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The gene encoding the main signaling molecules of the Wnt signaling pathways (the Wnt proteins) was discovered almost four decades ago by Nüsslein-Volhard and Wieschaus. They identified and originally named the gene "wingless" (wg) after a phenotype discovered during their landmark genetic screen in Drosophila for body pattern defects. At around the same time, another researcher named Harold Varmus found that a murine tumor virus activates the mammalian wg homolog, Int-1, which...
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Wnt is a zygotic effect gene that is expressed during very early embryonic development. It regulates various processes in animals starting from early development through the adult stage, such as organogenesis in the embryo and maintenance of neuronal and blood stem cells. Wnt proteins can induce a wide variety of intracellular pathways depending upon the specific abilities of different Wnt ligands to form a complex with shared and cognate receptors in the presence of different co-receptors. The...
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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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Insulin secretory vesicles release insulin to stimulate blood glucose uptake and regulate carbohydrate metabolism. When the blood glucose levels increase, glucose enters the pancreatic β-islet cells through glucose transporters. Once inside, glucose is metabolized through glycolysis, the citric acid cycle, and the electron transport chain, producing ATP. This increase in ATP concentration closes ATP-sensitive potassium channels, leading to depolarization of the membrane and the opening of...
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Complement C3 promotes islet β-cell dedifferentiation by activating Wnt/β-catenin pathway.

Lei Zhuang1,2, Qi Li3, Wenjun You2

  • 1Department of Endocrinology, The Second Affiliated Hospital of Soochow University, Suzhou, China.

Iscience
|December 5, 2024
PubMed
Summary

Complement C3 drives islet beta-cell dedifferentiation in type 2 diabetes mellitus (T2DM) by activating the Wnt/beta-catenin pathway. Targeting C3 may offer a new therapeutic approach for T2DM.

Keywords:
Biological sciencesImmunologyMolecular biologyPhysiology

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Area of Science:

  • Endocrinology
  • Immunology
  • Cell Biology

Background:

  • Islet beta-cell dedifferentiation is crucial in type 2 diabetes mellitus (T2DM) progression.
  • Complement C3 is implicated in T2DM, enhancing inflammatory mediator secretion.

Purpose of the Study:

  • To elucidate the mechanisms by which complement C3 contributes to islet beta-cell dedifferentiation in T2DM.
  • To investigate the therapeutic potential of targeting C3 for T2DM.

Main Methods:

  • Quantified C3 protein levels in T2DM patients, mice, and islet beta-cells.
  • Assessed the effects of insulin, gliclazide, and metformin on C3, dedifferentiation markers, and beta-cell function in vitro and in vivo.
  • Investigated the role of C3 in beta-cell dedifferentiation and its interaction with the Wnt/beta-catenin pathway.

Main Results:

  • Elevated C3 protein levels were observed in T2DM blood and islet beta-cells.
  • Insulin, gliclazide, and metformin treatments reduced C3 levels and inhibited beta-cell dedifferentiation.
  • C3 promoted, while C3 knockdown inhibited, beta-cell dedifferentiation.
  • C3 activated the Wnt/beta-catenin pathway, evidenced by increased p-beta-catenin, and pathway inhibitors blocked C3-induced dedifferentiation.

Conclusions:

  • Complement C3 promotes islet beta-cell dedifferentiation in T2DM through Wnt/beta-catenin pathway activation.
  • Targeting complement C3 presents a promising therapeutic strategy for T2DM.