiple functions that are both, directly and indirectly, involved in digestion.
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Hormones Regulating Blood Glucose01:16

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Insulin is released by beta cells of the pancreas when blood glucose levels are high. It facilitates glucose absorption and utilization in insulin-dependent cells with insulin receptors on their plasma membranes. Insulin promotes glucose uptake by increasing the number of glucose transport proteins in the cell membrane, allowing glucose to enter the cell. As a result, glucose utilization and ATP production are enhanced.
In addition to accelerating glucose uptake and utilization, insulin has...
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Regulation of the Digestive System01:25

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Digestive activity regulation hinges on three primary components. Activation is prompted by a multitude of mechanical and chemical indicators, primarily detected by receptors within the stomach and intestines' walls. These receptors predominantly respond to factors such as mechanical stretching of the organ walls, changes in pH and osmolarity, and the presence of digesting materials and their by-products.
The effectors in this regulation system are glands and smooth muscles. Activation of...
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Glucose Homeostasis: Regulation of Blood Glucose01:02

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Carbohydrates consumed through foods are converted into glucose, a crucial energy source for the body. In the prandial state, high blood glucose levels stimulate the secretion of insulin from the pancreas. Insulin inhibits hepatic glucose production and stimulates glucose uptake and metabolism by muscle and adipose tissue. The excess glucose is converted into glycogen and stored in the liver and muscles.
During fasting, when blood glucose levels are low, the pancreas secretes glucagon. it...
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Glucose Homeostasis: Pancreatic Islets and Insulin Secretion01:27

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The pancreatic islets comprising only 1%-2% of the volume are highly vascularized and innervated mini-organs. They contain five endocrine cell types, including β cells that secrete insulin, which is synthesized as a single polypeptide chain, preproinsulin, processed to proinsulin, and finally to insulin and C-peptide. This process is complex and regulated, involving the Golgi complex, the endoplasmic reticulum, and the secretory granules of the β cell.
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Glucagon-like Receptor Agonists01:24

Glucagon-like Receptor Agonists

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Incretins include glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP), which stimulate insulin secretion post-meals. In type 2 diabetes, GIP's efficacy is reduced, making GLP-1 a viable drug target. GIP originates from preproGIP.
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Related Experiment Video

Updated: May 5, 2026

Hyperinsulinemic-euglycemic Clamps in Conscious, Unrestrained Mice
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Factors controlling gastric-glucagon release

P J Lefèbvre, A S Luyckx

    The Journal of Clinical Investigation
    |April 1, 1977
    PubMed
    Summary

    This study shows that insulin is needed for high blood sugar to reduce gastric glucagon secretion. An isolated dog stomach model helps investigate alpha-cell function without insulin interference.

    Area of Science:

    • Endocrinology
    • Gastroenterology
    • Physiology

    Background:

    • Gastric glucagon plays a role in glucose homeostasis.
    • Understanding factors influencing gastric glucagon secretion is crucial for metabolic research.

    Purpose of the Study:

    • To investigate the regulation of gastric glucagon secretion using an isolated perfused dog stomach model.
    • To determine the effects of arginine, somatostatin, hyperglycemia, and hyperinsulinemia on gastric glucagon release.

    Main Methods:

    • Utilized an isolated dog stomach perfused with whole blood.
    • Measured basal and stimulated gastric glucagon release.
    • Administered arginine, somatostatin, and induced hyperglycemia and hyperinsulinemia.

    Main Results:

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    • Basal gastric glucagon release ranged from 0.0-3.1 ng/100g/min.
    • Arginine stimulated rapid glucagon release, which was inhibited by somatostatin.
    • Hyperglycemia alone did not affect gastric glucagon release, but it was reduced by 40% when combined with physiological hyperinsulinemia.

    Conclusions:

    • Adequate insulin levels are necessary for hyperglycemia to inhibit gastric glucagon secretion.
    • The isolated perfused dog stomach is a valuable tool for studying alpha-cell function independently of endogenous insulin.