Control of body weight: a physiologic and transgenic perspective

Frühbeck, Gema; Gómez-Ambrosi, Javier

doi:10.1007/s00125-003-1053-4

Cited by 104 publications

(80 citation statements)

References 203 publications

(252 reference statements)

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“…BMI was calculated as weight in kilograms divided by the square of height in meters. Obesity was defined as a BMI of ≥30 kg/ m 2 and normal weight as a BMI of <25 kg/m 2 . Obese patients were sub-classified into three groups (normoglycaemia, impaired glucose tolerance or type 2 diabetes) following the criteria of the Expert Committee on the Diagnosis and Classification of Diabetes [18].…”

Section: Methodsmentioning

confidence: 99%

“…Ghrelin, a 28 amino-acid peptide with an n-octanoyl group at the serine 3 residue, is the endogenous ligand of the growth hormone secretagogue receptor (GHS-R) [1,2]. Ghrelin is synthesised predominantly in X/A cells of the oxyntic glands in the mucosa layer of the gastric fundus and secreted to the bloodstream in two major forms: acylated (∼5% of total ghrelin) and desacyl ghrelin (the form lacking n-octanoylation and representing ∼95% of total ghrelin) [1,3,4].…”

Section: Introductionmentioning

confidence: 99%

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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: Methodsmentioning

confidence: 99%

Section: Introductionmentioning

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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“…The balance between these factors is crucial for determining homeostasis (Frühbeck and Gómez-Ambrosi 2003;Leal Vde and Mafra 2013;Ouchi et al 2011). In states of obesity, we have previously described that adipose tissue produces higher levels of novel adipokines including chemerin, chitinase-3-like protein 1 (YKL-40), lipocalin-2 (LCN-2) and osteopontin (OPN) (Catalán et al 2009(Catalán et al , 2011(Catalán et al , 2013Gómez-Ambrosi et al 2007).…”

Section: Introductionmentioning

confidence: 99%

Peripheral mononuclear blood cells contribute to the obesity-associated inflammatory state independently of glycemic status: involvement of the novel proinflammatory adipokines chemerin, chitinase-3-like protein 1, lipocalin-2 and osteopontin

et al. 2015

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Inflammation is a critical contributor to the pathogenesis of metabolic disorders with adipose tissue being crucial in the inflammatory response by releasing multiple adipokines with either pro-or anti-inflammatory activities with potential functions as metabolic regulators. Peripheral blood mononuclear cells (PBMC) have been proposed as representative of the inflammatory status in obesity. The aim of the present study was to evaluate the contribution of PBMC to the obesity-associated chronic inflammation analyzing the expression of novel adipokines. Samples obtained from 69 subjects were used in the study. Real-time PCR determinations were performed to quantify gene expression levels in PBMC of novel adipokines including chemerin, chitinase-3-like protein 1 (YKL-40), lipocalin-2 (LCN-2) and osteopontin (OPN), and their circulating concentrations were also determined by ELISA. We show, for the first time, that PBMC gene expression levels of chemerin (P \ 0.0001), chitinase-3-like protein 1 (P = 0.010), lipocalin-2 (P \ 0.0001) and osteopontin (P \ 0.0001) were strongly upregulated in obesity independently of the glycemic state. Circulating concentrations of these adipokines followed the same trend being significantly higher (P \ 0.05) in obese normoglycemic and type 2 diabetic patients compared to lean volunteers and also associated (P \ 0.05) with their corresponding mRNA levels in PBMC. These results provide evidence that alterations in inflammation-related adipokines are manifest in PBMC, which might contribute to the low-grade chronic inflammation that characterizes obesity.

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“…leptin, CCK, GLP1) of energy intake are more vulnerable to disruption than the physiological regulators of energy expenditure. 5,6 In contrast to the rapid progress at the molecular level, our understanding of precisely how the modern obesogenic environment so readily undermines the innate control of energy balance has progressed remarkably little and, although some epidemiological studies have linked dietary energy density or low levels of physical activity with weight gain, the data are not consistent. 7 One reason is that almost all appetite research has employed very short-term experimental approaches involving the 'pre-load and test-meal' paradigm often performed within a single day.…”

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confidence: 99%

Variability of appetite control mechanisms in response to 9 weeks of progressive overfeeding in humans

et al. 2006

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Background:The current epidemic of obesity demonstrates that mechanisms for maintaining human energy balance are readily subverted by adverse environmental conditions. The critical elements of this dysregulation are poorly understood. Most previous research into what regulates the intake side of the energy balance equation has been handicapped by the use of short-term within-day experimental tests. Objective: We enrolled six non-obese men to a 17-week protocol involving three 21 days periods of progressive overfeeding ( þ 20, þ 40 and þ 60%) separated by free diet periods to test for compensatory satiety. Results: Responses to overfeeding differed markedly with evidence of 'compensators' and 'non-compensators', but on average, subsequent food intake was stimulated rather than suppressed after overfeeding in spite of markedly elevated body fat ( þ 13%) and fasting leptin ( þ 116%).

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Control of body weight: a physiologic and transgenic perspective

Cited by 104 publications

References 203 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

Peripheral mononuclear blood cells contribute to the obesity-associated inflammatory state independently of glycemic status: involvement of the novel proinflammatory adipokines chemerin, chitinase-3-like protein 1, lipocalin-2 and osteopontin

Variability of appetite control mechanisms in response to 9 weeks of progressive overfeeding in humans

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