Effect of a high-protein breakfast on the postprandial ghrelin response

Abstract

The HP breakfast decreased postprandial ghrelin concentrations more strongly over time than did the HC breakfast. High associations between ghrelin and glucose-dependent insulinotropic polypeptide and glucagon suggest that stimulation of these peptides may mediate the postprandial ghrelin response. The HP breakfast also reduced gastric emptying, probably through increased secretion of cholecystokinin and glucagon-like peptide 1.

Effect of the glycemic index of carbohydrates on day-long (10 h) profiles of plasma glucose, insulin, cholecystokinin and ghrelin

“…There was no correlation, however, between GHR and blood glucose concentration in this study. In some studies, but not others (Blom et al, 2006), protein ingestion increased postprandial GHR secretion (Erdmann et al, 2006). The protein in the meals in this study may therefore have partly masked any inhibitory effect of carbohydrate.…”

“…While the acute control of feeding is partly mediated by gut peptides such as cholecystokinin (CCK) and ghrelin (GHR) (Tschop et al, 2000;Wren and Bloom, 2007), the macronutrient composition of a food is a recognized determinant of feeding drive. Dietary protein is the most satiating macronutrient in experimental meal settings (Poppitt et al, 1998), with high-protein meals increasing blood concentrations of CCK (Blom et al, 2006;Bowen et al, 2006). Fat (Matzinger et al, 1999) and to a lesser extent carbohydrate (Holt et al, 1992;Parker et al, 2005) also stimulate CCK production from I cells in the duodenum and jejunum (Buffa et al, 1978).…”

Safety, tolerability and pharmacokinetics of intravenous ghrelin for cancer-related anorexia/cachexia: a randomised, placebo-controlled, double-blind, double-crossover study

“…A high intrapatient variability of symptoms and nutritional intake is reported in patients with advanced, incurable cancer (Stromgren et al, 2006). Baseline food intake (Gilg and Lutz, 2006) and dietary patterns with high protein or liquid intake (Blom et al, 2006) may influence ghrelin regulation. Drugs for symptom control (eg, haloperidol (Jaszberenyi et al, 2006), 5-HT-3 antagonist ) may interact with ghrelin metabolism.…”

“…The limitations of this study design include the lack of chronic efficacy data beyond two weekly infusions; namely, body composition (lean body mass, fat mass (Theander-Carrillo et al, 2006)), objective subconscious locomotive motor and physical activity (Jaszberenyi et al, 2006), energy expenditure measurements (Lejeune et al, 2006), and gastrointestinal motility (Binn et al, 2006;Blom et al, 2006). Our results on dose responsiveness may be influenced by unbalanced groups: UD patients had more metastases, greater weight loss, lower dietary intake, more early satiety, and were closer to death.…”

“…The safety and tolerability data support further exploration of the therapeutic potential of natural ghrelin, namely escalation of dose and frequency and chronic administration. The patient population may be stratified for baseline ghrelin levels (Garcia et al, 2005;Wolf et al, 2006), and other factors need to be controlled for, namely genetic alterations of the ghrelin gene (Holst and Schwartz, 2006), cytokine levels (Dixit et al, 2004), stress level (Kristenssson et al, 2006), hypogonadism (Strasser et al, 2006), patients' eating preferences (Blom et al, 2006), baseline food intake (Gilg and Lutz, 2006), and gastric emptying (Binn et al, 2006). These strategies may counteract the series of many negative cachexia phase III trials (EPA, cannabinoids) or single not confirmed studies (ATP, thalidomide), treating uniformly all patients having loss of weight and appetite, despite promising pathophysiological concepts.…”