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Glucose Homeostasis: Pancreatic Islets and Insulin Secretion01:27

Glucose Homeostasis: Pancreatic Islets and Insulin Secretion

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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.
Insulin and C-peptide are...
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Dipeptidyl peptidase 4 (DPP-4) is a serine protease widely distributed in the body. It's involved in the inactivation of GLP-1 and GIP hormones, which are crucial for insulin regulation. DPP-4 inhibitors, such as sitagliptin (Januvia), saxagliptin (Onglyza), linagliptin (Tradjenta), alogliptin (Nesina), and vildagliptin (Galvus), help increase the proportion of active GLP-1, enhancing insulin secretion. These inhibitors work by competitively binding to DPP-4. This binding causes a...
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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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Multicellular organisms contain a variety of structurally and functionally distinct cell types, but the DNA in all the cells originated from the same parent cells. The differences in the cells can be attributed to the differential gene expression. Liver cells, whose functions include detoxification of blood, production of bile to metabolize fats, and synthesis of proteins essential for metabolism, must express a specific set of genes to perform their functions. Gene expression also varies with...
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  1. ホーム
  3. デキサメソンが誘発する炎症性臓β細胞アポトーシスに対するジェニステインの作用
  1. ホーム
  3. デキサメソンが誘発する炎症性臓β細胞アポトーシスに対するジェニステインの作用

関連する実験動画

Isolated Pancreatic Islet Treatment and Apoptosis Measurement
09:36

Isolated Pancreatic Islet Treatment and Apoptosis Measurement

Published on: May 2, 2025

512

デキサメソンが誘発する炎症性臓β細胞アポトーシスに対するジェニステインの作用

Nattinee Jitprawet1, Jatuporn Sujjitjoon2, Petcharee Maneethorn1

  • 1Department Physiology, Faculty of Medicine, Siriraj Hospital, Mahidol University, Bangkok, Thailand.

Molecular nutrition & food research
|August 23, 2025

PubMed で要約を見る

まとめ
この要約は機械生成です。

ゲニステインは,エンドプラズマ網膜のストレスとNLRP3炎症体の活性化を低下させることで,ステロイド誘発糖尿病から臓のβ細胞を保護する. この植物エストロゲンは,グルココルチコイド誘発の細胞損傷に対する潜在的な治療戦略を提供します.

キーワード:
ER ストレスNLRP3 インフラマソームデキサメタゾンジェニステイン臓のβ細胞アポトーシス

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A Murine Pancreatic Islet Cell-based Screening for Diabetogenic Environmental Chemicals
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Surgical Injury to the Mouse Pancreas through Ligation of the Pancreatic Duct as a Model for Endocrine and Exocrine Reprogramming and Proliferation
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Surgical Injury to the Mouse Pancreas through Ligation of the Pancreatic Duct as a Model for Endocrine and Exocrine Reprogramming and Proliferation

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関連する実験動画

Isolated Pancreatic Islet Treatment and Apoptosis Measurement
09:36

Isolated Pancreatic Islet Treatment and Apoptosis Measurement

Published on: May 2, 2025

512
A Murine Pancreatic Islet Cell-based Screening for Diabetogenic Environmental Chemicals
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A Murine Pancreatic Islet Cell-based Screening for Diabetogenic Environmental Chemicals

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Surgical Injury to the Mouse Pancreas through Ligation of the Pancreatic Duct as a Model for Endocrine and Exocrine Reprogramming and Proliferation
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Surgical Injury to the Mouse Pancreas through Ligation of the Pancreatic Duct as a Model for Endocrine and Exocrine Reprogramming and Proliferation

Published on: August 7, 2015

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科学分野:

  • 内分泌学
  • 細胞生物学
  • 薬理学について

背景:

  • ステロイド誘発糖尿病は,長期にわたるグルココルチコイド (GC) 治療の既知の合併症である.
  • グルココルチコイドは,エンドプラズマ網膜 (ER) ストレスを通して,臓ベータ細胞のアポトーシスを誘発する.
  • ERストレスとNLRP3炎症体の活性化は,細胞死を促進する関連経路です.

研究 の 目的:

  • ジェニステインがデキサメタゾーン誘発の臓β細胞アポトーシスを軽減するかどうかを調査する.
  • このモデルでは,ジェニステインがERストレスとNLRP3炎症体の活性化を低下させるかどうかを判断する.

主な方法:

  • デキサメタゾンは,臓のベータ細胞でアポトーシスを誘発するために使用されました.
  • アポトーシスマーカー (cPARP, Bax, Bcl-2),ERストレス指標 (SERCA, IRE1-α, sXBP),および炎症体成分 (TXNIP, NLRP3, ASC, IL- 1β) のタンパク質発現レベルを分析した.
  • ゲニステインとデキサメタゾンの保護効果を評価するために併用した.

主要な成果:

  • デキサメタゾンはベータ細胞アポトーシス,ERストレスマーカー,TXNIP,NLRP3炎症体活性化 (NLRP3,ASC,IL- 1β) を増加させた.
  • ジェニステインの併用治療はこれらの効果を逆転させ,アポトーシスとERストレスマーカーを減少させた.
  • ジェニステインはTXNIP,NLRP3,ASC,およびIL- 1βの発現を著しく低下させ,炎症体の活性化が低下したことを確認した.

    • 結論:

    • ゼニステインはデキサメタゾンが誘発するアポトーシスから 臓のベータ細胞を保護する.
    • この保護は,ERストレスとNLRP3炎症体の活性化のダウンレギュレーションによって媒介されます.
    • ジェニステインは,ステロイド誘発糖尿病の潜在的な治療薬です.