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関連する概念動画

Glucose Homeostasis: Regulation of Blood Glucose01:02

Glucose Homeostasis: Regulation of Blood Glucose

2.5K
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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Hormones Regulating Blood Glucose01:16

Hormones Regulating Blood Glucose

4.0K
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...
4.0K
Insulin: The Receptor and Signaling Pathways01:28

Insulin: The Receptor and Signaling Pathways

1.5K
Insulin action is mediated through a receptor tyrosine kinase, akin to the IGF-1 receptor. The number of receptors per cell varies significantly, from 40 on erythrocytes to 300,000 on adipocytes and hepatocytes. The insulin receptor consists of linked α/β subunit dimers, forming a heterotetramer glycoprotein with two extracellular α subunits and two β subunits spanning the membrane. The α subunits inhibit the inherent tyrosine kinase activity of the β subunits, but...
1.5K
Glucagon-like Receptor Agonists01:24

Glucagon-like Receptor Agonists

416
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.
GLP-1, when administered in high doses intravenously, triggers insulin secretion, inhibits glucagon release, slows gastric emptying, reduces food intake, and restores normal insulin secretion. However, its rapid inactivation by...
416
Hypoglycemia and Glucagon01:15

Hypoglycemia and Glucagon

334
Without prolonged fasting, healthy individuals maintain blood glucose levels above 3.5 mM due to a well-adapted neuroendocrine counterregulatory system that effectively prevents acute hypoglycemia, a potentially life-threatening condition. The primary clinical scenarios for hypoglycemia encompass diabetes treatment, inappropriate production of endogenous insulin or insulin-like substances by tumors, and the use of glucose-lowering agents in non-diabetic individuals. Notably, hypoglycemia in the...
334
Glucose Homeostasis: Pancreatic Islets and Insulin Secretion01:27

Glucose Homeostasis: Pancreatic Islets and Insulin Secretion

1.4K
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.
Insulin and C-peptide are...
1.4K

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関連する実験動画

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Live Images of GLUT4 Protein Trafficking in Mouse Primary Hypothalamic Neurons Using Deconvolution Microscopy
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Live Images of GLUT4 Protein Trafficking in Mouse Primary Hypothalamic Neurons Using Deconvolution Microscopy

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肝臓のグルココルチコイド受容体作用とグルコースホメオスタシス

Maggie Chang1, Jen-Chywan Wang1

  • 1Endocrinology Graduate Group and Department of Nutritional Sciences & Toxicology, University of California Berkeley, Berkeley, CA 94720, USA.

Endocrine reviews
|September 2, 2025
PubMed
まとめ

グルココルチコイド (GC) は血糖値を維持しますが,慢性的に使用するとインスリン抵抗性が生じます. 肝臓のGC受容体 (GR) 調節を理解することは,GC療法と代謝障害の治療を改善するための鍵です.

科学分野:

  • 内分泌学
  • 代謝の調節
  • 分子生物学

背景:

  • グルコースチオイド (Glucocorticoids,GC) は,ストレスのときのグルコースホメオスタシスの維持に不可欠です.
  • GCは,抗炎症および免疫調節効果のために広く使用されています.
  • 慢性的なGC曝露は,高血糖症やインスリン抵抗性などの副作用をもたらし,その治療的使用を制限します.

研究 の 目的:

  • 肝臓のグルコース代謝におけるGC受容体 (GR) 活性化トランスクリプションのメカニズムをレビューする.
  • 肝臓のGR標的遺伝子がインスリン感受性とグルコースホメオスタシスをどのように調節するかを調査する.
  • GC誘発のグルコース障害におけるトランスクリプションの共同調節器,シグナル伝達経路,および肝臓特異的なGRノックアウトマウスモデルについて議論する.

主な方法:

  • 肝臓のグルコース代謝におけるGR活性化転写に焦点を当てた文献レビュー.
  • 肝臓のGR標的遺伝子とインスリン感受性におけるその役割に関する研究の分析
  • GC誘発の代謝障害に関与するトランスクリプションの共同調節およびシグナル伝達経路の検査.

主要な成果:

  • GCは主に肝臓のGC受容体 (GR) を介してグルコースホメオスタシスを調節する.
キーワード:
グルココルチコイド受容体グルココルチコイドグルコネオゲネシスグルコース代謝インスリン抵抗性肝臓

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Hyperinsulinemic-euglycemic Clamps in Conscious, Unrestrained Mice
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Hyperinsulinemic-euglycemic Clamps in Conscious, Unrestrained Mice

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Biochemical Reconstitution of Steroid Receptor•Hsp90 Protein Complexes and Reactivation of Ligand Binding
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Biochemical Reconstitution of Steroid Receptor•Hsp90 Protein Complexes and Reactivation of Ligand Binding

Published on: September 21, 2011

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関連する実験動画

Last Updated: Sep 9, 2025

Live Images of GLUT4 Protein Trafficking in Mouse Primary Hypothalamic Neurons Using Deconvolution Microscopy
08:47

Live Images of GLUT4 Protein Trafficking in Mouse Primary Hypothalamic Neurons Using Deconvolution Microscopy

Published on: December 7, 2017

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Hyperinsulinemic-euglycemic Clamps in Conscious, Unrestrained Mice
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Hyperinsulinemic-euglycemic Clamps in Conscious, Unrestrained Mice

Published on: November 16, 2011

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Biochemical Reconstitution of Steroid Receptor•Hsp90 Protein Complexes and Reactivation of Ligand Binding
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Biochemical Reconstitution of Steroid Receptor•Hsp90 Protein Complexes and Reactivation of Ligand Binding

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  • GR活性化による慢性的なGC曝露は,高血糖症とインスリン抵抗性につながる可能性があります.
  • 特定の標的遺伝子とシグナル伝達経路がこれらの有害な代謝効果を媒介する.

    • 結論:

    • GR媒介による肝臓のグルコース代謝の理解は,GCの副作用の管理に極めて重要です.
    • GRの調節に関するさらなる研究は,代謝障害に対する新しい治療戦略を導き出すことができる.
    • パーソナライズされた薬剤療法については,GC応答の個々の変動により,さらなる調査が必要である.