Obesity and susceptibility to autoimmune diseases

Abstract

For decades, obesity has been considered to be the result of the complex interaction between genes and the environment and its pathogenesis is still unresolved. The discovery of hormones and neural mediators responsible for the control of food intake and metabolism at the hypothalamic level has provided fundamental insights into the complicated pathways that control food intake. However, the molecular basis for the association between obesity and low-degree chronic inflammation is still unknown. More recently, the discovery of leptin, one of the most abundant adipocyte-derived hormones, has suggested that nutritional status, through leptin secretion, can control immune self-tolerance modulating Treg suppressive function and responsiveness. Furthermore, recent experimental evidence has shown the presence of an abundant adipose tissue-resident Treg population responsible for the control of metabolic parameters and glucose homeostasis. Better knowledge of the intricate network of interactions among leptin-related energy regulation, Treg activities and obesity could lead to valuable strategies for therapeutic intervention in obesity and obesity-associated insulin resistance.

Keywords::

• inflammation
• leptin
• metabolism
• obesity
• Tregs

Dedication

This work is dedicated to the memory of Eugenia Papa and Serafino Zappacosta.

Acknowledgement

The authors thank Salvatore De Simone for critically reading the manuscript and ideation of the art graphic models.

Financial & competing interests disclosure

Giuseppe Matarese is supported by grants from the EU Ideas Programme, ERC-Starting Independent Grant ‘LeptinMS’ number 202579 and Telethon-JDRF grant number GJT08004. The authors have no other relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript. This includes employment, consultancies, honoraria, stock ownership or options, expert testimony, grants or patents received or pending, or royalties.

No writing assistance was utilized in the production of this manuscript.