How does adipose tissue contribute to inflammageing?

doi:10.1016/j.exger.2020.111162

Experimental Gerontology

Volume 143, January 2021, 111162

https://doi.org/10.1016/j.exger.2020.111162 Get rights and content

Highlights

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Aging is associated with an increase in visceral fat, ectopic fat and a decline in gluteofemoral subcutaneous fat.
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Dysfunctional fat is characterized by preadipocytes differentiation decline, senescent cells accumulation and inflammation.
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Adipose tissue changes may be responsible for the systemic pro-inflammatory state (inflammageing) typical of aging itself.

Abstract

Across aging, white adipose tissue (WAT) undergoes significant changes in quantity and distribution, with an increase in visceral adipose tissue, ectopic fat deposition and a decline in gluteofemoral subcutaneous depot.

In particular, WAT becomes dysfunctional with an increase in production of inflammatory peptides and a decline of those with anti-inflammatory activity and infiltration of inflammatory cells. Moreover, dysfunction of WAT is characterized by preadipocyte differentiation decline, increased oxidative stress and mitochondrial dysfunction, reduction in vascularization and hypoxia, increased fibrosis and senescent cell accumulation.

WAT changes represent an important hallmark of the aging process and may be responsible for the systemic pro-inflammatory state (“inflammageing”) typical of aging itself, leading to age-related metabolic alterations.

This review focuses on mechanisms linking age-related WAT changes to inflammageing.

Introduction

Aging is the main risk factor for multiple chronic diseases, decline in physical function and frailty. Such conditions are frequently preceded by metabolic alterations and low-grade chronic inflammation. Adipose tissues are organized to form a large adipose organ with discrete anatomy, vasculature and innervation, high plasticity and complex cytology where the main cells, the adipocytes, are defined as white or brown in relation to their different morphology and function (Cinti, 2012). Across aging, both white adipose tissue adipose (WAT) and brown adipose tissue (BAT) undergo changes in quantity, distribution and function. WAT changes represent an important hallmark of the aging process itself and may be responsible for the systemic pro-inflammatory state typical of aging itself (Kirkland et al., 2002). This age-related state of chronic sterile low-grade inflammation has been named “inflammageing” and participate in the development of frailty, disability and most chronic degenerative diseases including age-related cardiovascular and cerebrovascular diseases (Franceschi, 2007; Franceschi and Campisi, 2014). Even if a variety of tissues and organs participate in inflammageing (Franceschi and Campisi, 2014; Franceschi et al., 2018; Liberale et al., 2020), WAT plays a major role. Moreover, WAT plays a major role in human physiology by constituting the main reservoir of energy stores, deposited as triglycerides and by serving as an endocrine organ secreting several peptides which have a fundamental role in the regulation of energy homeostasis, insulin sensitivity and cardiovascular function (Cinti et al., 2005; Giordano et al., 2013). WAT is usually divided into visceral (VAT) and subcutaneous (SAT) adipose tissue (Bosello and Zamboni, 2000). SAT is where the majority of excess lipids are stored, and is considered healthier than VAT in both lean and obese subjects while, VAT, being more metabolically active and sensitive to lipolytic stimulus, is strongly related to the onset of metabolic syndrome and to increased cardiovascular morbidity and mortality (Bosello and Zamboni, 2000).

Therefore, the aim of this review is to revise current literature about the contribution of WAT to inflammageing and explore potential mechanisms at the systemic, tissutal and cellular levels.

Section snippets

Age related body fat redistribution

As people age, a progressive increase in fat mass occurs, in response to chronic positive calorie balance, reduced physical activity and lower basal metabolic rate (Mancuso and Bouchard, 2019). An increase in total adiposity may be independent of body weight changes due to a concomitant decrease in muscle mass observed with aging, so-called sarcopenia (Prentice and Jebb, 2001), as well as a decrement in total body water, especially the intracellular compartment, and a decreasing trend of bone

Age related WAT dysfunction

WAT is organized in a large adipose organ with discrete anatomy, vasculature and innervation, specific cytology and high plasticity (Cinti, 2012). WAT is composed of different cell types including the adipocyte fraction, which contains primarily mature adipocytes and the stromal fraction, composed of adipogenic stem cells, preadipocytes, macrophages, lymphocytes, endothelial cells, pericytes, and fibroblasts (Cinti et al., 2005; Cinti, 2012; Cawthorn et al., 2012; Senesi et al., 2019). With

Conclusions

Sterile inflammation, or the presence of inflammation in the absence of a known identifiable infection is a common feature of aging, a condition that was defined years ago by Franceschi et al., as inflammageing (Franceschi, 2007; Franceschi et al., 2018). WAT may be a major contributor to inflammageing in the elderly (Zamboni et al., 2014; Stout et al., 2016). This may depend on the fact that WAT has recognized immunological functions (Kershaw and Kershaw and Flier, 2004; Grant and Dixit, 2015;

Declaration of competing interest

None.

Acknowledgements

This project was supported by grants from Fondazione Cariplo (2016-1006 to Mauro Zamboni).

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Citation Excerpt :
Indeed, fat tissue mass increases through midlife and declines during the old age. Moreover, aging is associated with a redistribution of body WAT, characterized by an increased fat accumulation in vWAT, as well as ectopic fat deposition, with a decline in scWAT mass [7,8]. Certainly, WAT is the most plastic organ among the metabolically relevant tissues [9].
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How does adipose tissue contribute to inflammageing?

Highlights

Abstract

Introduction

Section snippets

Age related body fat redistribution

Age related WAT dysfunction

Conclusions

Declaration of competing interest

Acknowledgements

Aging alters tissue resident mesenchymal stem cell properties

Stem Cell Res.

T cells in adipose tissue in aging

Front. Immunol.

Adipokines and aging: findings from centenarians and the very old

Front. Endocrinol.

Adiponectin levels and genotype: a potential regulator of life span in humans

J. Gerontol. A Biol. Sci. Med. Sci.

Clearance of p16 Ink4a -positive senescent cells delays ageing-associated disorders

Nature

Depletion of fat resident T reg cells prevents age-associated insulin resistance

Nature

Adipose tissue as a potential source of hematopoietic stem/progenitor cells

Obesity (Silver Spring)

High-fat diet induced obesity and age influence the telomere shelterin complex and telomerase gene expression in mouse adipose tissue

Physiol Rep.

Visceral obesity and metabolic syndrome

Obes. Rev.

Body composition variations in ageing

Coll. Antropol.

Aging induces Nlrp3 inflammasome-dependent adipose B cell expansion to impair metabolic homeostasis

Innov. Aging

Role of leptin resistance in the development of obesity in older patients

Clin. Interv. Aging

Peripheral fat loss and decline in adipogenesis in older humans

Metabolism

Adipose tissue stem cells meet preadipocyte commitment: going back to the future

J. Lipid Res.

Adipocyte mTORC1 deficiency promotes adipose tissue inflammation and NLRP3 inflammasome activation via oxidative stress and de novo ceramide synthesis

J. Lipid Res.

Innate immune cells in the adipose tissue

Reviews in Endocrine and Metabolic Disorders

The adipose organ at a glance

Dis. Model. Mech.

Adipocyte death defines macrophage localization and function in adipose tissue of obese mice and humans

J. Lipid Res.

Biochemistry of adipose tissue: an endocrine organ

Arch. Med. Sci.

The senescence-associated secretory phenotype: the dark side of tumor suppression

Annual Review of Pathology Mechanisms of Disease

Immune cells gate white adipose tissue expansion

Endocrinology

Adipose tissue quality in aging: how structural and functional aspects of adipose tissue impact skeletal muscle quality

Nutrients

The impact of ageing on adipose structure, function and vasculature in the B6D2F1 mouse: evidence of significant multisystem dysfunction

J. Physiol.

Low steady-state oxidative stress inhibits adipogenesis by altering mitochondrial dynamics and decreasing cellular respiration

Redox Biol.

Oxidative stress accumulates in adipose tissue during aging and inhibits adipogenesis

PLoS One

Inflammageing as a major characteristic of old people: can it be prevented or cured?

Nutr. Rev.

Chronic inflammation (inflammageing) and its potential contribution to age-associated diseases

The Journals of Gerontology: Series A

Inflammageing: a new immune-metabolic viewpoint for age-related diseases

Nat Rev Endocrinol.

Adipose tissue: a tertiary lumphoid organ: does it change with age?

Gerontology.

Leptin resistance during aging is independent of fat mass

Diabetes

Changes in adipose tissue macrophages and T cells during aging

Crit. Rev. Immunol.

Impaired autophagy activity is linked to elevated ER-stress and inflammation in aging adipose tissue

Aging

Obese adipocytes show ultrastructural features of stressed cells and die of pyroptosis

J. Lipid Res.

Obesity, regional body fat distribution, and the metabolic syndrome in older men and women

Arch. Intern. Med.

Adipose tissue as an immunological organ

Obesity