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Updated: May 31, 2026

Isolation, Characterization, and Purification of Macrophages from Tissues Affected by Obesity-related Inflammation
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Published on: April 3, 2017

Inflammation, oxidative stress, and obesity.

Alba Fernández-Sánchez1, Eduardo Madrigal-Santillán, Mirandeli Bautista

  • 1Instituto de Ciencias de la Salud, Universidad Autónoma del Estado de Hidalgo, Ex-Hacienda de la Concepción, Tilcuautla, 42080 Pachuca de Soto, Hgo, Mexico; E-Mails: alba_mfs@hotmail.com (A.F.-S.); eomsmx@yahoo.com.mx (E.M.-S.); mirandeli@hotmail.com (M.B.); m.valadezvega@lycos.com (C.V.-V.).

International Journal of Molecular Sciences
|June 21, 2011
PubMed
Summary

Obesity increases body fat and triggers oxidative stress through adipokines and altered metabolism. This imbalance diminishes antioxidant defenses, leading to endothelial dysfunction and promoting atherosclerotic disease.

Keywords:
adipokinesobesityreactive oxygen species

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Published on: May 22, 2013

Area of Science:

  • Endocrinology
  • Metabolic Syndrome
  • Cardiovascular Health

Background:

  • Obesity is a chronic disease characterized by excessive body fat accumulation.
  • Adipose tissue produces bioactive adipokines, including inflammatory Interleukin-6 (IL-6) and weight-regulating leptin.
  • Adipokines contribute to oxidative stress (OS) by inducing reactive oxygen species (ROS) production.

Purpose of the Study:

  • To explore the mechanisms by which obesity generates oxidative stress.
  • To investigate the link between adipose tissue, adipokines, and systemic OS.
  • To understand how obesity-induced OS impacts antioxidant capacity and endothelial function.

Main Methods:

  • Review of mechanisms linking obesity to OS, including fatty acid oxidation and mitochondrial function.
  • Analysis of adipokine roles in ROS generation and their impact on antioxidant enzymes.
  • Examination of the consequences of OS on endothelial function and atherosclerotic disease development.

Main Results:

  • Adipose tissue is an independent source of systemic OS due to adipokine-secreted ROS.
  • Obesity involves ROS generation via fatty acid oxidation and mitochondrial oxygen over-consumption.
  • Increased adipose tissue correlates with diminished activity of antioxidant enzymes like superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GPx).

Conclusions:

  • Obesity-induced oxidative stress, driven by adipokines and metabolic alterations, significantly reduces antioxidant capacity.
  • This imbalance promotes endothelial dysfunction, characterized by reduced nitric oxide (NO) bioavailability.
  • The resulting pro-oxidative and pro-atherosclerotic environment contributes to the development of cardiovascular diseases.