Abstract

The adipose tissue is a central metabolic organ in the regulation of whole-body energy homeostasis. The white adipose tissue functions as a key energy reservoir for other organs, whereas the brown adipose tissue accumulates lipids for cold-induced adaptive thermogenesis. Adipose tissues secrete various hormones, cytokines, and metabolites (termed as adipokines) that control systemic energy balance by regulating appetitive signals from the central nerve system as well as metabolic activity in peripheral tissues. In response to changes in the nutritional status, the adipose tissue undergoes dynamic remodeling, including quantitative and qualitative alterations in adipose tissue-resident cells. A growing body of evidence indicates that adipose tissue remodeling in obesity is closely associated with adipose tissue function. Changes in the number and size of the adipocytes affect the microenvironment of expanded fat tissues, accompanied by alterations in adipokine secretion, adipocyte death, local hypoxia, and fatty acid fluxes. Concurrently, stromal vascular cells in the adipose tissue, including immune cells, are involved in numerous adaptive processes, such as dead adipocyte clearance, adipogenesis, and angiogenesis, all of which are dysregulated in obese adipose tissue remodeling. Chronic overnutrition triggers uncontrolled inflammatory responses, leading to systemic low-grade inflammation and metabolic disorders, such as insulin resistance. This review will discuss current mechanistic understandings of adipose tissue remodeling processes in adaptive energy homeostasis and pathological remodeling of adipose tissue in connection with immune response.

Highlights

  • The adipose tissue is a critical regulator of systemic energy homeostasis by acting as a caloric reservoir

  • high-fat diet (HFD)-fed IFNγ knockout mice show no difference in adipose tissue mass, adipose tissue inflammation, and glucose tolerance are ameliorated compared to wild-type mice [142]. These findings suggest that proinflammatory immune cells amplify the inflammatory response via cell-to-cell interactions with adipocytes and other immune cells, which in turn induces chronic inflammation, adipose tissue dysfunction, and insulin resistance

  • We have focused on the physiological and pathological roles of the adipose tissue and its remodeling in regulating whole-body energy metabolism by sensing the nutritional status and crosstalk between adipocytes and stromal vascular cells

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Summary

INTRODUCTION

The adipose tissue is a critical regulator of systemic energy homeostasis by acting as a caloric reservoir. In response to alterations in the energy status, the adipose tissue is rapidly and dynamically remodeled through changes in the number and/or size of adipocytes. Pathophysiological Role of Adipose Tissue Remodeling cells in the adipose tissue undergo numerical and/or functional changes, contributing to the maintenance of the adipose tissue function as an energy reservoir and endocrine organ. This series of events is called “adipose tissue remodeling.”. Under pathophysiological conditions, such as obesity, aberrant adipose tissue remodeling may induce dysregulation of adipose tissue-derived cytokines, hormones, and metabolites, leading to metabolic stresses and disorders in metabolic organs [2,3,4] This series of events is called “adipose tissue remodeling.” under pathophysiological conditions, such as obesity, aberrant adipose tissue remodeling may induce dysregulation of adipose tissue-derived cytokines, hormones, and metabolites, leading to metabolic stresses and disorders in metabolic organs [2,3,4]

The Adipose Tissue as a Specialized Energy Storage Organ
The Adipose Tissue as an Endocrine Organ Regulating Energy Homeostasis
The Adipose Tissue as a Thermal Regulator
Two Modes of Adipose Tissue Expansion
Hypertrophic Adipocytes
Hyperplastic Adipocytes
Obesity and Adipose Tissue Inflammation
Tissue Immune Cell Balance
Adipose Tissue Angiogenesis and Macrophages
Clearance of Dead Adipocytes and Macrophages
Adaptive Thermogenesis and Adipose Tissue Macrophages
Findings
CONCLUSION
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