Naringenin suppresses macrophage infiltration into adipose tissue in an early phase of high-fat diet-induced obesity

Yoshida, Hiroki; Watanabe, Hideaki; Ishida, Akiko; Watanabe, Wataru; Narumi, Keiko; Atsumi, Toshiyuki; Sugita, Chihiro; Kurokawa, Mineo

doi:10.1016/j.bbrc.2014.10.038

Cited by 61 publications

(46 citation statements)

References 23 publications

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“…The mediators of ATM increase during rapid WAT expan-sion require further investigation, but candidates include IL4, IL6, and OPN. 30,[37][38][39][40][41][42][43] Adipocyte hypertrophy is observed as early as 3d of HFD and is associated with elevated chemoattractants and surface expression of stress markers in obesity. 22,36,44 These observations support the possibility that adipocyte hypertrophy regulates ATM proliferation.…”

Section: Discussionmentioning

confidence: 99%

Frontline Science: Rapid adipose tissue expansion triggers unique proliferation and lipid accumulation profiles in adipose tissue macrophages

Muir

Kiridena

Griffin

et al. 2018

Journal of Leukocyte Biology

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Obesity-related changes in adipose tissue leukocytes, in particular adipose tissue macrophages (ATMs) and dendritic cells (ATDCs), are implicated in metabolic inflammation, insulin resistance, and altered regulation of adipocyte function. We evaluated stromal cell and white adipose tissue (WAT) expansion dynamics with high fat diet (HFD) feeding for 3-56 days, quantifying ATMs, ATDCs, endothelial cells (ECs), and preadipocytes (PAs) in visceral epididymal WAT and subcutaneous inguinal WAT. To better understand mechanisms of the early response to obesity, we evaluated ATM proliferation and lipid accumulation. ATMs, ATDCs, and ECs increased with rapid WAT expansion, with ATMs derived primarily from a CCR2-independent resident population. WAT expansion stimulated proliferation in resident ATMs and ECs, but not CD11c ATMs or ATDCs. ATM proliferation was unperturbed in Csf2- and Rag1-deficient mice with WAT expansion. Additionally, ATM apoptosis decreased with WAT expansion, and proliferation and apoptosis reverted to baseline with weight loss. Adipocytes reached maximal hypertrophy at 28 days of HFD, coinciding with a plateau in resident ATM accumulation and the appearance of lipid-laden CD11c ATMs in visceral epididymal WAT. ATM increases were proportional to tissue expansion and adipocyte hypertrophy, supporting adipocyte-mediated regulation of resident ATMs. The appearance of lipid-laden CD11c ATMs at peak adipocyte size supports a role in responding to ectopic lipid accumulation within adipose tissue. In contrast, ATDCs increase independently of proliferation and may be derived from circulating precursors. These changes precede and establish the setting in which large-scale adipose tissue infiltration of CD11c ATMs, inflammation, and adipose tissue dysfunction contributes to insulin resistance.

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Section: Discussionmentioning

confidence: 99%

Frontline Science: Rapid adipose tissue expansion triggers unique proliferation and lipid accumulation profiles in adipose tissue macrophages

Muir

Kiridena

Griffin

et al. 2018

Journal of Leukocyte Biology

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“…Immune cells, particularly monocytes, migrate to areas of hypoxia, where they differentiate into proinflammatory macrophages (13,14). Macrophage infiltration into AT occurs within one day of HFF (15). Although few studies have directly addressed the effect of mild hypoxia during early AT expansion on AT inflammatory processes, there have been reports of both pro-and antiinflammatory responses during the first four days of HFF.…”

Section: The Adipocyte Stress Signal: Mild Hypoxiamentioning

confidence: 99%

The ominous triad of adipose tissue dysfunction: inflammation, fibrosis, and impaired angiogenesis

Crewe¹,

An²,

Scherer³

2017

Journal of Clinical Investigation

565

461

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There are three dominant contributors to the pathogenesis of dysfunctional adipose tissue (AT) in obesity: unresolved inflammation, inappropriate extracellular matrix (ECM) remodeling and insufficient angiogenic potential. The interactions of these processes during AT expansion reflect both a linear progression as well as feed-forward mechanisms. For example, both inflammation and inadequate angiogenic remodeling can drive fibrosis, which can in turn promote migration of immune cells into adipose depots and impede further angiogenesis. Therefore, the relationship between the members of this triad is complex but important for our understanding of the pathogenesis of obesity. Here we untangle some of these intricacies to highlight the contributions of inflammation, angiogenesis, and the ECM to both "healthy" and "unhealthy" AT expansion.

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“…This inflammation is derived from an infiltration of macrophages in the adipose tissue [74]. The protective effects of naringenin were elucidated in one study where mice fed a high fat diet along with naringenin had decreased levels of macrophage infiltration and thus lower obesity-related adipose tissue inflammation [75]. Another study shows naringenin administered to rats in conjunction with cholesterol-rich diet reduced total cholesterol and triglyceride levels as well as increased antioxidant activity [76].…”

Section: Phytochemicals In Obesitymentioning

confidence: 99%

Phytochemicals as novel agents for the induction of browning in white adipose tissue

et al. 2016

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Obesity and its associated metabolic syndrome continue to be a health epidemic in westernized societies and is catching up in the developing world. Despite such increases, little headway has been made to reverse adverse weight gain in the global population. Few medical options exist for the treatment of obesity which points to the necessity for exploration of anti-obesity therapies including pharmaceutical and nutraceutical compounds. Defects in brown adipose tissue, a major energy dissipating organ, has been identified in the obese and is hypothesized to contribute to the overall metabolic deficit observed in obesity. Not surprisingly, considerable attention has been placed on the discovery of methods to activate brown adipose tissue. A variety of plant-derived, natural compounds have shown promise to regulate brown adipose tissue activity and enhance the lipolytic and catabolic potential of white adipose tissue. Through activation of the sympathetic nervous system, thyroid hormone signaling, and transcriptional regulation of metabolism, natural compounds such as capsaicin and resveratrol may provide a relatively safe and effective option to upregulate energy expenditure. Through utilizing the energy dissipating potential of such nutraceutical compounds, the possibility exists to provide a therapeutic solution to correct the energy imbalance that underlines obesity.

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Naringenin suppresses macrophage infiltration into adipose tissue in an early phase of high-fat diet-induced obesity

Cited by 61 publications

References 23 publications

Frontline Science: Rapid adipose tissue expansion triggers unique proliferation and lipid accumulation profiles in adipose tissue macrophages

Frontline Science: Rapid adipose tissue expansion triggers unique proliferation and lipid accumulation profiles in adipose tissue macrophages

The ominous triad of adipose tissue dysfunction: inflammation, fibrosis, and impaired angiogenesis

Phytochemicals as novel agents for the induction of browning in white adipose tissue

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