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Differentiated Mouse Adipocytes in Primary Culture: A Model of Insulin Resistance
Published on: February 17, 2023
Loxin polymorphism is associated with increased resistin levels and with oxidative status
Roberto Gambino1, Simona Bo, Giovanni Musso
1Department of Internal Medicine, University of Turin, Corso Dogliotti 14, 10126 Torino, Italy. roberto.gambino@unito.it
Clinical Biochemistry
|June 18, 2011
Summary
The LOX-1 G allele is linked to higher resistin and nitrotyrosine levels, increasing cardiovascular risk. This suggests enhanced oxidized-low-density lipoprotein uptake contributes to inflammation.
Area of Science:
- Cardiovascular Genetics
- Molecular Biology
- Inflammation Research
Background:
- The scavenger receptor LOX-1 plays a role in oxidized-low-density lipoprotein (ox-LDL) uptake.
- Genetic variations in the LOX-1 gene (OLR1) may influence inflammatory processes and cardiovascular disease risk.
- Resistin is a pro-inflammatory adipokine implicated in metabolic and cardiovascular conditions.
Purpose of the Study:
- To investigate the association between the LOX-1 IVS4-14 A>G polymorphism and systemic resistin expression.
- To determine if LOX-1 polymorphism modulates inflammation and cardiovascular risk markers.
Main Methods:
- A population-based cohort of 276 men was studied.
- Metabolic and inflammatory markers, including plasma resistin and nitrotyrosine, were measured at baseline and after 6 years.
- The OLR1 IVS4-14 A>G polymorphism was genotyped.
Main Results:
- Individuals homozygous for the G allele (G/G genotype) exhibited significantly higher plasma resistin and nitrotyrosine levels compared to A/A homozygotes.
- Total antioxidant status (TAS) was significantly lower in G/G individuals.
- The G allele showed a significant direct association with both resistin and nitrotyrosine levels.
Conclusions:
- Carriers of the LOX-1 G allele demonstrate enhanced ox-LDL uptake.
- This enhanced uptake is associated with increased oxidative stress (higher nitrotyrosine) and elevated resistin levels.
- These findings suggest a mechanism linking LOX-1 polymorphism to inflammation and cardiovascular risk through macrophage, smooth muscle cell, and monocyte ox-LDL uptake.
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