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Glucose Transporters01:27

Glucose Transporters

15.2K
Glucose transporters facilitate the transport of glucose across the cell membrane. In addition to glucose, some glucose transporters can also aid the movement of other hexoses such as fructose, mannose, and galactose.
Facilitated diffusion-glucose transporters (GLUTs) are encoded by the solute-linked carrier (SLC) family 2, subfamily A gene family, or SLC2A. The 14 GLUT protein members are distributed into three classes:
15.2K
Diabetes Mellitus: Introduction01:26

Diabetes Mellitus: Introduction

24
Diabetes mellitus consists of chronic metabolic disorders characterized by persistent hyperglycemia. This elevated blood glucose results from defects in insulin secretion, impaired insulin action, or both. Insulin, produced by pancreatic β-cells, is essential for maintaining glucose homeostasis by facilitating cellular glucose uptake for energy or storage. Disruptions in insulin production or function lead to glucose accumulation in the bloodstream, causing the clinical features and...
24
Type I Diabetes I: Introduction01:12

Type I Diabetes I: Introduction

45
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...
45
Type I Diabetes III: Clinical Manifestations01:19

Type I Diabetes III: Clinical Manifestations

26
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...
26
Type II Diabetes I: Introduction01:26

Type II Diabetes I: Introduction

17
Type 2 diabetes mellitus (T2DM) is a chronic metabolic disorder characterized by insulin resistance, in which target tissues such as the liver, muscle, and adipose tissue respond poorly to insulin. It is also associated with inadequate compensatory insulin secretion, where pancreatic β-cells fail to produce sufficient insulin. Together, these abnormalities lead to persistent hyperglycemia.EtiologyT2DM develops through a complex interaction of genetic predisposition and environmental or...
17
Hyperglycemia01:29

Hyperglycemia

25
Hyperglycemia is an abnormally high blood glucose level. It is diagnosed by fasting glucose ≥126 mg/dL, 2-hour oral glucose tolerance test (or OGTT) ≥200 mg/dL, random glucose ≥200 mg/dL with symptoms, or HbA1c ≥6.5%. However, HbA1c results may be unreliable in certain conditions, such as anemia or hemoglobinopathies, and the diagnosis should be confirmed unless classic symptoms are present. Postprandial hyperglycemia is typically considered significant when glucose...
25

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Updated: May 3, 2026

Dual Effects of Melanoma Cell-derived Factors on Bone Marrow Adipocytes Differentiation
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クラスEの異常な脂質結合オリゴサッカライドThy-1-ネガティブな変異性リンパ腫

I S Trowbridge, R Hyman

    Cell
    |July 1, 1979
    PubMed
    まとめ

    Thy-1変異性リンパ腫は,脂質結合オリゴサッカリド前駆体の合成が阻害されているため,グリコシル化欠陥を示します. 変異細胞の異常な,エンドグリコシダゼH耐性オリゴサッカライドは,グリコプロテイン前駆体形成の欠陥を示している.

    科学分野:

    • バイオケミストリー バイオケミストリー
    • 分子生物学は分子生物学である.
    • 細胞生物学 細胞生物学

    背景:

    • Thy-1は,細胞の相互作用に関与する細胞表面のグリコタンパク質です.
    • グライコシレーションは,タンパク質の機能に影響を与える重要な翻訳後の修正である.
    • クラスE補足群 型-1-変異性リンパ腫は,特定のグリコシル化欠陥を示します.

    研究 の 目的:

    • クラスEのThy-1-変異性リンパ腫における特定のグリコシル化欠陥を特定するために.
    • これらの変異細胞の脂質結合オリゴサッカライド (LLO) を特徴付けるため.
    • 新しく合成されたポリペプチドで発見された異常なオリゴサッカライドの起源を決定する.

    主な方法:

    • Thy-1変異性および野生型リンパ腫細胞からのLLOsの分離および特徴付け.
    • エンドグリコシダゼH消化を用いたLLOsの分析.
    • 変異細胞から新たに合成されたポリペプチドのオリゴサッカライドの分析.

    主要な成果:

    • 変異細胞から2つの主要なLLOが分離され,どちらも野生型LLOよりも小さい.
    • 変異したLLOは,野生型のLLOとは異なり,エンドグリコシダゼH消化に抵抗性がありました.

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    Author Spotlight: Insights into Cardiometabolic Diseases with Subcutaneous Adipose Tissue Microvasculature Studies
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    An Advanced Murine Model for Nonalcoholic Steatohepatitis in Association with Type 2 Diabetes
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  • 変異細胞で新たに合成されたポリペプチドのオリゴサッカリドも,エンドグリコシダゼH耐性であった.
  • 結論:

    • クラスE Thy-1リンパ腫におけるグリコシル化欠陥は,LLO前駆体合成のブロックである.
    • 異常な,エンドグリコシダゼH耐性LLOは,変異細胞で形成される.
    • これらの異常なLLOsは,変異細胞のグリコプロテイン上のエンドグリコシダゼH耐性オリゴサッカリドの発生源である可能性が高い.