Link between Adipose Tissue Angiogenesis and Fat Accumulation in Severely Obese Subjects

Lemoine, A.; Ledoux, Séverine; Quéguiner, Isabelle; Caldérari, Sophie; Mechler, Charlotte; Msika, Simon; Corvol, Pierre; Larger, Étienne

doi:10.1210/jc.2011-2649

Cited by 42 publications

(31 citation statements)

References 20 publications

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“…Chronic overfeeding leads to AT expansion due to adipocyte hypertrophy and is accompanied by enhanced vascularization to assure adequate oxygen supply which requires substantial ECM remodeling (Lemoine et al, 2012). In our model, deletion of Postn resulted in a reduced ability for AT expansion during HFD feeding.…”

Section: Discussionmentioning

confidence: 99%

Loss of periostin occurs in aging adipose tissue of mice and its genetic ablation impairs adipose tissue lipid metabolism

et al. 2018

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Remodeling of the extracellular matrix is a key component of the metabolic adaptations of adipose tissue in response to dietary and physiological challenges. Disruption of its integrity is a well‐known aspect of adipose tissue dysfunction, for instance, during aging and obesity. Adipocyte regeneration from a tissue‐resident pool of mesenchymal stem cells is part of normal tissue homeostasis. Among the pathophysiological consequences of adipogenic stem cell aging, characteristic changes in the secretory phenotype, which includes matrix‐modifying proteins, have been described. Here, we show that the expression of the matricellular protein periostin, a component of the extracellular matrix produced and secreted by adipose tissue‐resident interstitial cells, is markedly decreased in aged brown and white adipose tissue depots. Using a mouse model, we demonstrate that the adaptation of adipose tissue to adrenergic stimulation and high‐fat diet feeding is impaired in animals with systemic ablation of the gene encoding for periostin. Our data suggest that loss of periostin attenuates lipid metabolism in adipose tissue, thus recapitulating one aspect of age‐related metabolic dysfunction. In human white adipose tissue, periostin expression showed an unexpected positive correlation with age of study participants. This correlation, however, was no longer evident after adjusting for BMI or plasma lipid and liver function biomarkers. These findings taken together suggest that age‐related alterations of the adipose tissue extracellular matrix may contribute to the development of metabolic disease by negatively affecting nutrient homeostasis.

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Section: Discussionmentioning

confidence: 99%

Loss of periostin occurs in aging adipose tissue of mice and its genetic ablation impairs adipose tissue lipid metabolism

et al. 2018

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“…Interestingly, there is evidence for a functional link between adipogenesis and angiogenesis during deposition of fat mass, whereby the angiogenic capacity of WAT may determine the extent of adipogenesis and propensity of a subject to gain weight (37,38). In addition, several studies have shown that endothelial cells control adipogenesis in WAT through VEGF and matrix metalloproteinases pathways (39)(40)(41)(42).…”

Section: Discussionmentioning

confidence: 99%

Endostatin Prevents Dietary-Induced Obesity by Inhibiting Adipogenesis and Angiogenesis

Wang

Chen

et al. 2015

Diabetes

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Endostatin is a well-known angiogenesis inhibitor. Although angiogenesis has been considered as a potential therapeutic target of obesity, the inhibitory effect of endostatin on adipogenesis and dietary-induced obesity has never been demonstrated. Adipogenesis plays a critical role in controlling adipocyte cell number, body weight, and metabolic profile in a homeostatic state. Here we reveal that endostatin inhibits adipogenesis and dietary-induced obesity. The antiadipogenic mechanism of endostatin lies in its interaction with Sam68 RNA-binding protein in the nuclei of preadipocytes. This interaction competitively impairs the binding of Sam68 to intron 5 of mammalian target of rapamycin (mTOR), causing an error in mTOR transcript. This consequently decreases the expression of mTOR, results in decreased activities of the mTOR complex 1 pathway, and leads to defects in adipogenesis. Moreover, our findings demonstrate that the antiangiogenic function of endostatin also contributes to its obesity-inhibitory activity. Through the combined functions on adipogenesis and angiogenesis, endostatin prevents dietary-induced obesity and its related metabolic disorders, including insulin resistance, glucose intolerance, and hepatic steatosis. Thus, our findings reveal that endostatin has a potential application for antiobesity therapy and the prevention of obesity-related metabolic syndromes.

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“…It has been shown that adipose tissue in severely obese patients produces proangiogenic factors, including vascular endothelial growth factor (VEGF) and placental growth factor and, in these patients, BMI correlated with vascular density in subcutaneous white adipose tissue. However, after effective weight-lowering treatment, these abnormalities are reversed 14. Taken together, these data suggest that obesity has the potentiality to initiate many of the known immune-inflammatory pathways underlying the pathogenesis of PsA.…”

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confidence: 87%

The link between obesity and psoriatic arthritis

Cañete

Mease

2012

Ann Rheum Dis

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Link between Adipose Tissue Angiogenesis and Fat Accumulation in Severely Obese Subjects

Abstract: Angiogenesis may influence WAT expansion and plasticity but does not appear to be involved in the development of insulin resistance in subjects with severe obesity.

Cited by 42 publications

References 20 publications

Loss of periostin occurs in aging adipose tissue of mice and its genetic ablation impairs adipose tissue lipid metabolism

Loss of periostin occurs in aging adipose tissue of mice and its genetic ablation impairs adipose tissue lipid metabolism

Endostatin Prevents Dietary-Induced Obesity by Inhibiting Adipogenesis and Angiogenesis

The link between obesity and psoriatic arthritis

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