アディプシンと補足因子Dの活性:肥満における免疫関連の欠陥
Science (New York, N.Y.)
|June 23, 1989
まとめ
肥満モデルで欠乏しているタンパク質であるアディプシンが,補完因子Dのように機能していることが,アディプシンと補完系が,エネルギーバランスの調節に意外と関与していることを示唆しています.
科学分野:
- バイオケミストリー バイオケミストリー
- 免疫学 免疫学とは
- メタボリズムは
背景:
- アディポサイトからのセリンプロテアゼであるアディプシン (adipsin) は,肥満モデルでは欠乏しています.
- 欠陥遺伝子発現は肥満と関連しています.
- アディプシンの機能は,ほとんど解明されていないままです.
研究 の 目的:
- リコンビネントマウスアディプシンを浄化し,特徴づけるために.
- アディプシン (adipsin) の生化学的および酵素学的性質を明らかにする.
- 補完体活性化とエネルギーバランスにおけるアディプシンの役割を調査する.
主な方法:
- 再結合マウスアディプシンの浄化.
- アディプシン活性を決定するための生化学および酵素分析.
- コンプリメントの代替経路活性化と赤血球溶解の評価.
- 様々な肥満モデルにおけるアディプシン活性の比較.
主要な成果:
- アクティベーションされたアディプシンには,補足因子Dのような活性があり,補足因子Bを分裂させます.
- アディプシンは,補完の代替経路を活性化させ,赤血球の溶解につながります.
- 多数の肥満モデル (ob/ob, db/db,MSGを注入したマウス,fa/faラット) で,補完因子Dの活性 (58-80%) が著しく低下することが観察されました.
結論:
- アディプシンは,補足因子Dの機能に類似しています.
- アディプシンは,補完の代替経路を活性化します.
- アディプシンと補完の代替経路は,全身のエネルギーバランスを調節する上で重要な役割を果たす可能性があります.
さらに関連する動画
06:08Semi-Automated Isolation of the Stromal Vascular Fraction from Murine White Adipose Tissue Using a Tissue Dissociator
Published on: May 19, 2023
10:40Characterization of Adipocyte-Derived Extracellular Vesicle Secretion Using a CD63-GFP Reporter Mouse Model In Vivo and In Vitro
Published on: December 5, 2025
関連する概念動画
01:36Humoral Immune Responses
Overview
01:24Obesity
The Body Mass Index (BMI) is a numerical value derived from a person's weight and height, used to categorize individuals into weight ranges. It is calculated using the formula: weight in kilograms divided by height in meters squared. Obesity is a health condition characterized by excessive accumulation of adipose tissue that poses health risks, often diagnosed with a BMI ≥ 30. This excess fat storage occurs when surplus dietary calories are converted into triglycerides and stored in adipocytes...
01:27Complement System
The complement system is a group of approximately 20 plasma proteins that strengthen the body's defenses against infections through opsonization, inflammation, and cell lysis. Opsonization involves coating pathogens with complement proteins, making them more recognizable and facilitating phagocyte engulfment. Certain complement proteins induce inflammation that attracts immune cells to the site of infection. Cell lysis involves the destruction of pathogens through the formation of a membrane...
01:12Type I Diabetes I: Introduction
Type 1 diabetes mellitus is a chronic metabolic disorder characterized by an absolute deficiency of insulin resulting from the autoimmune destruction of pancreatic β-cells. Although it can occur at any age, it is most commonly diagnosed in childhood, adolescence, or early adulthood. The loss of insulin production impairs cellular glucose uptake, resulting in persistent hyperglycemia and necessitating lifelong insulin therapy.Autoimmune Destruction of β-CellsThe hallmark of type 1 diabetes is an...
01:26Type I Diabetes II: Pathophysiology
Type 1 diabetes mellitus arises from an immune-mediated destruction of pancreatic β-cells, resulting in an absolute deficiency of insulin. This process develops in genetically susceptible individuals when autoimmunity, environmental exposures, and immunologic dysregulation converge to trigger a targeted attack on the insulin-producing cells of the pancreas. The β-cells are located within the islets of Langerhans and are essential for regulating blood glucose by facilitating cellular uptake of...
01:19Type I Diabetes III: Clinical Manifestations
Type 1 diabetes mellitus typically presents with rapid-onset symptoms due to the body’s inability to utilize glucose in the absence of insulin. Since insulin is required for glucose uptake into cells, its deficiency leads to hyperglycemia and cellular energy deprivation, resulting in characteristic clinical features.Polyuria and PolydipsiaOne of the earliest, most prominent symptoms is polyuria (excessive urination). When blood glucose concentrations rise above the renal threshold, the kidneys...