Adipose tissue: between the extremes

Abstract

Adipose tissue represents a critical component in healthy energy homeostasis. It fulfills important roles in whole-body lipid handling, serves as the body's major energy storage compartment and insulation barrier, and secretes numerous endocrine mediators such as adipokines or lipokines. As a consequence, dysfunction of these processes in adipose tissue compartments is tightly linked to severe metabolic disorders, including obesity, metabolic syndrome, lipodystrophy, and cachexia. While numerous studies have addressed causes and consequences of obesity-related adipose tissue hypertrophy and hyperplasia for health, critical pathways and mechanisms in (involuntary) adipose tissue loss as well as its systemic metabolic consequences are far less understood. In this review, we discuss the current understanding of conditions of adipose tissue wasting and review microenvironmental determinants of adipocyte (dys)function in related pathophysiologies.

Leptin in the regulation of the immunometabolism of adipose tissue-macrophages

“…87 SAT buffers the excess fat, which otherwise would be toxic if in the circulation and accumulated ectopically or in VAT. 88 Consistently, insulin resistance is associated with lower levels of circulating leptin and reduced adipogenic capacity in the SAT of obese individuals, compared to insulin sensitive subjects. 89 Among adipose tissue depots, SAT is also the main source of leptin in humans 86,90 and it is tempting to speculate whether the role of leptin in this fat depot is beneficial or detrimental.…”

“…On the other hand, subcutaneous adipose tissue (SAT, or also known as SQ WAT) is recognized for its greater capacity to store lipids and its contribution to proper glucose homeostasis . SAT buffers the excess fat, which otherwise would be toxic if in the circulation and accumulated ectopically or in VAT . Consistently, insulin resistance is associated with lower levels of circulating leptin and reduced adipogenic capacity in the SAT of obese individuals, compared to insulin sensitive subjects .…”

Jak-TGFβ cross-talk links transient adipose tissue inflammation to beige adipogenesis

“…Jak activity inhibited expression of Tgfb3 and Tgfb1 through Stat3 and counteracted TGF-Srf/Smad3 activation. It is tempting to speculate that chronic dysregulation of Tgfb3 and Tgfb1 in progenitor and stromal cells may promote fibrosis and inhibit adipogenesis and mitochondrial oxidative metabolism, contributing to adipose tissue dysfunction and metabolic disease (49,50).…”

Manifestations of systemic diseases and conditions that affect the periodontal attachment apparatus: Case definitions and diagnostic considerations

“…Dysfunction of processes in adipose tissue compartments may trigger various metabolic disorders, including obesity, metabolic syndrome, lipodystrophy, and cachexia. 65 Studies show that crosstalk between T cells and adipose tissue shapes the inflammatory environment in obesity-associated metabolic diseases. 66 Likewise, obesity-induced changes to macrophages and adipocytes may lead to chronic inflammation and insulin resistance.…”