Adipose tissue inflammation and ectopic lipid accumulation [Review]

Suganami, Takayoshi; Tanaka, Miyako; Ogawa, Yoshihiro

doi:10.1507/endocrj.ej12-0271

Cited by 168 publications

(130 citation statements)

References 79 publications

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“…However, the ability of AT to store excess energy as triglycerides is limited, as determined by both genetic and environmental factors. In fact, it has been proposed that when the lipid storage capacity of AT is exceeded, then lipids accumulate ectopically in the liver and muscle, causing insulin resistance and impaired pancreatic beta cell function by a lipotoxic mechanism (Suganami et al 2012).…”

Section: Introductionmentioning

confidence: 99%

Dietary fat modifies lipid metabolism in the adipose tissue of metabolic syndrome patients

et al. 2014

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Adipose tissue (AT) is a key organ in the regulation of total body lipid homeostasis, which is responsible for the storage and release of fatty acids according to metabolic needs. We aimed to investigate the effect of the quantity and quality of dietary fat on the lipogenesis and lipolysis processes in the AT of metabolic syndrome (MetS) patients. A randomized, controlled trial conducted within the LIPGENE study assigned MetS patients to one of four diets: (a) high-saturated fatty acid (HSFA) (b) highmonounsaturated fatty acid, and (c, d) two low-fat, highcomplex carbohydrate diets supplemented with long chain (LC) n-3 (LFHCC n-3) polyunsaturated fatty acids (PUFA) or placebo (LFHCC), for 12 weeks each. A fat challenge reflecting the same fatty acid composition as the original diets was conducted post-intervention. Long-term consumption of the LFHCC diet induced an increase in the fasting expression levels of the sterol regulatory element binding protein-1 and stearoyl-CoA desaturase D9-desaturase genes, whereas the supplementation of this diet with n-3 PUFA reversed this effect (p = 0.007). In contrast, long-term consumption of the HSFA diet increased the expression of the adipose triglyceride lipase (ATGL) gene, at both fasting and postprandial states (both, p \ 0.001). Our results showed the anti-lipogenic effect exerted by LC n-3 PUFA when administered together with a LFHCC diet. Conversely, a diet high in saturated fat increased the expression of the lipolytic gene ATGL relative to the other diets.

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Section: Introductionmentioning

confidence: 99%

Dietary fat modifies lipid metabolism in the adipose tissue of metabolic syndrome patients

et al. 2014

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“…Indeed, adipose tissue in obesity is characterized by adipocyte hypertrophy, followed by increased angiogenesis, immune cell infiltration, extracellular matrix overproduction, which is referred to as 'adipose tissue remodelling' 3,4 . As a molecular mechanism, we have provided evidence that a paracrine loop involving saturated fatty acids and tumour necrosis factor-a (TNFa) derived from adipocytes and macrophages, respectively, establishes a vicious cycle, thereby accelerating the inflammatory change in obese adipose tissue 5 .…”

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confidence: 99%

Macrophage-inducible C-type lectin underlies obesity-induced adipose tissue fibrosis

et al. 2014

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“…In this regard, excessive energy intake should affect adipose tissue function. Moreover, there is considerable evidence suggesting that the interaction between mature adipocytes and stromal cells in adipose tissue plays a critical role in the regulation of adipocytokine production and lipid storage 16,17) . Among a number of stromal cells, the role of macrophages has been *Correspondence: suganami@riem.nagoya-u.ac.jp most intensively studied.…”

Section: Obesity-induced Adipose Tissue Remodelingmentioning

confidence: 99%

“…In addition, Khan et al reported that mice lacking collagen VI, which is expressed abundantly in adipose tissue, exhibit uninhibited adipose tissue expansion and substantial improvement in insulin sensitivity on a high-fat diet 46) . It is known that, in response to nutritional conditions, the lipid storage function of adipose tissue is tightly regulated by hormones such as insulin and the sympathetic nervous system 17) . Chronic inflammation-induced adipose tissue fibrosis may be a novel mechanism of systemic energy homeostasis.…”

Section: Obesity-induced Adipose Tissue Fibrosismentioning

confidence: 99%

“…Another possible mediator may be free fatty acids. Adipose tissue inflammation increases insulin resistance in adipocytes, induces lipolysis and limits adipose tissue expandability, all of which contributes to increased serum free fatty acid levels 16,17) . Mincle-deficient mice consistently exhibit lower serum free fatty acid levels than wildtype mice on a highfat diet 44) .…”

Section: Adipose Tissue Inflammation and Systemic Metabolic Derangementsmentioning

confidence: 99%

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Molecular mechanism underlying nutritional control of inflammatory responses

Tanaka

Suganami

2017

JPFSM

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Storage of excessive energy as triglycerides is a fundamental function of adipose tissue. Adipose tissue also secrets a number of hormones termed "adipocytokines" or "adipokines" in response to the systemic nutritional status, thereby constituting a feedback mechanism of metabolic homeostasis. In this regard, adipose tissue senses systemic nutritional conditions and regulates systemic metabolic homeostasis. During the past decade, there has been remarkable progress in the molecular mechanism underlying obesity-induced adipose tissue dysfunction. Accumulating evidence has suggested that a variety of stromal cells induce adipose tissue remodeling, which impairs adipose tissue function such as lipid storage and adipocytokine production, thereby leading to systemic metabolic derangements. Namely, chronic inflammation provides a molecular basis underlying obesity-induced adipose tissue dysfunction. In contrast, nutritional deprivation or malnutrition results in immune dysfunction, at least partly, through adipocytokine dysregulation. Thus, adipose tissue links nutritional conditions and inflammatory responses.

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Adipose tissue inflammation and ectopic lipid accumulation [Review]

Cited by 168 publications

References 79 publications

Dietary fat modifies lipid metabolism in the adipose tissue of metabolic syndrome patients

Dietary fat modifies lipid metabolism in the adipose tissue of metabolic syndrome patients

Macrophage-inducible C-type lectin underlies obesity-induced adipose tissue fibrosis

Molecular mechanism underlying nutritional control of inflammatory responses

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