Apelin receptors: From signaling to antidiabetic strategy

Chaves-Almagro, Carline; Castan-Laurell, Isabelle; Dray, Cédric; Knauf, Claude; Valet, Philippe; Masri, Bernard

doi:10.1016/j.ejphar.2015.05.017

Cited by 85 publications

(83 citation statements)

References 135 publications

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“…Here, we discovered that central apelin exerts inverse effect on BAT function as opposed to its direct effects on the brown adipogenic capacity and browning28. This last result fits with the concept that we have previously highlighted demonstrating that over-expression of apelin in the brain participates to the establishment of T2D305051. Therefore, we speculate that the decrease in energy expenditure observed in these mice might be explained by the reduced expression of key factors characterizing BAT activity.…”

Section: Discussionsupporting

confidence: 89%

Central chronic apelin infusion decreases energy expenditure and thermogenesis in mice

Drougard

Fournel

Marlin

et al. 2016

Sci Rep

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Apelin is a bioactive peptide involved in the control of energy metabolism. In the hypothalamus, chronic exposure to high levels of apelin is associated with an increase in hepatic glucose production, and then contributes to the onset of type 2 diabetes. However, the molecular mechanisms behind deleterious effects of chronic apelin in the brain and consequences on energy expenditure and thermogenesis are currently unknown. We aimed to evaluate the effects of chronic intracerebroventricular (icv) infusion of apelin in normal mice on hypothalamic inflammatory gene expression, energy expenditure, thermogenesis and brown adipose tissue functions. We have shown that chronic icv infusion of apelin increases the expression of pro-inflammatory factors in the hypothalamus associated with an increase in plasma interleukin-1 beta. In parallel, mice infused with icv apelin exhibit a significant lower energy expenditure coupled to a decrease in PGC1alpha, PRDM16 and UCP1 expression in brown adipose tissue which could explain the alteration of thermogenesis in these mice. These data provide compelling evidence that central apelin contributes to the development of type 2 diabetes by altering energy expenditure, thermogenesis and fat browning.

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Section: Discussionsupporting

confidence: 89%

Central chronic apelin infusion decreases energy expenditure and thermogenesis in mice

Drougard

Fournel

Marlin

et al. 2016

Sci Rep

View full text Add to dashboard Cite

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“…Also, the ERK/Akt-p70S6K pathway regulates cell proliferation (Masri et al, 2004; Liu et al, 2010; Langelaan et al, 2013). It has been recently shown that a heterodimer is formed with APJ and K -opioid receptors and this leads to the phosphorylation of ERK, resulting in increasing cell proliferation (Li et al, 2012; Chaves-Almagro et al, 2015). Moreover, APJ/apelin system induces intercellular adhesion molecule-1 (ICAM-1) expression via the NF-κB/c-Jun N-terminal kinase (JNK) signal pathway (Lu et al, 2012).…”

Section: The Downstream and Upstream Factors Of Apelin/apjmentioning

confidence: 99%

“…Each isoform has distinct activity and the shorter isoform is a more potent activator for APJ. Both apelin-13 and apelin-17 have much stronger activity than apelin-36 (Kawamata et al, 2001; De Mota et al, 2004; Chaves-Almagro et al, 2015). The receptor binding affinities of apelin-13 and apelin-36 are different, which causes different intracellular signaling of APJ.…”

Section: Introductionmentioning

confidence: 97%

The Role of the Apelin/APJ System in the Regulation of Liver Disease

Kong

Chen

et al. 2017

Front. Pharmacol.

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Apelin is an endogenous peptide that is a ligand for the APJ receptor (angiotensin II receptor like-1, AT-1). The apelin/APJ system is distributed in diverse periphery organ tissues. It has been shown that the apelin/APJ system plays various roles in physiology and pathophysiology of many organs. It regulates cardiovascular development or cardiac disease, glycometabolism and fat metabolism as well as metabolic disease. The apelin/APJ system participates in various cell activities such as proliferation, migration, apoptosis or inflammation. However, apelin/APJ function in the liver is still under investigation. In the liver, the apelin-APJ system could play an inhibitory role in liver regeneration and promote Fas-induced apoptosis. It may participate in the formation of hepatic fibrosis or cirrhosis, and even cancer. In this review, we summarize the role of the apelin/APJ system in liver disease.

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“…Studies demonstrated that both short-and long-term apelin treatments improve insulin sensitivity in obese and insulin-resistant mice mainly by increasing glucose uptake in skeletal muscle (9)(10)(11). Apelin also modulates insulin secretion and increases pancreatic islet cell mass and b-cell insulin content in mice (12).…”

mentioning

confidence: 99%

“…Recently, apelin has been extensively described as a beneficial factor regarding glucose metabolism and as endowed with antidiabetes properties (9,10). Studies demonstrated that both short-and long-term apelin treatments improve insulin sensitivity in obese and insulin-resistant mice mainly by increasing glucose uptake in skeletal muscle (9)(10)(11).…”

mentioning

confidence: 99%

Apelin Controls Fetal and Neonatal Glucose Homeostasis and Is Altered by Maternal Undernutrition

et al. 2015

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The adequate control of glucose homeostasis during both gestation and early postnatal life is crucial for the development of the fetoplacental unit and adaptive physiological responses at birth. Growing evidences indicate that apelin and its receptor, APJ, which are expressed across a wide range of tissues, exert important roles in glucose homeostasis in adults. However, little is known about the function of the apelinergic system during gestation. In this study, we evaluated the activity of this system in rats, the role of apelin in fetal and neonatal glucose homeostasis, and its modulation by maternal food restriction. We found that 1) the apelinergic system was expressed at the fetoplacental interface and in numerous fetal tissues, 2) ex vivo, the placenta released high amounts of apelin in late gestation, 3) intravenous apelin injection in mothers increased the transplacental transport of glucose, and 4) intraperitoneal apelin administration in neonates increased glucose uptake in lung and muscle. Maternal food restriction drastically reduced apelinemia in both mothers and growth-restricted fetuses and altered the expression of the apelinergic system at the fetoplacental interface. Together, our data demonstrate that apelin controls fetal and neonatal glucose homeostasis and is altered by fetal growth restriction induced by maternal undernutrition.

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Apelin receptors: From signaling to antidiabetic strategy

Cited by 85 publications

References 135 publications

Central chronic apelin infusion decreases energy expenditure and thermogenesis in mice

Central chronic apelin infusion decreases energy expenditure and thermogenesis in mice

The Role of the Apelin/APJ System in the Regulation of Liver Disease

Apelin Controls Fetal and Neonatal Glucose Homeostasis and Is Altered by Maternal Undernutrition

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