Adipose Tissue Remodeling as Homeostatic Inflammation

Ichii, Michiko; Suganami, Takayoshi; Hachiya, Rumi; Ogawa, Yoshihiro

doi:10.4061/2011/720926

Cited by 72 publications

(63 citation statements)

References 67 publications

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“…Monocytes/macrophages: During the development of obesity, there is an increase in migration and infiltration activities of blood circulating monocytes, which are attracted by adipose tissue products: MCP-1, CXCL14, osteopontin, Angptl2, etc [91]. Macrophage infiltration in adipose tissue occurs before the development of insulin resistance in animal models [82,92].…”

Section: Cellular Adipose-lung Crosstalkmentioning

confidence: 99%

Adipose-Lung Cell Crosstalk in the Obesity-ARDS Paradox

Bustamante¹

2013

J Pulmon Resp Med

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Obesity is an increasingly frequent condition associated with increased adipose, systemic and pulmonary inflammation. There is an emerging and unexpected finding that obese individuals may not be at a greater risk for ARDS and, indeed, may even be partially protected against ARDS. This finding is known as the Obesity-ARDS Paradox. In this review we discuss the observations regarding this intriguing phenomenon and begin to elaborate on the theoretical rationale that obesity-triggered low-grade inflammatory processes may constitute pre-conditioning insults or trigger anti-inflammatory adaptive mechanisms that confer protection against ARDS. The Obesity-ARDS ParadoxObesity is an increasing global epidemic that increases cardiovascular abnormalities, diabetes, sleep apnea and mortality [1][2][3]. The Acute Respiratory Distress Syndrome (ARDS) is a highly fatal respiratory failure disorder [4,5]. Because both obesity and ARDS are characterized by increased inflammation and oxidative stress [6][7][8][9][10][11][12], obesity might reasonably be considered a risk factor for ARDS. However, the opposite seems to be the case. Although obese patients manifest a greater incidence of certain pro-inflammatory respiratory diseases, such as sleep apnea and asthma [13,14], they actually have a lower than expected incidence and/or severity of ARDS in a number of studies (Table 1) [15][16][17][18][19][20][21]. This unexplained finding is termed the "Obesity-ARDS Paradox. " Some of these studies are retrospective in nature or do not allow the investigation of the concept that has been termed "Metabolically Healthy Obesity" (MHO) [22,23] terminology that refers to obese individuals with no associated metabolic comorbidities (insulin resistance, atherosclerosis, liver dysfunction). Interestingly, this MHO concept has been linked to lower adiposerelated inflammatory profiles and a lower mortality risk compared to individuals with metabolically unhealthy obesity [24]. How obesity may affect systemic and even pulmonary inflammatory responses is the key focus of this review. The differences in the metabolic and inflammatory backgrounds of patients in studies that do not fully support the Obesity ARDS Paradox phenomenon may explain their different conclusions. However, the finding of multiple studies showing a lower-than-expected mortality (including lower mortality [15,19,20] or similar mortality [17,18,21] than normal weight patients) in obese individuals after ARDS is provocative. Elucidating the causes of this observation should increase understanding of the causes of ARDS and, perhaps, lead to new and needed therapeutic approaches. Pre-Conditioning as a Mechanism Contributing to the Obesity-ARDS ParadoxThe underlying mechanism responsible for the Obesity-ARDS Paradox is unknown. Confronted with trying to elucidate a reason, we hypothesized earlier [25] that obesity-induces a low-grade inflammation that generates a process that subsequently protects the lung against later insults. We termed this protective response the "pre-co...

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Section: Cellular Adipose-lung Crosstalkmentioning

confidence: 99%

Adipose-Lung Cell Crosstalk in the Obesity-ARDS Paradox

Bustamante¹

2013

J Pulmon Resp Med

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“…In other words, stromal cells change dramatically in number and cell type during the course of obesity. Such dynamic histological changes observed in obese adipose tissue can be referred to as "adipose tissue remodeling" [10,17,18]. In this regard, recent evidence suggests that the interaction between mature adipocytes and stromal cells in adipose tissue plays a critical role in the regulation of adipocytokine production [18].…”

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confidence: 99%

Adipose tissue inflammation and ectopic lipid accumulation [Review]

2012

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“…Adaptive expansion of the adipose tissue is enabled by combination of adipocyte hypertrophy and hyperplasia. Expansion of adipose tissue requires quite extensive tissue remodeling, in order to maintain adequate energy and oxygen supply, active neuronal network as well as integrity and functional properties of cellular membranes (Itoh et al 2011;Pietilainen et al 2011). Broader knowledge of the fat cell life-cycle dynamics is critical for our understanding the pathophysiological mechanisms limiting adipose tissue hyperplastic expansion.…”

Section: Adipose Tissue In Metabolic Health and Diseasementioning

confidence: 99%

“…Adipose tissue secretory products, "adipokines", could modulate food intake, energy expenditure, or tissue oxidative capacity (Trayhurn et al 1998;Ukropec et al 2001;Ahima & Lazar 2008;Henry & Clarke 2008;Friedman 2011). In addition, adipose tissue dynamically changes its structure (tissue remodeling, lipid composition), function (lipid storage & lipolysis) a s w e l l a s e n d o c r i n e a c t i o n i n r e s p o n s e t o d i f f e r e n t physiological (fasting / refeeding, exercise, microgravity) and pathophysiological (obesity, prediabetes, diabetes, cachexia, lipodystrophy, growth hormone deficiency) conditions (Ukropec et al 2008;Itoh et al 2011;Pietilainen et al 2011). It is important to understand that adipose tissue is a mixture of very different cell-types.…”

Section: Adipose Tissue In Metabolic Health and Diseasementioning

confidence: 99%