Cellular and Molecular Basis of Functional Differences among Fat Depots

Thomou, Thomas; Tchkonia, Tamar; Kirkland, James L.

doi:10.1002/9783527629527.ch2

Cited by 11 publications

(18 citation statements)

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“…Adipose tissue also has immune, endocrine, regenerative, mechanical, and thermal functions (reviewed in Thomou et al, 2010). Both the fuel and nonfuel functions of adipose tissue vary among depots, with depot size, and with body-fat distribution.…”

Section: Fat-tissue Functionmentioning

confidence: 99%

“…Once inflamed, adipose tissue shifts from storing to releasing fatty acids, potentially driven in part through local proinflammatory cytokine release (Faty et al, 2012; Zhang et al, 1996). The proinflammatory response of fat tissue to bacterial antigens such as lipopolysaccharide may combine with high local concentrations of fatty acids during ensuing cytokine-induced lipolysis to mitigate infection (Chung et al, 2006; Desbois and Smith, 2010; Tchkonia et al, 2006a; Thomou et al, 2010). Obesity, aging, and lipodystrophies are associated with sustained fat-tissue immune-response activation, proinflammatory cytokine release, impaired insulin responsiveness, reduced incorporation of fatty acid as triglycerides, and increased lipolysis (Tchkonia et al, 2010; Thomou et al, 2010).…”

Section: Fat-tissue Functionmentioning

confidence: 99%

“…The proinflammatory response of fat tissue to bacterial antigens such as lipopolysaccharide may combine with high local concentrations of fatty acids during ensuing cytokine-induced lipolysis to mitigate infection (Chung et al, 2006; Desbois and Smith, 2010; Tchkonia et al, 2006a; Thomou et al, 2010). Obesity, aging, and lipodystrophies are associated with sustained fat-tissue immune-response activation, proinflammatory cytokine release, impaired insulin responsiveness, reduced incorporation of fatty acid as triglycerides, and increased lipolysis (Tchkonia et al, 2010; Thomou et al, 2010). This contributes to low-grade “sterile” systemic inflammation, metabolic dysregulation, and lipotoxicity, with different fat depots potentially contributing in distinct ways.…”

Section: Fat-tissue Functionmentioning

confidence: 99%

“…Several adipokines are secreted in a fat-depot-dependent fashion (Table 1). Like macrophages, preadipocytes exhibit robust innate immune responses to bacterial antigens, recruit macrophages and other immune effectors, and participate in initiating and regulating fat-tissue immune activation (Gustafson et al, 2009; Lacasa et al, 2007; Thomou et al, 2010). Preadipocyte gene-expression profiles are closer to those of macrophages, into which they may be able to convert, than to those of fat cells (Charrière et al, 2003; Prunet-Marcassus et al, 2006).…”

Section: Cellular Mechanisms Of Fat Growth and Functionmentioning

confidence: 99%

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Mechanisms and Metabolic Implications of Regional Differences among Fat Depots

et al. 2013

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Fat distribution is closely linked to metabolic disease risk. Distribution varies with sex, genetic background, disease state, certain drugs and hormones, development, and aging. Preadipocyte replication and differentiation, developmental gene expression, susceptibility to apoptosis and cellular senescence, vascularity, inflammatory cell infiltration, and adipokine secretion vary among depots, as do fatty-acid handling and mechanisms of enlargement with positive-energy and loss with negative-energy balance. How interdepot differences in these molecular, cellular, and pathophysiological properties are related is incompletely understood. Whether fat redistribution causes metabolic disease or whether it is a marker of underlying processes that are primarily responsible is an open question.

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Section: Fat-tissue Functionmentioning

confidence: 99%

Section: Fat-tissue Functionmentioning

confidence: 99%

Section: Fat-tissue Functionmentioning

confidence: 99%

Section: Cellular Mechanisms Of Fat Growth and Functionmentioning

confidence: 99%

See 2 more Smart Citations

Mechanisms and Metabolic Implications of Regional Differences among Fat Depots

et al. 2013

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“…(22) Obesity, aging, and lipodystrophies are associated with sustained fat-tissue immuneresponse activation, proinlammatory cytokine release, impaired insulin responsiveness, reduced incorporation of fatty acid as triglycerides, and increased lipolysis. (8,22) This contributes to low-grade ''sterile'' systemic inlammation, metabolic dysregulation, and lipotoxicity, with different fat depots potentially contributing in distinct ways.…”

Section: Introductionmentioning

confidence: 99%

Hypertrophic Obesity and Subcutaneous Adipose Tissue Dysfunction

Meiliana

Wijaya

2014

Indones Biomed J

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BACKGROUND: Over the past 50 years, scientists have recognized that not all adipose tissue is alike, and that health risk is associated with the location as well as the amount of body fat. Different depots are sufficiently distinct with respect to fatty-acid storage and release as to probably play unique roles in human physiology. Whether fat redistribution causes metabolic disease or whether it is a marker of underlying processes that are primarily responsible is an open question.CONTENT: The limited expandability of the subcutaneous adipose tissue leads to inappropriate adipose cell expansion (hypertrophic obesity) with local inflammation and a dysregulated and insulin-resistant adipose tissue. The inability to store excess fat in the subcutaneous adipose tissue is a likely key mechanism for promoting ectopic fat accumulation in tissues and areas where fat can be stored, including the intra-abdominal and visceral areas, in the liver, epi/pericardial area, around vessels, in the myocardium, and in the skeletal muscles. Many studies have implicated ectopic fat accumulation and the associated lipotoxicity as the major determinant of the metabolic complications of obesity driving systemic insulin resistance, inflammation, hepatic glucose production, and dyslipidemia.SUMMARY: In summary, hypertrophic obesity is due to an impaired ability to recruit and differentiate available adipose precursor cells in the subcutaneous adipose tissue. Thus, the subcutaneous adipose tissue may be particular in its limited ability in certain individuals to undergo adipogenesis during weight increase. Inability to promote subcutaneous adipogenesis under periods of affluence would favor lipid overlow and ectopic fat accumulation with negative metabolic consequences.KEYWORDS: obesity, adipogenesis, subcutaneous adipose tissue, visceral adipose tissue, adipocyte dysfunction

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