Abstract

Background. Obesity is a global health problem of epidemic proportions, which is characterized by increased adipose tissue (AT) mass and significant repercussions in different body apparati and systems. AT is a special connective tissue, which contains several types of cells, in addition to adipocytes, and is a highly active endocrine and immune organ, which directly modulates many processes, including energy balance, metabolism, and inflammation. Summary. In this paper, the authors list and attempt to answer in a brief and simple way several questions regarding the complex relationships between obesity, adipose tissue, and inflammation, with the objective to provide an easy way to understand the main changes that occur in this pathological state. The questions are the following: Is adipose tissue only made up of adipocytes? Are adipocytes just a reservoir of free fatty acids? Do different types of fatty tissue exist? If so, which types? Can we further subcategorize the types of adipose tissue? Is it possible to form new adipocytes during adulthood? What is the role of inflammation? What is the role of macrophages? Are macrophages central mediators of obesity-induced adipose tissue inflammation and insulin resistance? What causes macrophage infiltration into adipose tissue? What is the role of hypoxia in AT alterations? Is there cross talk between adipocytes and immune cells? What other changes occur in AT in obesity? Does metabolically healthy obesity really exist? Is this a benign condition? Key messages. Obesity is a complex disease with numerous metabolic consequences, which are mainly the result of dysfunction that occurs in the adipose tissue of patients with this pathology. Understanding the pathophysiology of AT and the changes that occur in obesity would contribute to a better approach to patients with obesity, with the inherent medical implications that could result from this.

Highlights

  • During the past few decades, the prevalence of both obesity (which is defined in Caucasians to be a body mass index (BMI) of over 30 kg/m2) and being overweight (25 ≤ BMI < 30 kg/m2) has been increasing rapidly in Western societies and in developing countries [1] and is a health problem of epidemic proportions.Since 1980, the prevalence of obesity has doubled in more than 70 countries

  • When the storage capacity of the subcutaneous adipose tissue (SCAT) is exceeded, or if its ability to generate new adipocytes is impaired, either due to stress or a genetic predisposition, an accumulation of fat is found in visceral fat tissue or in other areas outside the SCAT [49], such as muscle, liver, and bone, which are not adapted to lipid storage, causing toxic effects—a process known as ectopic lipid accumulation [50]

  • E underlying mechanisms that could explain the existence of this phenotype are still being elucidated. ere is a growing evidence suggesting that subclinical inflammation and macrophage phenotypes could be the underlying mechanisms, which determine whether an individual is Metabolically healthy obesity (MHO) or not [110, 111]

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Summary

Background

Obesity is a global health problem of epidemic proportions, which is characterized by increased adipose tissue (AT) mass and significant repercussions in different body apparati and systems. AT is a special connective tissue, which contains several types of cells, in addition to adipocytes, and is a highly active endocrine and immune organ, which directly modulates many processes, including energy balance, metabolism, and inflammation. The authors list and attempt to answer in a brief and simple way several questions regarding the complex relationships between obesity, adipose tissue, and inflammation, with the objective to provide an easy way to understand the main changes that occur in this pathological state. Do different types of fatty tissue exist? Are macrophages central mediators of obesity-induced adipose tissue inflammation and insulin resistance? Obesity is a complex disease with numerous metabolic consequences, which are mainly the result of dysfunction that occurs in the adipose tissue of patients with this pathology. Understanding the pathophysiology of AT and the changes that occur in obesity would contribute to a better approach to patients with obesity, with the inherent medical implications that could result from this

Introduction
Is Adipose Tissue Only Made Up of Adipocytes?
Are Adipocytes Just a Reservoir of Free Fatty Acids?
Can We Further Subcategorize the Types of Adipose Tissue?
Is It Possible to Form New Adipocytes during Adulthood?
What Is the Role of Immune Cells in the Adipose Tissue of Obese Individuals?
10. Which Other Changes Occur in AT in Obesity?
Findings
12. Conclusion
Full Text
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