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Lethal Alleles02:41

Lethal Alleles

Agouti: A Lethal Allele
Lucien Cuénot discovered lethal alleles in 1905 while studying the inheritance of coat color in mice. The agouti gene is responsible for the color of the coat in mice. This gene codes for an agouti-signaling protein, which is responsible for melanin distribution in mammals. The wild-type allele gives rise to gray-brown coat color in mice, while the mutant allele gives rise to yellow coat color. In addition to coat color, the agouti gene is associated with the yellow...

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Tumor necrosis factor-alpha induces endothelial dysfunction in Lepr(db) mice.

Xue Gao1, Souad Belmadani, Andrea Picchi

  • 1Department of Veterinary Physiology and Pharmacology, Texas A&M University, College Station, TX, USA.

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|January 4, 2007
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Tumor necrosis factor-alpha (TNF) drives endothelial dysfunction in type 2 diabetes by increasing oxidative stress. Blocking TNF or its downstream effects restores vascular function in diabetic mice.

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Area of Science:

  • Cardiovascular Research
  • Endocrinology
  • Immunology

Background:

  • Type 2 diabetes is associated with endothelial dysfunction.
  • Inflammatory cytokines, such as tumor necrosis factor-alpha (TNF), are implicated in this dysfunction.

Purpose of the Study:

  • To investigate the role of TNF in mediating endothelial dysfunction in a mouse model of type 2 diabetes.
  • To explore the mechanisms by which TNF contributes to vascular impairment.

Main Methods:

  • Utilized Lepr(db) mice (type 2 diabetes model) and control mice.
  • Assessed vasodilation responses to various agents (acetylcholine, sodium nitroprusside).
  • Measured TNF levels, nuclear factor-kappaB (NF-κB) expression, and oxidative stress markers (superoxide generation, NAD(P)H oxidase activity).
  • Administered anti-TNF therapies and evaluated their effects.

Main Results:

  • Diabetic Lepr(db) mice exhibited blunted endothelium-dependent vasodilation compared to controls.
  • TNF levels and NF-κB expression were significantly elevated in diabetic mice.
  • Genetic deletion of TNF or administration of anti-TNF therapy improved vasodilation in diabetic mice.
  • Increased TNF correlated with elevated NAD(P)H oxidase activity and reactive oxygen species production.

Conclusions:

  • TNF plays a critical role in type 2 diabetes-associated endothelial dysfunction.
  • Advanced glycation end products/receptor for advanced glycation end products and NF-κB signaling contribute to increased TNF production.
  • TNF activation of NAD(P)H oxidase and subsequent oxidative stress lead to endothelial dysfunction in type 2 diabetes.