1.
Influence of age, gender, and glucose tolerance on fasting and fed acylated ghrelin in Prader Willi syndrome.
Prodam, F, Bellone, S, Grugni, G, Crinò, A, Ragusa, L, Franzese, A, Di Battista, E, Corrias, A, Walker, G, Rapa, A, et al
Clinical nutrition (Edinburgh, Scotland). 2009;(1):94-9
Abstract
BACKGROUND & AIMS Prader Willi syndrome (PWS) is a genetic syndrome characterized by hyperphagia, morbid obesity, relative hypoinsulinemia and normal insulin sensitivity. PWS presents higher total (TG) and acylated ghrelin (AG) levels. The cause of this increase as well as the modulation of ghrelin secretion in fasting and feeding in relation to other metabolic parameters and glucose tolerance in PWS is largely unknown. METHODS We studied TG and AG at fasting in PWS children (14) and adults (18). We also studied TG and AG response to a mixed standardized light breakfast (SLB) in PWS adults without (AD-GT) and with glucose intolerance (AD-GI) at OGTT. RESULTS TG and AG were higher in children than in adults (p<0.05). AG was higher in adult males (p<0.001). Fasting AG and AG/TG ratio were lower in AD-GI than in AD-GT (p<0.05). TG, but not AG, decreased in AD-GT (p<0.006), whereas AG, but not TG, increased in AD-GI (p<0.03) post-SLB. Fasting TG and AG were negatively predicted by fasting insulin (p<0.05). Post-SLB AG was positively predicted by glucose during OGTT (p<0.04). CONCLUSIONS Fasting and post-meal AG levels are influenced by glucose tolerance in PWS, suggesting that AG derangement might have a role in the development of glucose intolerance.
2.
The nutritional control of ghrelin secretion in humans: the effects of enteral vs. parenteral nutrition.
Prodam, F, Me, E, Riganti, F, Gramaglia, E, Bellone, S, Baldelli, R, Rapa, A, van der Lely, AJ, Bona, G, Ghigo, E, et al
European journal of nutrition. 2006;(7):399-405
Abstract
BACKGROUND The nutritional control of ghrelin has not been fully clarified yet. Particularly, the influence of aminoacids and lipids is controversial and, moreover, whether the intraluminal gastric contact with nutrients is required or if the modulatory action of nutrients on ghrelin secretion is mediated by insulin is still matter of debate. AIM OF THE STUDY To clarify the role of nutrients in the control of ghrelin secretion evaluating the effects of intravenous and oral lipids and aminoacids compared with glucose and fructose load in healthy subjects. METHODS A total of 6 healthy overnight-fasted volunteers underwent the following testing sessions: (a) iv arginine (ARG, 0.5 g/kg); (b) oral protein load (PRO, 50 g); (c) iv lipid-heparin infusion (Li He, Intralipid 10% 250 ml); (d) oral fat load (OIL, soy oil 40 g); (e) oral glucose load (OGL, 100 g); (f) oral fructose load (OFL, 100 g); (g) iv saline (SAL, 3 ml); (h) oral water load (WL, 200 ml). Total ghrelin, insulin, and glucose were assayed every 15 min from 0 up to +180 min. RESULTS WL and SAL did not modify insulin, glucose and ghrelin. ARG induced a prompt but transient increase (P < 0.05) of insulin and glucose (P < 0.01), without modifying ghrelin secretion. PRO induced a mild but sustained increase of insulin secretion (P < 0.05) without affecting glucose and ghrelin. Li-He progressively increased circulating glucose (P < 0.01) without modifying insulin and ghrelin secretion. No significant variations in circulating glucose, insulin, and ghrelin occurred after OIL. OGL significantly (P < 0.01) increased insulin and glucose levels and progressively decreased (P < 0.05) ghrelin levels. OFL induced a mild (P < 0.05) increase of insulin without modifying glucose levels. Similarly, OFL was followed by a milder decrease (P < 0.05) of ghrelin levels. CONCLUSIONS Differently from carbohydrates and independently from their modulatory effect on insulin secretion and glucose levels, both lipids and aminoacids play a negligible role in the acute control of ghrelin secretion either after acute enteral and parenteral administration.