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Related Concept Videos

Type I Diabetes II: Pathophysiology01:26

Type 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...
Type II Diabetes II: Pathophysiology01:24

Type II Diabetes II: Pathophysiology

PathophysiologyType 2 diabetes mellitus (T2DM ) is a chronic metabolic disorder characterized by insulin resistance and progressive pancreatic β-cell dysfunction, leading to impaired glucose homeostasis. It results from interactions among genetic predisposition, environmental factors, and metabolic stressors, such as overnutrition and a sedentary lifestyle.Insulin Resistance and Glucose DysregulationEarly T2DM involves insulin resistance in skeletal muscle, adipose tissue, and the liver.
Pathophysiology of Diabetes01:20

Pathophysiology of Diabetes

Diabetes mellitus is a chronic metabolic disorder characterized by hyperglycemia. The four categories of diabetes are type 1 diabetes, type 2 diabetes, other specific types of diabetes, and gestational diabetes.
Type 1 diabetes is characterized by autoimmune-mediated destruction of pancreatic β cells, with environmental factors potentially triggering this process in genetically susceptible individuals. Despite many not having a family history, certain genes increase susceptibility, suggesting a...
Insulin Secretory Vesicles01:05

Insulin Secretory Vesicles

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...
Diabetic Nephropathy01:28

Diabetic Nephropathy

Definition Diabetic nephropathy is a chronic kidney complication that results from prolonged hyperglycemia.Prevalence It is the most common cause of chronic kidney disease (CKD) and end-stage renal disease (ESRD) worldwide, affecting up to half of individuals with diabetes.Pathophysiology • Sustained hyperglycemia triggers multiple hemodynamic and metabolic changes in the kidney. • Early in the disease, increased renal blood flow and glomerular hyperfiltration occur due to afferent arteriolar...
Protein and Protein Structure02:15

Protein and Protein Structure

Proteins are one of the most abundant organic molecules in living systems and have the most diverse range of functions of all macromolecules. Proteins may be structural, regulatory, contractile, or protective. They may serve in transport, storage, or membranes; or they may be toxins or enzymes. Their structures, like their functions, vary greatly. They are all, however, amino acid polymers arranged in a linear sequence.
A protein's shape is critical to its function. For example, an enzyme can...

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Updated: Jun 29, 2026

Coculture Analysis of Extracellular Protein Interactions Affecting Insulin Secretion by Pancreatic Beta Cells
05:51

Coculture Analysis of Extracellular Protein Interactions Affecting Insulin Secretion by Pancreatic Beta Cells

Published on: June 15, 2013

Diabetes Alters Protein Corona to Reprogram Wear Particle-Cell Interaction.

Congxiu Mao1, Dongqi Fan1, Zhixin Qiu1

  • 1College of Stomatology, Chongqing Medical University, Chongqing, China; Chongqing Key Laboratory of Oral Diseases, Chongqing, China; Chongqing Municipal Key Laboratory of Oral Biomedical Engineering of Higher Education, Chongqing, China; Chongqing Municipal Health Commission Key Laboratory of Oral Biomedical Engineering, Chongqing, China.

Acta Biomaterialia
|June 27, 2026
PubMed
Summary
This summary is machine-generated.

Diabetes alters implant wear particle protein corona (PC), enhancing immune responses and bone loss. This diabetic-derived PC (DM-PC) activates inflammatory pathways, increasing implant failure risk in diabetic patients.

Keywords:
Diabetes mellitusImmune responseMacrophage recognitionProtein coronaTitanium nanoparticle

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Last Updated: Jun 29, 2026

Coculture Analysis of Extracellular Protein Interactions Affecting Insulin Secretion by Pancreatic Beta Cells
05:51

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

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Published on: December 7, 2017

Area of Science:

  • Biomaterials Science
  • Immunology
  • Diabetic Complications

Background:

  • Implant stability relies on immune homeostasis; wear particles trigger inflammation and bone loss.
  • Diabetes disrupts immune balance, increasing implant complication risks.
  • The protein corona (PC) influences particle-cell interactions, but its role in diabetes is unclear.

Purpose of the Study:

  • Investigate how diabetes remodels the PC on wear particles.
  • Elucidate the impact of this altered PC on immune responses and bone destruction.

Main Methods:

  • Characterized the protein corona formed on wear particles in diabetic conditions (DM-PC).
  • Assessed DM-PC interactions with macrophages and activation of signaling pathways (JAK1-STAT3).
  • Evaluated DM-PC's effect on M1 polarization and osteoclast activation.

Main Results:

  • Diabetes induces a distinct DM-PC enriched in signaling proteins.
  • DM-PC enhances wear particle interaction with macrophage receptors, activating the JAK1-STAT3 pathway.
  • DM-PC exacerbates particle-induced M1 polarization and osteoclast activation, promoting inflammation and bone loss.

Conclusions:

  • The DM-PC mechanism explains how diabetes exacerbates implant-related inflammation and bone destruction.
  • Findings offer insights into implant complications in diabetic patients.
  • Identifies potential targets for preventing implant failure in metabolic diseases.