Ghrelin Gene‐Related Peptides Modulate Rat White Adiposity

Giovambattista, Andrés; Gaillard, Rolf C.; Spinedi, Eduardo

doi:10.1016/s0083-6729(06)77008-x

Cited by 49 publications

(52 citation statements)

References 102 publications

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“…51 In line with this, our findings show that acylated and desacyl ghrelin treatment reduced adipophilin levels, the protein surrounding lipid droplets of preadipocytes, and increased the expression of perilipin, the protein coating lipid droplets in mature adipocytes. On the basis of our results, as well as on the studies carried out in experimental models, [19][20][21] it can be concluded that acylated and desacyl ghrelin directly increase adiposity in human visceral adipocytes, independently of its orexigenic action.…”

Section: Discussionsupporting

confidence: 66%

“…6,[9][10][11] Earlier studies suggest that the adipose tissue also constitutes an important target for the adipogenic actions of ghrelin in rodents. 19,21 This study has explored whether acylated and desacyl ghrelin directly act on visceral adipose tissue for regulating adipocyte metabolism in humans. The main findings are that: (1) circulating acylated ghrelin concentrations are increased in obese patients; (2) GHS-R 1a is expressed in omental adipose tissue; (3) the expression of this ghrelin receptor is decreased in obesity and obesityassociated T2D; and (4) acylated and desacyl ghrelin stimulate lipid accumulation in human visceral adipocytes.…”

Section: Discussionmentioning

confidence: 99%

“…6,18 Moreover, it has been suggested that acylated ghrelin directly acts on adipocytes for stimulating adipogenesis in rodents. [19][20][21] Nonetheless, these data are not univocal, as other authors have reported that overexpression of ghrelin inhibits adipocyte differentiation in 3T3-L1 adipocytes, and that the genetic deletion of ghrelin or its receptor in mice induces thymic adipogenesis. 22,23 These contradictory observations raise some questions regarding the involvement of ghrelin in the control of adipocyte metabolism.…”

Section: Introductionmentioning

confidence: 96%

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Acylated and desacyl ghrelin stimulate lipid accumulation in human visceral adipocytes

et al. 2009

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Objectives: The orexigenic hormone ghrelin circulates mainly in two forms, acylated and desacyl ghrelin. We evaluated the impact of obesity and obesity-associated type 2 diabetes (T2D) on ghrelin forms and the potential role of acylated and desacyl ghrelin in the control of adipogenesis in humans. Methods: Plasma concentrations of the different ghrelin forms were measured in 80 subjects. The expression of the ghrelin receptor (growth hormone secretagogue receptor, GHS-R) was analyzed in omental adipose tissue using western blot and immunohistochemistry, and the effect of acylated ghrelin and desacyl ghrelin (0.1-1000 pmol l À1 ) on adipogenesis was determined in vitro in omental adipocytes. Results: Circulating concentrations of acylated ghrelin were increased, whereas desacyl ghrelin levels were decreased, in obesity and obesity-associated T2D. Body mass index, waist circumference, insulin and HOMA (homeostasis model assessment) index were positively correlated with acylated ghrelin levels. Obese individuals showed a lower protein expression of GHS-R in omental adipose tissue. In differentiating omental adipocytes, incubation with both acylated and desacyl ghrelin significantly increased PPARg (peroxisome proliferator-activated receptor g) and SREBP1 (sterol-regulatory element binding protein-1) mRNA levels, as well as several fat storage-related proteins, including acetyl-CoA carboxylase, fatty acid synthase, lipoprotein lipase and perilipin. Consequently, both the ghrelin forms stimulated intracytoplasmatic lipid accumulation. Conclusions: Both acylated and desacyl ghrelin stimulate lipid accumulation in human visceral adipocytes. Given the lipogenic effect of acylated ghrelin on visceral adipocytes, the herein-reported elevation of its circulating concentrations in obese individuals may play a role in excessive fat accumulation in obesity.

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Section: Discussionsupporting

confidence: 66%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 96%

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Acylated and desacyl ghrelin stimulate lipid accumulation in human visceral adipocytes

et al. 2009

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“…APC differentiation is highly modulated by endocrine and metabolic factors such as insulin and glucocorticoid (GC) working either individually or in combination [19] . On the other hand, WAT mass expansion could result from either cell tissue hyperplasia (increased number of normal mature "small-size" adipocytes) or their hypertrophy (increase in the size of dysfunctional adipocytes).…”

Section: Looking For a Dysfunctional Starting Pointmentioning

confidence: 99%

White Adipose Tissue and Circadian Rhythm Dysfunctions in Obesity: Pathogenesis and Available Therapies

2016

Self Cite

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A combined neuroendocrine, metabolic, and chronobiological view can help to better understand the multiple and complex mechanisms involved in obesity development and maintenance, as well as to provide new effective approaches for its control and treatment. Indeed, we have currently updated data on the whole adipogenic process involved in white adipose tissue (WAT) mass expansion, namely due to a mechanism whereby WAT cells become hypertrophic, thus inducing a serious local (WAT) inflammatory condition that in turn, will impair not only the cross-talk between the hypothalamus and the WAT, but also favoring the development of deep and widespread neuroendocrine-metabolic dysfunction. Moreover, we also have revisited the circadian clock genes involved in dysfunctional WAT mass expansion and the mechanisms that may lead to obesity development, including early metabolic dysfunctions, enhanced oxidative stress and distorted energy homeostasis. The epigenetic changes of clock genes driving metabolic disease and obesity development have also been included in this review. Finally, we have also underlined the relevance of metabolic homeostasis regulation by central and peripheral organ clocks, sleep disturbances, nutrients, and feeding time, as key factors in obesity development as well as both, classical and chronotherapeutic approaches for its prevention and treatment.

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“…Both peptides promote the differentiation of skeletal myoblasts, preadipocytes, and embryonic stem cells toward cardiomyocytes (Filigheddu et al 2007;Gao et al 2012Gao et al , 2013Giovambattista et al 2008;Miegueu et al 2011). Moreover, they affect, either positively or negatively, proliferation of numerous cell types including osteoblasts, pancreatic b cells, islets and islet microendothelial cells, myoblasts, and adrenocortical tumor cells (Delhanty et al 2006(Delhanty et al , 2007Favaro et al 2012;Filigheddu et al 2007;Granata et al 2007).…”

Section: Introductionmentioning

confidence: 99%

Ghrelin Gene Products in Acute and Chronic Inflammation

Prodam,

Filigheddu

2014

Arch. Immunol. Ther. Exp.

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Ghrelin gene products-the peptides ghrelin, unacylated ghrelin, and obestatin-have several actions on the immune system, opening new perspectives within neuroendocrinology, metabolism and inflammation. The aim of this review is to summarize the available evidence regarding the less known role of these peptides in the machinery of inflammation and autoimmunity, outlining some of their most promising therapeutic applications.

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Ghrelin Gene‐Related Peptides Modulate Rat White Adiposity

Cited by 49 publications

References 102 publications

Acylated and desacyl ghrelin stimulate lipid accumulation in human visceral adipocytes

Acylated and desacyl ghrelin stimulate lipid accumulation in human visceral adipocytes

White Adipose Tissue and Circadian Rhythm Dysfunctions in Obesity: Pathogenesis and Available Therapies

Ghrelin Gene Products in Acute and Chronic Inflammation

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