Ghrelin Interacts with Human Plasma Lipoproteins

Vriese, Carine De; Hacquebard, Mirjam; Grégoire, Françoise; Carpentier, Yvon; Delporte, Christine

doi:10.1210/en.2006-1281

Cited by 99 publications

(57 citation statements)

References 41 publications

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“…Moreover, transcript levels of MBOAT4 in omental adipose tissue were positively associated with serum LDL-cholesterol. Interestingly, LDL-cholesterol interacts with acylated ghrelin, and a plausible role of triacylglycerol-rich LDL-and HDLcholesterol particles as ghrelin transporters in the bloodstream has been suggested [37]. Although correlation does not imply causality, the association between GOAT and LDL-cholesterol may reflect an increased transport of ghrelin into the bloodstream, thereby contributing to the high levels of circulating acylated ghrelin in insulin resistance.…”

Section: Discussionmentioning

confidence: 99%

The ghrelin O-acyltransferase–ghrelin system reduces TNF-α-induced apoptosis and autophagy in human visceral adipocytes

et al. 2012

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Aims/hypothesis Proinflammatory and proapoptotic cytokines such as TNF-α are upregulated in human obesity. We evaluated the association between ghrelin isoforms (acylated and desacyl ghrelin) and TNF-α in obesity and obesity-associated type 2 diabetes, as well as the potential role of ghrelin in the control of apoptosis and autophagy in human adipocytes. Methods Plasma concentrations of the ghrelin isoforms and TNF-α were measured in 194 participants. Ghrelin and ghrelin O-acyltransferase (GOAT) levels were analysed by western-blot, immunohistochemistry and real-time PCR in 53 biopsies of human omental adipose tissue. We also determined the effect of acylated and desacyl ghrelin (10 to 1,000 pmol/l) on TNF-α-induced apoptosis and autophagy-related molecules in omental adipocytes. Results Circulating concentrations of acylated ghrelin and TNF-α were increased, whereas desacyl ghrelin levels were decreased in obesity-associated type 2 diabetes. Ghrelin and GOAT were produced in omental and subcutaneous adipose tissue. Visceral adipose tissue from obese patients with type 2 diabetes showed higher levels of GOAT, increased adipocyte apoptosis and increased expression of the autophagyrelated genes ATG5, BECN1 and ATG7. In differentiating Diabetologia (2012) human omental adipocytes, incubation with acylated and desacyl ghrelin reduced TNF-α-induced activation of caspase-8 and caspase-3, and cell death. In addition, acylated ghrelin reduced the basal expression of the autophagyrelated genes ATG5 and ATG7, while desacyl ghrelin inhibited the TNF-α-induced increase of ATG5, BECN1 and ATG7 expression. Conclusions/interpretation Apoptosis and autophagy are upregulated in human visceral adipose tissue of patients with type 2 diabetes. Acylated and desacyl ghrelin reduce TNF-α-induced apoptosis and autophagy in human visceral adipocytes.

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Section: Discussionmentioning

confidence: 99%

The ghrelin O-acyltransferase–ghrelin system reduces TNF-α-induced apoptosis and autophagy in human visceral adipocytes

et al. 2012

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“…In mammals, ghrelin is derived from a 117-amino-acid polypeptide termed pro-ghrelin, following cleavage after the 28th amino acid residue by prohormone convertase 1 [20]. It circulates in the bloodstream, bound to lipoproteins [21]. A portion of ghrelin has a fatty acid modification, an n-octanoylation, attached to the serine at position 3.…”

Section: Ghrelinmentioning

confidence: 99%

Ghrelin and feeding behaviour in preterm infants

Savino¹,

Lupica²,

Liguori³

et al. 2012

Early Human Development

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a b s t r a c t a r t i c l e i n f o Available online xxxx Keywords: Ghrelin Feeding behaviour Preterm infantThe importance of early life events in the development of metabolic diseases is well recognized. Early postnatal environment, including nutrition, is key to future health, and this is particularly true for preterm infants. It is important that these infants receive sufficient nutrients to prevent growth restriction and promote neurodevelopment, while minimizing predisposition to metabolic diseases later in life. Feeding habits are the fundamental elements of nutrition and are influenced by many factors, including personal and familial habits, socioeconomic status, and cultural environment. In the last decades, there has been an important scientific interest toward the comprehension of the molecular and neural mechanisms regulating appetite. In these networks, act many peptide hormones produced in brain or gut, among which ghrelin is important because of its action in the short-term regulation of food intake and the long-term regulation of body weight. Ghrelin stimulates appetite and plays a role in regulating feeding behaviour. Ghrelin levels vary from fetal life through to early adulthood, with the highest levels observed in the very early years. Cord ghrelin levels have been evaluated in term and preterm newborns and high ghrelin levels have been observed in smallfor-gestational age newborns and in newborns with intrauterine growth restriction. Moreover, ghrelin has been detected in term and preterm human breast milk, suggesting that it may play a role in the development of neuroendocrine pathways regulating appetite and energy homeostasis in early life. However, more research is required to better define ghrelin's role in breast milk and on feeding behaviour.

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“…Regarding the second theory, numerous enzymes were proposed to be responsible for this deacylation. It has been demonstrated that ghrelin is deacylated in human serum by butyrylcholinesterase and platelet-activating factor acetylhydrolase, while in rat serum only carboxylesterase is involved [40]. Paraoxonase may also intervene in ghrelin deacylation, although there is controversy about this issue [9,40].…”

Section: Ghrelin Gene-derived Peptides In Circulationmentioning

confidence: 99%

“…It has been demonstrated that ghrelin is deacylated in human serum by butyrylcholinesterase and platelet-activating factor acetylhydrolase, while in rat serum only carboxylesterase is involved [40]. Paraoxonase may also intervene in ghrelin deacylation, although there is controversy about this issue [9,40]. Interestingly, these enzymes are associated with serum lipoproteins, which also participate in the transport of circulating ghrelin (see below).…”

Section: Ghrelin Gene-derived Peptides In Circulationmentioning

confidence: 99%

Ghrelin, des-acyl ghrelin and obestatin: Three pieces of the same puzzle

2008

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a b s t r a c tThe major active product of ghrelin gene is a 28-amino acid peptide acylated at the serine 3 position with an octanoyl group, called simply ghrelin. Ghrelin has a multiplicity of physiological functions, affecting GH release, food intake, energy and glucose homeostasis, This suggests the existence of a novel endocrine system with multiple effector elements which not only may have opposite actions but may regulate the action of each other. In this review, we summarize the steps which lead to the production of the different ghrelin gene products and examine the most significant differences between them in terms of structure and actions.

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Ghrelin Interacts with Human Plasma Lipoproteins

Cited by 99 publications

References 41 publications

The ghrelin O-acyltransferase–ghrelin system reduces TNF-α-induced apoptosis and autophagy in human visceral adipocytes

The ghrelin O-acyltransferase–ghrelin system reduces TNF-α-induced apoptosis and autophagy in human visceral adipocytes

Ghrelin and feeding behaviour in preterm infants

Ghrelin, des-acyl ghrelin and obestatin: Three pieces of the same puzzle

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