PYY-67HK Sigma-AldrichHuman PYY (3-36) Specific RIA

Context: Acute energy deficits imposed by food restriction increase appetite and energy intake; however, these outcomes remain unchanged when energy deficits are imposed by exercise. Objective: Our objective was to determine the potential role of acylated ghrelin and peptide YY(3-36) (PYY(3-36)) in mediating appetite and energy intake responses to identical energy deficits imposed by food restriction and exercise. Design: Twelve healthy males completed three 9-h trials (exercise deficit, food deficit, and control) in a randomized counterbalanced design. Participants ran for 90 min (70% of VO(2) max) at the beginning of the exercise deficit trial and then rested for 7.5 h. Participants remained sedentary throughout the food deficit and control trials. Test meals were consumed by participants at 2 and 4.75 h in all trials. The amount provided in the food deficit trial was restricted so that an energy deficit (equivalent to that imposed by exercise) was induced relative to control. Participants were permitted access to a buffet meal at 8 h. Results: The energy deficits imposed by food restriction (4820 ± 151 kJ) and exercise (4715 ± 113 kJ) were similar. Appetite and ad libitum energy intake responded in a compensatory fashion to food restriction yet were not influenced by exercise. Plasma acylated ghrelin concentrations increased, whereas PYY(3-36) decreased, in response to food restriction (two-way ANOVA, trial × time interaction, P < 0.001 for each). Exercise did not induce such compensatory responses. Conclusions: These findings suggest a mediating role of acylated ghrelin and PYY(3-36) in determining divergent feeding responses to energy deficits imposed by food restriction and exercise.

Epidemiological evidence shows an inverse relationship between dietary fibre intake and body weight gain. Oat beta-glucan, a soluble fibre alters appetite hormones and subjective satiety in acute meal test studies, but its effects have not been demonstrated with chronic consumption. The present study aimed to test the effects in women of two different doses of oat beta-glucan on weight loss and hormones associated with appetite regulation. In a 3-month parallel trial, sixty-six overweight females were randomised into one of three 2 MJ energy-deficit diets: a control and two interventions including 5-6 g or 8-9 g beta-glucan. Anthropometric and metabolic variables (blood glucose level, insulin, total cholesterol (TC), LDL, HDL, TAG and leptin), together with markers of appetite regulation (cholecystokinin (CCK), glucagon-like peptide-1 (GLP-1), ghrelin, peptide YY (PYY) and PYY3-36) were measured at baseline and at 3 months. After 3 months, all groups lost weight (P < 0.001) and showed a reduced waist circumference (P < 0.001). The study sample also showed reductions in TC, LDL, HDL, leptin, PYY, GLP-1 values (all P < 0.001) and an increase in CCK levels (P < 0.001). No significant differences were noted between the groups for all outcome values except PYY levels (P = 0.018). In broad terms, the addition of oat beta-glucan did not enhance the effect of energy restriction on weight loss in mildly overweight women, although wide variations in observed results suggests that individual responsiveness may be an issue.

BACKGROUND: Epidemiologic and clinical data indicate that nuts can be incorporated into the diet without compromising body weight. This has been attributed to strong satiety properties, increased resting energy expenditure, and limited lipid bioaccessibility. OBJECTIVE: The role of mastication was explored because of evidence that the availability of nut lipids is largely dependent on the mechanical fracture of their cell walls. DESIGN: In a randomized, 3-arm, crossover study, 13 healthy adults (body mass index, in kg/m(2): 23.1 +/- 0.4) chewed 55 g almonds 10, 25, or 40 times. Blood was collected and appetite was monitored during the following 3 h. Over the next 4 d, all foods were provided, including 55 g almonds, which were consumed under the same chewing conditions. Complete fecal samples were collected. RESULTS: Hunger was acutely suppressed below baseline (P 0.05), and fullness was elevated above baseline longer (P 0.05) after 40 chews than after 25 chews. Two hours after consumption, fullness levels were significantly lower and hunger levels were significantly higher after 25 chews than after 10 and 40 chews (P 0.05). Initial postingestive glucagon-like peptide-1 concentrations were significantly lower after 25 chews than after 40 chews (P 0.05), and insulin concentrations declined more rapidly after 25 and 40 chews than after 10 chews (both P 0.05). Fecal fat excretion was significantly higher after 10 chews than after 25 and 40 chews (both P 0.05). All participants had higher fecal energy losses after 10 and 25 chews than after 40 chews (P 0.005). CONCLUSION: The results indicate important differences in appetitive and physiologic responses to masticating nuts and likely other foods and nutrients. This trial was registered at clinicaltrials.gov as NCT00768417.

Dipeptidyl peptidase IV inhibitors are a new class of antidiabetic drugs. It is urgent, therefore, to fully understand the pharmacology of these inhibitors. Although dipeptidyl peptidase IV metabolizes at least 24 endogenous substrates, the pharmacological consequences of inhibiting the metabolism of most of these substrates is unknown. Our previous results show that Y(1) receptors, but not Y(2) receptors, enhance renovascular responses to angiotensin II in kidneys from genetically susceptible animals (spontaneously hypertensive rats). Dipeptidyl peptidase IV converts peptide YY(1-36) (circulating hormone) to peptide YY(3-36), and peptide YY(1-36) is a Y(1)-receptor agonist, whereas peptide YY(3-36) is a selective Y(2)-receptor agonist. Therefore, it is conceivable that inhibition of dipeptidyl peptidase IV in genetically susceptible kidneys may increase the ability of peptide YY(1-36) to potentiate angiotensin II-induced renal vasoconstriction. Here we demonstrate that in kidneys from spontaneously hypertensive rats 1) peptide YY(1-36) potentiates renovascular responses to angiotensin II, whereas peptide YY(3-36) has little effect, 2) 3-N-[(2S,3S)-2-amino-3-methylpentanoyl]-1,3-thiazolidine (P32/98) (dipeptidyl peptidase IV inhibitor) augments the ability of peptide YY(1-36) to enhance renovascular responses to angiotensin II, 3) dipeptidyl peptidase IV is expressed in preglomerular microvessels and glomeruli, 4) kidneys metabolize arterial PYY(1-36) to PYY(3-36) via a mechanism blocked by P32/98, and 5) preglomerular microvessels and glomeruli convert peptide YY(1-36) to peptide YY(3-36), and this conversion is inhibited by P32/98. We conclude that dipeptidyl peptidase IV is expressed in the renal microcirculation and inhibition of this ecto-enzyme causes arterial PYY(1-36) to more effectively enhance angiotensin II-induced renal vasoconstriction in genetically susceptible kidneys.