Immune Modulation and Macrophage Polarization in the Pathogenesis of Pancreatic Dysfunction and Obesity


Yazıhan N., Akdas S.

Pathophysiology of Obesity-Induced Health Complications, Tappia,Paramjit S.,Ramjiawan,Bram,Dhalla,Naranjan, Editör, Springer Nature, Berlin, ss.135-151, 2020

  • Yayın Türü: Kitapta Bölüm / Araştırma Kitabı
  • Basım Tarihi: 2020
  • Yayınevi: Springer Nature
  • Basıldığı Şehir: Berlin
  • Sayfa Sayıları: ss.135-151
  • Editörler: Tappia,Paramjit S.,Ramjiawan,Bram,Dhalla,Naranjan, Editör
  • Ankara Üniversitesi Adresli: Evet

Özet

The prevalence of obesity and metabolic syndrome continue to increase by years and now obesity is a growing public health problem. World Health Organization (WHO) reports that more than 1.9 billion adults were overweight in 2016, 39% of them obese and 8.5–12.2% of adults aged 18 years and older had diabetes. Nutritional imbalance (over- or under-nutrition), lifestyles or environmental factors can affect the hemostasis of the body. Hormonal, inflammatory, oxidative and nutritional status determines the activation of cellular and systemic pathways in the body. Chronic disturbances of the nutritional status of the body especially obesity increases the prevalence of chronic non-communicable diseases (NCD) (WHO Diabetes []). Body weight and metabolism are determined by a complex orchestration of the function of several cells, organs and tissues. Underlying mechanisms of obesity and insulin resistance are still unknown. Immune cells within the metabolism related organs also likely contribute to systemic control of glucose, lipid. Increased production of local and systemic adipokines and cytokines, polarization of macrophages, T helper subtype changes could contribute to pathologies linking obesity to diabetes, both by decreasing insulin sensitivity, by compromising β-cell function and disturbing adipose tissue metabolism and distribution. Recent studies show that oxidative stress, systemic chronic inflammation or dysregulation of immune system contribute to development of NCD. Metabolic syndrome and diabetes have similar pathophysiological mechanisms with other NCD. For this reason, relevant interventions to modulate oxidative and inflammatory status of the body will make meaningful improvements in the mortality and morbidity associated with NCD. Chronic nutrition imbalance and obesity promote low-grade inflammation. “Metainflammation” is a term used for chronic inflammation of organs consists of the gastrointestinal system (including liver), muscle and adipose tissue. Macrophages are guardians of the tissues. They regulate immune responses, homeostasis in the different physiological and pathological conditions. Clarification of the underlying mechanisms of chronic inflammation will provide an explanation for mechanisms of obesity and the associated complications and will supply information for new therapeutic approaches. This noteworthy perception is allowing us to more assuredly define the role that macrophages involve in health and in obesity and how inflammatory mediators behave as signaling molecules in this pathway. Additionally, on a molecular level, we are beginning to figure out how such factors as nutritional, metabolic status, hormonal changes, lifestyle, genetic and epigenetic factors interrelate and terminate in different phenotypes and characteristics, and which interventions may modulate immune functions. Therefore, this chapter will review the metabolic regulation of plasticity of macrophages and role of inflammation and macrophage polarization in obesity, diabetes and pathogenesis.