Apelin/APJ signaling system: a potential link between adipose tissue and endothelial angiogenic processes

Kunduzova, Oksana; Alet, Nathalie; Delesque-Touchard, Nathalie; Millet, Larry J.; Castan-Laurell, Isabelle; Müller, Cathérine; Dray, Cédric; Schaeffer, Paul; Hérault, Jean-Pascal; Savi, Pierre; Bono, Françoise; Valet, Philippe

doi:10.1096/fj.07-104018

Cited by 113 publications

(87 citation statements)

References 34 publications

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“…The VEGF receptor-2 (KDR) gene, encoding an early marker of endothelial cell differentiation, was also decreased ( 28 ). Interestingly, the APJ receptor (Agtrl1), which is part of the apelin/APJ-R signaling system that plays a critical role in the development of a functional network in WAT ( 29 ), is equally decreased in the 6HFD-fed mice. Last, but not least, expression of adiponectin (Adipoq), which has been reported to promote proliferation and function of endothelial cells ( 30 ), So far, studies have been mainly focused on the relationships between diet-induced obesity in female rodents and the development of adult offspring adiposity and associated diseases ( 46,47 ).…”

Section: Genes Regulated By Regimenmentioning

confidence: 99%

A Western-like fat diet is sufficient to induce a gradual enhancement in fat mass over generations

Massiéra

Barbry

Guesnet

et al. 2010

Journal of Lipid Research

166

128

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This article is available online at http://www.jlr.org able to genetic factors as it has occurred relatively recently and is observed in a wide range of human populations. High-fat diets are considered to be obesogenic in that they produce a consistent increase in fat mass that is directly related to the content of the diet and duration of feeding. However, the contribution of dietary fats compared with an excess energy intake in increasing body weight remains controversial, as no major change in the total amount of ingested fats has occurred in the last two decades ( 1, 2 ).In addition to caloric excess, a qualitative issue has emerged as a risk factor for obesity in rodents and possibly in humans; i.e., the disequilibrium in polyunsaturated fatty acid (PUFA) metabolism with a high ratio of linoleic acid (C18:2 6, LA) versus ␣ -linolenic acid (C18:3 3, LNA) ( 3 ). Notably, in rodents, reducing this ratio from 59 to 2 under isolipidic, isoenergetic conditions (40% energy as fat) by inclusion of dietary LNA counteracted the enhancing effects of LA on body weight and fat mass, which then became similar to that observed with a chow diet ( 4 ).6 PUFAs were more potent than 3 PUFAs in promoting adipogenesis ( 5-7 ). When combined with high carbohydrate content, a linoleic acid-enriched diet was found to be pro-adipogenic in vivo through cAMP-dependent signaling ( 8 ). LA acts through arachidonic acid (C20:4 6, ARA) and prostacyclin, as pups from mice invalidated for the prostacyclin receptor (IP-R) and fed a LA-rich diet exhibit reduced body weight and fat mass compared with wild-type mice fed the same diet ( 4 ). Overall, these results emphasize the importance of adipose tissue development Abstract The prevalence of obesity has steadily increased over the last few decades. During this time, populations of industrialized countries have been exposed to diets rich in fat with a high content of linoleic acid and a low content of ␣ -linolenic acid compared with recommended intake. To assess the contribution of dietary fatty acids, male and female mice fed a high-fat diet (35% energy as fat, linoleic acid: ␣ -linolenic acid ratio of 28) were mated randomly and maintained after breeding on the same diet for successive generations. Offspring showed, over four generations, a gradual enhancement in fat mass due to combined hyperplasia and hypertrophy with no change in food intake. Transgenerational alterations in adipokine levels were accompa nied by hyperinsulinemia. Gene expression analyses of the stromal vascular fraction of adipose tissue, over generations, revealed discrete and steady changes in certain important players, such as CSF3 and Nocturnin. Thus, under conditions of genome stability and with no change in the regimen over four generations, we show that a Western-like fat diet induces a gradual fat mass enhancement, in accordance with the increasing prevalence of obesity observed in humans. -Massiera, F., P. Barbry, P. Guesnet, A. Joly, S. The prevalence of obesity and the risk of developing associated diseases ha...

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Section: Genes Regulated By Regimenmentioning

confidence: 99%

A Western-like fat diet is sufficient to induce a gradual enhancement in fat mass over generations

Massiéra

Barbry

Guesnet

et al. 2010

Journal of Lipid Research

166

128

View full text Add to dashboard Cite

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“…The apelin-APJ conjugate is widely distributed throughout human tissues, including adipose, brain, liver, lung, and heart, and its expression profile is similar to that of the angiotensin II (Ang II)-angiotensin II type 1 (AT1) receptor complex [3]. In adipose tissue, the apelin/APJ signaling pathway was demonstrated to play a key role in the development of the functional vascular network [4]. As to the cardiovascular system, apelin could protect the heart against ischemia reperfusion injury and induce nitric oxide-dependent arterial vasodilation [5].…”

Section: Introductionmentioning

confidence: 99%

Increased apelin serum levels and expression in human chondrocytes in osteoarthritic patients

Tang

Chen

et al. 2010

International Orthopaedics (SICOT)

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Apelin is a recently discovered hormone secreted by adipocytes. The aim of this study, therefore, was to evaluate the distribution of apelin in paired serum and synovial fluid (SF) of osteoarthritis (OA) patients, as compared to that in healthy controls, and to characterise the expression profile of apelin and its cognate receptor APJ in human chondrocytes. Apelin levels in serum and SF were analysed by enzyme-linked immunosorbent assay (ELISA). Expression of apelin and APJ in human chondrocytes was determined by real-time quantitative polymerase chain reaction (PCR). Apelin was found to be present in OA SF, and concentrations were positively correlated with the severity of OA. OA serum exhibited significantly elevated levels of apelin (2.18±0.22 ng/ml) as compared to normal serum (1.31±0.12 ng/ml) (p<0.05), and serum apelin levels exceeded those in paired SF (p < 0.001). The apelin and APJ transcripts were identified in chondrocytes, and levels were significantly higher in OA cartilage than in healthy donors. These findings suggest that apelin may contribute to the onset and/or progression of OA, and may provide new insights into the pathophysiology of OA.

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“…The overproduction of apelin observed in obesity has been suggested to be an adaptive response that attempts to prevent the onset of obesity related disorders. Thus, current research focuses on the potential link of apelin with obesity associated insulin resistance [117].…”

Section: Apelinmentioning

confidence: 99%

Adipocytokines in Particular Pregnancy Disorders

Canverenler¹

2015

Ann Clin Lab Res

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Apelin/APJ signaling system: a potential link between adipose tissue and endothelial angiogenic processes

Cited by 113 publications

References 34 publications

A Western-like fat diet is sufficient to induce a gradual enhancement in fat mass over generations

A Western-like fat diet is sufficient to induce a gradual enhancement in fat mass over generations

Increased apelin serum levels and expression in human chondrocytes in osteoarthritic patients

Adipocytokines in Particular Pregnancy Disorders

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