Changes in serum ghrelin predict weight loss after Roux-en-Y gastric bypass in rats

Stylopoulos, Nicholas; Davis, Philip J.; Pettit, Jeffrey; Rattner, David W.; Kaplan, Lee M.

doi:10.1007/s00464-004-8825-x

Cited by 44 publications

(38 citation statements)

References 22 publications

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“…Many studies have shown gastric bypass operations to be associated with significant reduction of ghrelin levels (Cummings et al, 2002a;Geloneze et al, 2003;Lin et al, 2004;Roth et al, 2009;Stylopoulos et al, 2005;Suzuki et al, 2005). In addition, the normal, meal-related fluctuation and the diurnal rhythm of ghrelin level was found to be absent after gastric bypass surgery (Cummings et al, 2002a).…”

Section: Ghrelin and Bariatric Surgerymentioning

confidence: 99%

Ghrelin in obesity and endocrine diseases

Scerif

Goldstone

Korbonits

2011

Molecular and Cellular Endocrinology

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Section: Ghrelin and Bariatric Surgerymentioning

confidence: 99%

Ghrelin in obesity and endocrine diseases

Scerif

Goldstone

Korbonits

2011

Molecular and Cellular Endocrinology

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“…PYY and GLP-1 are satiety signals released by the endocrine L cells of the gastrointestinal tract after meals that have been shown to reduce food intake and body weight gain in obese Zucker rats [43][44][45]. In humans, fasting and post-prandial plasma levels of PYY increase progressively 6 and 12 months after vertical banded gastroplasty surgery [46].…”

Section: Discussionmentioning

confidence: 99%

Increase in Ghrelin Levels After Weight Loss in Obese Zucker Rats is Prevented by Gastric Banding

et al. 2007

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Background Gastric banding is thought to decrease appetite in addition to the mechanical effects of food restriction, although this has been difficult to demonstrate in human studies. Our aim was to investigate the changes in orexigenic signals in the obese Zucker rat after gastric banding. Methods Obese Zucker rats ( fa/fa) were submitted to gastric banding (GBP), sham gastric banding fed ad libitum (sham), or sham operation with food restriction, pair-fed to the gastric banding group (sham-PF). Lean Zucker rats ( fa/+) were used as additional controls. Body weight and food intake were daily recorded for 21 days after surgery when epididymal fat was weighed and fasting ghrelin and hypothalamic NPY mRNA expression were measured. Results Gastric banding in obese Zucker rats resulted in a significant decrease of cumulative body weight gain and food intake. Furthermore, gastric banded rats were leaner than Sham-PF, as expressed by a significantly lower epididymal fat weight. Ghrelin levels of gastric banded rats were not increased when compared to sham-operated animals fed ad libitum and were significantly lower than the levels of weight matched sham-PF rats (1116.9±103.3 g GBP vs 963.2±54.3 g sham, 3,079.5±221.6 sham-PF and 2,969.9±150.9 g lean rats, p<0.001); hypothalamic NPY mRNA expression was not increased in GBP when compared to sham-operated rats. Conclusion In obese Zucker rats, GBP prevents the increase in orexigenic signals that occur during caloric deprivation. Our data support the hypothesis that sustained weight loss observed after gastric banding does not depend solely on food restriction.

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“…Much is known regarding life with chronically reduced ghrelin levels because thousands of individuals have undergone Rouxen-Y gastric bypass surgery, which reduces ghrelin levels by 50-70% for weeks relative to weight-loss controls. Postsurgical ghrelin levels are even lower after total gastrectomy or sleeve gastrectomy (removal of the fundus) and remain so in the long-term (34)(35)(36)(37)(38)(67)(68)(69)(70)(71)(72)(73)(74)(75)(76)(77). The Roux-en-Y gastric bypass and sleeve gastrectomy surgeries both produce massive weight reduction, greater than those of other surgical procedures that less effectively reduce ghrelin levels and improve the health of previously morbidly obese patients with low complication rates (37,78,79).…”

Section: Resultsmentioning

confidence: 99%

“…Subchronic neutralization of the ghrelin molecule with the biostable aptamer l-NOX-B11-2, an l-RNA-spiegelmer based therapeutic, similarly reduced spontaneous food intake and feed efficiency, promoted weight loss, and reduced fat mass (31). Finally, active immunization with Nterminal-inclusive ghrelin haptens slowed weight gain and fat accrual in adult rats in direct relation to the elicited anti-ghrelin antibody response (32).Ghrelin levels increase during voluntary energy restriction (i.e., dieting); these increases predict weight regain and are thought to impede sustained weight loss (7,(33)(34)(35)(36)(37)(38), so new approaches to oppose ghrelin action may be therapeutically important. From a chemical standpoint, ghrelin is the first peptide isolated from natural sources in which the hydroxyl group of a Ser residue (Ser-3) is acylated by n-octanoic acid (3, 39).…”

mentioning

confidence: 99%

“…Ghrelin levels increase during voluntary energy restriction (i.e., dieting); these increases predict weight regain and are thought to impede sustained weight loss (7,(33)(34)(35)(36)(37)(38), so new approaches to oppose ghrelin action may be therapeutically important. From a chemical standpoint, ghrelin is the first peptide isolated from natural sources in which the hydroxyl group of a Ser residue (Ser-3) is acylated by n-octanoic acid (3, 39).…”

mentioning

confidence: 99%

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Catalytic antibody degradation of ghrelin increases whole-body metabolic rate and reduces refeeding in fasting mice

Mayorov

Amara

Chang

et al. 2008

Proc. Natl. Acad. Sci. U.S.A.

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Obesity is a chronic, costly, and globally prevalent condition, with excess caloric intake a suspected etiologic factor. Nonsurgical treatments are modestly efficacious, and weight loss maintenance is hampered by anti-famine homeostatic mechanisms. Ghrelin, a gastric hormone linked to meal initiation, energy expenditure, and fuel partitioning, is hypothesized to facilitate weight gain and impede weight loss. Unique among known animal peptides, the serine-3 residue of ghrelin is posttranslationally acylated with an n-octanoic acid, a modification important for the peptide's active blood-brain transport and growth hormone secretagogue receptor-1 agonist activity. Pharmacological degradation of ghrelin would be hypothesized to reduce ghrelin's biological effects. To study endogenous ghrelin's role in appetite and energy expenditure, we generated antibodies that hydrolyze the octanoyl moiety of ghrelin to form des-acyl ghrelin. The most proficient antibody catalyst, GHR-11E11, was found to display a second-order rate constant of 18 M ؊ 1⅐s ؊1 for the hydrolysis of ghrelin to des-acyl ghrelin. I.v. administration of GHR-11E11 (50 mg/kg) maintained a greater metabolic rate in fasting C57BL/6J mice as compared with mice receiving a control antibody and suppressed 6-h refeeding after 24 h of food deprivation. Indirect respiratory measures of metabolism after refeeding and relative fuel substrate utilization were unaffected. The results support the hypothesis that acylated ghrelin stimulates appetite and curbs energy expenditure during deficient energy intake, whereas des-acyl ghrelin does not potently share these functions. Catalytic anti-ghrelin antibodies might thereby adjunctively aid consolidation of caloric restrictioninduced weight loss and might also be therapeutically relevant to Prader-Willi syndrome, characterized after infancy by hyperghrelinemia, hyperphagia, and obesity.hormone inactivation ͉ obesity ͉ neuropeptides A pproximately 1 billion people worldwide are overweight or obese (body mass index ϭ 25-29.9 or Ͼ30 kg/m 2 , respectively) (1), conditions associated with significant morbidity and mortality and for which new treatments are needed (2). Among recently characterized molecules implicated in energy homeostasis, ghrelin was identified in 1999 during a search for the endogenous ligand for the GH secretagogue receptor (GHSR) (ghrelin receptor), previously localized to peripheral tissues and to several CNS sites, including the arcuate nucleus and ventromedial hypothalamic nucleus (3). Human ghrelin is a 28-amino acid acylated peptide (GSS(n-octanoyl)FLSPEHQRVQQRKESKKPPAKLQPR) released mainly from endocrine cells of the stomach and upper gastrointestinal tract but also expressed in testes, kidney, pituitary, pancreas, lymphocytes, and brain (3-7). Several findings establish gastric ghrelin as an indicator of energy insufficiency and anabolic modulator of energy homeostasis (3). Ghrelin secretion is thought to stimulate food intake, slow metabolic rate, and spare lipid oxidation via central (8) and, possi...

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Changes in serum ghrelin predict weight loss after Roux-en-Y gastric bypass in rats

Cited by 44 publications

References 22 publications

Ghrelin in obesity and endocrine diseases

Ghrelin in obesity and endocrine diseases

Increase in Ghrelin Levels After Weight Loss in Obese Zucker Rats is Prevented by Gastric Banding

Catalytic antibody degradation of ghrelin increases whole-body metabolic rate and reduces refeeding in fasting mice

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