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Open AccessJournal ArticleDOI

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

TLDR
It is demonstrated that >90% of all macrophages in WAT of obese mice and humans are localized to dead adipocytes, where they fuse to form syncytia that sequester and scavenge the residual “free” adipocyte lipid droplet and ultimately form multinucleate giant cells, a hallmark of chronic inflammation.
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This article is published in Journal of Lipid Research.The article was published on 2005-11-01 and is currently open access. It has received 2235 citations till now. The article focuses on the topics: Crown-Like Structure & Adipocyte hypertrophy.

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Inflammation and metabolic disorders

TL;DR: Dysfunction of the immune response and metabolic regulation interface can be viewed as a central homeostatic mechanism, dysfunction of which can lead to a cluster of chronic metabolic disorders, particularly obesity, type 2 diabetes and cardiovascular disease.
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Exploring the full spectrum of macrophage activation.

TL;DR: This Review suggests a new grouping of macrophages based on three different homeostatic activities — host defence, wound healing and immune regulation, and proposes that similarly to primary colours, these three basic macrophage populations can blend into various other 'shades' of activation.
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Adipokines in inflammation and metabolic disease

TL;DR: The role of adipokines in inflammatory responses is focused on and their potential as regulators of metabolic function is discussed.
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Macrophage biology in development, homeostasis and disease

TL;DR: This Review discusses how macrophage regulate normal physiology and development, and provides several examples of their pathophysiological roles in disease, and defines the ‘hallmarks’ of macrophages according to the states that they adopt during the performance of their various roles.
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Type 2 diabetes as an inflammatory disease.

TL;DR: Preliminary results from clinical trials with salicylates and interleukin-1 antagonists support the notion that inflammation participates in the pathogenesis of type 2 diabetes and have opened the door for immunomodulatory strategies for the treatment of T2D that simultaneously lower blood glucose levels and potentially reduce the severity and prevalence of the associated complications of this disease.
References
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Journal ArticleDOI

Obesity is associated with macrophage accumulation in adipose tissue

TL;DR: Transcript expression in perigonadal adipose tissue from groups of mice in which adiposity varied due to sex, diet, and the obesity-related mutations agouti (Ay) and obese (Lepob) found that the expression of 1,304 transcripts correlated significantly with body mass.
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Adipose expression of tumor necrosis factor-alpha: direct role in obesity-linked insulin resistance

TL;DR: A role for TNF-alpha in obesity and particularly in the insulin resistance and diabetes that often accompany obesity is indicated.
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Chronic inflammation in fat plays a crucial role in the development of obesity-related insulin resistance.

TL;DR: It is proposed that obesity-related insulin resistance is, at least in part, a chronic inflammatory disease initiated in adipose tissue, and that macrophage-related inflammatory activities may contribute to the pathogenesis of obesity-induced insulin resistance.
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Increased oxidative stress in obesity and its impact on metabolic syndrome

TL;DR: It is suggested that increased oxidative stress in accumulated fat is an early instigator of metabolic syndrome and that the redox state in adipose tissue is a potentially useful therapeutic target for obesity-associated metabolic syndrome.
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Endoplasmic Reticulum Stress Links Obesity, Insulin Action, and Type 2 Diabetes

TL;DR: It is shown that obesity causes endoplasmic reticulum (ER) stress, which leads to suppression of insulin receptor signaling through hyperactivation of c-Jun N-terminal kinase (JNK) and subsequent serine phosphorylation of insulin receptors substrate–1 (IRS-1).
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