Effect of somatostatin infusion on peptide YY secretion: studies in the acute and recovery phase of anorexia nervosa and in obesity

Abstract

Objective: Changes in many gastrointestinal peptides, including the anorexigenic peptide YY (PYY), which is produced by L cells, occur in both anorexia nervosa (AN) and obesity (OB). High PYY levels are present in AN, whereas in morbid OB fasting and postprandial PYY secretion is blunted. Somatostatin (somatotropin release-inhibiting factor (SRIF)) reportedly inhibits plasma PYY concentrations in animals and healthy humans, but the effect of a SRIF infusion on spontaneous PYY secretion in AN and OB is unknown. Methods: A total of 18 young women, seven with acute AN (A-AN), four with AN in the recovery phase (R-AN), and seven with morbid OB, were studied. All subjects underwent an infusion of SRIF (9 mg/kg i.v./h, over 60 min), with blood samples drawn before and at different time intervals after SRIF administration. Plasma PYY levels were measured at each time point. Results: SRIF significantly inhibited plasma PYY concentrations in R-AN and OB, without affecting PYY titers in A-AN. In OB, the inhibitory effect of SRIF also persisted at 90 min. Withdrawal of SRIF infusion in R-AN resulted in a prompt restoration of basal plasma PYY levels, whereas termination of SRIF infusion in OB was followed by a slower increase of PYY titers toward baseline levels. After infusion, PYY D area under the curve (DAUC) in R-AN was significantly higher than those in A-AN and OB patients. A significant difference in PYY DAUC between A-AN and OB was present. Conclusions: These results suggest the existence of a hypo-and hyper-sensitivity of L cells to the inhibitory effect of SRIF in A-AN and OB respectively.

Impact of a Three-Week in-Hospital Multidisciplinary Body Weight Reduction Program on Body Composition, Muscle Performance and Fatigue in a Pediatric Obese Population with or without Metabolic Syndrome

“…Therefore, one might argue that the success of our BWRP on specific outcomes in obese children and adolescents with metabolic syndrome may rely on the "reversibility" of the metabolic-syndrome-induced alterations in the youth and that any therapeutic intervention against obesity and, particularly, metabolic syndrome, should be adopted as early as possible in childhood and adolescence [7]. This might have some implications when our public health stakeholders are called to make decisions to fight pediatric obesity [37][38][39][40][41][42].…”

Central Inflammation and Leptin Resistance Are Attenuated by Ginsenoside Rb1 Treatment in Obese Mice Fed a High-Fat Diet

“…The mechanism by which Rb1 treatment increased circulating PYY levels remains to be determined. However, PYY is predominantly secreted by intestinal L cells located in the distal gastrointestinal tract [40], and it has been reported that the PYY levels are decreased in patients with inflammatory bowel disease [41]. In addition, three days of oral Rb1 treatment potently inhibited the expression of TNF-α and IL-1β in the inflamed colon of mice with colitis [19].…”

Gastrointestinal alterations in anorexia nervosa — A systematic review

“…The secretion CCK (Phillipp et al, 1991;Tamai et al, 1993), vasoactive intestinal peptide, leptin, betaendorphin, gastrin, somatostatin (Baranowska et al, 2000), and peptide YY (Rigamonti et al, 2011) are elevated in AN compared with controls. Additionally, there is data indicating an altered insulin response (Blickle et al, 1984;Stephan et al, 1982) in AN.…”

“…A significant increase of plasma vasoactive intestinal peptide, responsible for smooth muscle relaxation, and a significant decrease of leptin, beta-endorphin, gastrin, and somatostatin was detected in AN (Baranowska, Radzikowska, Wasilewska-Dziubinska, Roguski, & Borowiec, 2000), illustrating a disturbed GI hormone state in AN, which likely impacts on GI functions. Increased peptide YY values in AN were reduced by somatotropin release-inhibiting factor only in the recovery phase but not in acute AN (Rigamonti et al, 2011) pointing towards a hyposensitivity of L-cells to somatotropin release-inhibiting factor in acute AN. Whether also other products of the L-cells such as glucagon-like peptide, incretin, and oxyntomodulin are affected in AN should be further investigated.…”

“…-Loss of fat mass, reduced gastric filling, hypoglycaemia ➔ compensatory increase of orexigenic and compensatory decrease of anorexigenic mediators (Baranowska et al, 2000;Cuntz et al, 2013;Phillipp et al, 1991;Rigamonti et al, 2011;Tamai et al, 1993) Diminished insulin secretion -Altered sensitivity of beta cells (Blickle et al, 1984;Brown, Treasure, & Campbell, 2001;Stephan et al, 1982) Reduced water absorption -Impaired gut permeability (Russell, 1966) Impaired permeability -Reduced colonic claudin-1 expression (Jésus et al, 2014;Monteleone et al, 2004) Increased risk of celiac disease -Impaired gut barrier, immunological alterations (Marild et al, 2017;Passananti et al, 2013;Ricca et al, 2000) Microbiotic changes -Reduced short chain fatty acid intake, hormonal dysregulation, undernutrition (Continues) is not a typical feature of AN, and therefore, differential diagnoses should be considered. However, it is to note that the findings of the early study are yet to be confirmed.…”