EZHPYYT66K MilliporeHuman PYY (Total) ELISA

Nutritional management is essential for patients with inborn errors of metabolism, such as urea cycle disorders (UCDs). Lack of appetite is common in these patients and can lead to underconsumption of calories, catabolism, and subsequently loss of metabolic control. The etiology of anorexia in these patients is largely unexplored. The neuroendocrine hormone peptide tyrosine tyrosine (PYY), secreted postprandially from endocrine cells of the ileum and colon, induces feelings of satiety and decreases food intake. While plasma PYY levels have been characterized in a number of populations, they have not been examined in UCD patients. In a retrospective study, plasma PYY concentrations were measured in UCD (n=42) patients and controls (n=28) via an ELISA to determine if levels of this anorexigenic hormone are altered in this patient population. Median PYY levels were significantly higher in UCD patients compared to controls (p=3.5×10(-5)). Body mass index was significantly associated with increased PYY levels in controls (p=0.02), while UCD diagnosis subtype was associated with PYY levels (p=1×10(-3)) in cases. Median PYY levels were significantly lower in ornithine carbamoyltransferase deficient patients compared with all other UCD subtypes (p=9×10(-3)), but significantly higher compared to controls (p=1.6×10(-3)). Overall, this study demonstrates that UCD cases have increased PYY levels compared to controls, suggesting that regulation of PYY may be altered in these patients. These observations may lead to a better understanding of the development of anorexia in UCD patients.

There have been reports of an inverse relationship between meal frequency (MF) and adiposity. It has been postulated that this may be explained by favourable effects of increased MF on appetite control and possibly on gut peptides as well. The main goal of the present study was to investigate whether using a high MF could lead to a greater weight loss than that obtained with a low MF under conditions of similar energy restriction. Subjects were randomised into two treatment arms (high MF = 3 meals+3 snacks/d or low MF = 3 meals/d) and subjected to the same dietary energy restriction of - 2931 kJ/d for 8 weeks. Sixteen obese adults (n 8 women and 8 men; age 34.6 (sd 9.5); BMI 37.1 (sd 4.5) kg/m2) completed the study. Overall, there was a 4.7 % decrease in body weight (P < 0.01); similarly, significant decreases were noted in fat mass ( - 3.1 (sd 2.9) kg; P < 0.01), lean body mass ( - 2.0 (sd 3.1) kg; P < 0.05) and BMI ( - 1.7 (sd 0.8) kg/m2; P < 0.01). However, there were NS differences between the low- and high-MF groups for adiposity indices, appetite measurements or gut peptides (peptide YY and ghrelin) either before or after the intervention. We conclude that increasing MF does not promote greater body weight loss under the conditions described in the present study.

Obesity is a heritable trait that contributes to hypertension and subsequent cardiorenal disease risk; thus, the investigation of genetic variation that predisposes individuals to obesity is an important goal. Circulating peptide YY (PYY) is known for its appetite and energy expenditure-regulating properties; linkage and association studies have suggested that PYY genetic variation contributes to susceptibility for obesity, rendering PYY an attractive candidate for study of disease risk.

Peptide Y-Y (PYY) is an anorexigenic hormone implicated in appetite control, and beta-glucan is a fiber known to affect appetite. We hypothesized that plasma PYY levels would increase in overweight human adults consuming increasing doses of beta-glucan. The objective was to test whether the effect could be seen with beta-glucan delivered through extruded cereals containing a high beta-glucan oat bran with demonstrated high molecular weight and solubility. Fourteen subjects consumed a control meal and 3 cereals of varying beta-glucan concentration (between 2.2 and 5.5 g), and blood samples were collected over 4 hours. Analysis of raw PYY data showed a trend toward significant increases over 4 hours. An increasing dose of beta-glucan resulted in higher levels of plasma PYY, with significant differences between groups from 2 to 4 hours post test-meal. Data for the area under the curve analysis also approached significance, with post hoc analysis showing a difference (P = .039) between the control and the highest dose of beta-glucan (5.5 g). The PYY levels at 4 hours were significantly different between the control and high-dose meal test (P = .036). There was a significant dose response, with a positive correlation between the grams of beta-glucan and PYY area under the curve (r(2) = 0.994, P = .003). The optimal dose of beta-glucan appears to lie between 4 and 6 g, with the effects on PYY mediated by viscosity and concentration. Meal-test studies examining a range of hormones should measure hormones over a minimum of 4 hours and record meal intake for even longer time frames.