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Related Concept Videos

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Diabetic Retinopathy

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DefinitionDiabetic retinopathy is a microvascular complication of diabetes affecting the retinal blood vessels.Risk FactorsDiabetic retinopathy is present in almost all individuals with type 1 diabetes and more than 60% of those with type 2 diabetes after two decades of disease.The risk increases with poor glycemic control, hypertension, dyslipidemia, smoking, pregnancy, and puberty.Although cataracts and glaucoma are also more frequent in people with diabetes, retinopathy remains the leading...
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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...
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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...
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Pathophysiology of Diabetes01:20

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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.
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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.
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Rapidly dividing tumors, embryos, and wounded tissues require more oxygen than usual, lowering the oxygen concentration in the blood. At low oxygen or hypoxic conditions, an oxygen-sensitive transcription factor called the hypoxia-inducible factor 1 or HIF1 is activated. HIF1 is a dimeric protein of alpha (ɑ) and beta (β) subunits.  Under optimal oxygen conditions, HIF1β is present in the nucleus while HIF1ɑ remains in the cytosol. HIF1ɑ is hydroxylated by prolyl...
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Endothelial PGC-1α mediates vascular dysfunction in diabetes.

Naoki Sawada1, Aihua Jiang2, Fumihiko Takizawa3

  • 1Department of Molecular Endocrinology and Metabolism, Tokyo Medical and Dental University, Tokyo 113-8510, Japan; Global COE Program, Tokyo Medical and Dental University, Tokyo 113-8510, Japan; Cardiovascular Institute and Center for Vascular Biology Research, Beth Israel Deaconess Medical Center, Boston, MA 02215, USA; Section of Cardiology, Department of Medicine, University of Chicago, Chicago, IL 60637, USA.

Cell Metabolism
|February 11, 2014
PubMed
Summary

High levels of Peroxisome proliferator-activated receptor gamma coactivator 1-alpha (PGC-1α) in endothelial cells worsen diabetes-related vascular dysfunction. Reducing PGC-1α improves healing and blood flow recovery in diabetic models.

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Area of Science:

  • Vascular Biology
  • Metabolic Diseases
  • Molecular Endocrinology

Background:

  • Endothelial dysfunction is a key feature of diabetes.
  • The role of transcriptional coactivator PGC-1α in endothelial cells is not well understood.

Purpose of the Study:

  • To investigate the role of endothelial PGC-1α in diabetes-induced vascular dysfunction.
  • To determine the mechanisms by which PGC-1α affects endothelial cell function.

Main Methods:

  • Assessed endothelial PGC-1α expression in diabetic rodents and humans.
  • Utilized cell culture and in vivo models to study endothelial cell migration and vasculogenesis.
  • Employed transgenic models with endothelial PGC-1α overexpression and deletion.
  • Examined signaling pathways including Notch, Rac/Akt/eNOS, and angiogenic factor responses.

Main Results:

  • Endothelial PGC-1α expression is elevated in diabetic conditions.
  • PGC-1α inhibits endothelial cell migration, vasculogenesis, re-endothelialization, wound healing, and blood flow recovery.
  • PGC-1α induces Notch signaling and blunts Rac/Akt/eNOS activation.
  • Deletion of endothelial PGC-1α ameliorates diabetic vascular complications.

Conclusions:

  • Endothelial PGC-1α significantly impairs endothelial function and angiogenesis.
  • Increased endothelial PGC-1α is a contributing factor to vascular complications in diabetes.
  • Targeting endothelial PGC-1α may offer therapeutic potential for diabetic vascular disease.