Influence of acute and chronic energy balance changes on circulating concentrations of human peptide YY

2005 ◽  
Vol 43 (10) ◽  
Author(s):  
B Otto ◽  
F Lippl ◽  
P Pfluger ◽  
J Spranger ◽  
U Cuntz ◽  
...  
Keyword(s):  
Author(s):  
B Otto ◽  
H Rochlitz ◽  
M Möhlig ◽  
L Burget ◽  
J Kampe ◽  
...  
Keyword(s):  

2005 ◽  
Vol 51 (11) ◽  
pp. 2131-2137 ◽  
Author(s):  
Tania Siahanidou ◽  
Helen Mandyla ◽  
Maria Vounatsou ◽  
Dimitris Anagnostakis ◽  
Ioannis Papassotiriou ◽  
...  

Abstract Background: Peptide YY (PYY) and ghrelin are gastrointestinal tract–derived hormones that play roles in the regulation of food intake and energy balance. Negative energy balance often occurs in hospitalized preterm infants. Methods: To measure serum concentrations of PYY in preterm and full-term infants and to investigate their correlations with anthropometric characteristics, food intake, and serum ghrelin concentrations, we measured serum PYY and ghrelin concentrations by RIA in 62 healthy preterm infants [mean (SD) gestational age, 32.0 (2.1) weeks; postnatal age, 40.9 (14.8) days] and 15 healthy full-term infants of comparable postnatal age. All of the infants were formula-fed every 3 h. Results: PYY concentrations were significantly higher in preterm [1126.2 (215.4) ng/L] than in full-term infants [825.3 (234.4) ng/L; P <0.001]. In the entire study population, serum PYY concentrations correlated negatively with gestational age and anthropometric measurements (birth weight, body weight, body length, body mass index, and head circumference) and positively with serum ghrelin concentrations, whereas there was no significant correlation between PYY concentration and caloric intake or weight gain. Multiple regression analysis, after correction for prematurity, revealed that serum PYY concentrations correlated independently with serum ghrelin concentrations and infant body weight or body mass index. Conclusions: Circulating concentrations of PYY may increase in preterm infants to compensate for the negative body-weight balance. The physiologic mechanisms behind the correlation between PYY and ghrelin remain to be elucidated.


2014 ◽  
Vol 74 (3) ◽  
pp. 227-234 ◽  
Author(s):  
Michael Blaut

The microbial community populating the human digestive tract has been linked to the development of obesity, diabetes and liver diseases. Proposed mechanisms on how the gut microbiota could contribute to obesity and metabolic diseases include: (1) improved energy extraction from diet by the conversion of dietary fibre to SCFA; (2) increased intestinal permeability for bacterial lipopolysaccharides (LPS) in response to the consumption of high-fat diets resulting in an elevated systemic LPS level and low-grade inflammation. Animal studies indicate differences in the physiologic effects of fermentable and non-fermentable dietary fibres as well as differences in long- and short-term effects of fermentable dietary fibre. The human intestinal microbiome is enriched in genes involved in the degradation of indigestible polysaccharides. The extent to which dietary fibres are fermented and in which molar ratio SCFA are formed depends on their physicochemical properties and on the individual microbiome. Acetate and propionate play an important role in lipid and glucose metabolism. Acetate serves as a substrate for de novo lipogenesis in liver, whereas propionate can be utilised for gluconeogenesis. The conversion of fermentable dietary fibre to SCFA provides additional energy to the host which could promote obesity. However, epidemiologic studies indicate that diets rich in fibre rather prevent than promote obesity development. This may be due to the fact that SCFA are also ligands of free fatty acid receptors (FFAR). Activation of FFAR leads to an increased expression and secretion of enteroendocrine hormones such as glucagon-like-peptide 1 or peptide YY which cause satiety. In conclusion, the role of SCFA in host energy balance needs to be re-evaluated.


2019 ◽  
Vol 3 (Supplement_1) ◽  
Author(s):  
Arashdeep Singh ◽  
Prasanth Chelikani

Abstract Objectives Fermentation of fiber in the gut generates short-chain fatty acids (SCFA), such as butyrate, which decrease food intake and promote weight loss in rodent models. SCFA have been shown to enhance secretion of the gut satiety hormone peptide YY (PYY). However, it is unknown whether PYY is causative to SCFA-induced changes in energy balance. Our Objectives were to determine the dose-response effects of butyrate on energy balance, and assess whether PYY signaling is essential for mediating the satiety effects of butyrate. Methods Male Sprague Dawley rats (8 wks old, n = 39) were randomized to one of three isocaloric (4.63 kcal/g) diets: 1) control (0% sodium butyrate, n = 14), 2) 5% sodium butyrate (n = 13), or 3) 10% sodium butyrate (n = 12), and followed for upto 4 weeks. A PYY Y-2 receptor antagonist (BIIE0246) or vehicle were administered IP acutely during the study. Measurements included food intake, respiratory quotient, and energy expenditure (CLAMS®), and body composition (Minispec LF110 NMR). Results Compared to control, 10% sodium butyrate decreased food intake and respiratory quotient for 4 days, whereas, 5% sodium butyrate was ineffective. Notably, compared to control, 10% sodium butyrate decreased body weight and fat gain without changing energy expenditure. Importantly, systemic Y-2 receptor blockade stimulated food intake and increased respiratory quotient, without altering energy expenditure, only in 10% sodium butyrate group. Conclusions We found that dietary butyrate dose-dependently decreases food intake and respiratory quotient. Importantly, Y-2 receptor blockade attenuated butyrate-induced hypophagia, which supports a role for endogenous PYY in the satiety effects of dietary butyrate. Funding Sources NSERC, Heart and Stroke Foundation of Canada.  


2012 ◽  
Vol 71 (4) ◽  
pp. 463-477 ◽  
Author(s):  
Thomas Riediger

The hypothalamic arcuate nucleus (ARC) and the area postrema (AP) represent targets for hormonal and metabolic signals involved in energy homoeostasis, e.g. glucose, amylin, insulin, leptin, peptide YY (PYY), glucagon-like peptide 1 (GLP-1) and ghrelin. Orexigenic neuropeptide Y expressing ARC neurons are activated by food deprivation and inhibited by feeding in a nutrient-dependent manner. PYY and leptin also reverse or prevent fasting-induced activation of the ARC. Interestingly, hypothalamic responses to fasting are blunted in different models of obesity (e.g. diet-induced obesity (DIO) or late-onset obesity). The AP also responds to feeding-related signals. The pancreatic hormone amylin acts via the AP to control energy intake. Amylin-sensitive AP neurons are also glucose-responsive. Furthermore, diet-derived protein attenuates amylin responsiveness suggesting a modulation of AP sensitivity by macronutrient supply. This review gives an overview of the receptive function of the ARC and the AP to hormonal and nutritional stimuli involved in the control of energy balance and the possible implications in the context of obesity. Collectively, there is consistency between the neurophysiological actions of these stimuli and their effects on energy homoeostasis under experimental conditions. However, surprisingly little progress has been made in the development of effective pharmacological approaches against obesity. A promising way to improve effectiveness involves combination treatments (e.g. amylin/leptin agonists). Hormonal alterations (e.g. GLP-1 and PYY) are also considered to mediate body weight loss observed in obese patients receiving bariatric surgery. The effects of hormonal and nutritional signals and their interactions might hold the potential to develop poly-mechanistic therapeutic strategies against obesity.


BMJ Open ◽  
2021 ◽  
Vol 11 (3) ◽  
pp. e044519
Author(s):  
Jonathan Lim ◽  
Uazman Alam ◽  
Daniel Cuthbertson ◽  
John Wilding

IntroductionRespiratory quotient (RQ) provides an indication of the relative balance of carbohydrate and fat oxidation. RQ could serve as an early biomarker of negative energy balance during weight loss. Restriction of energy intake relative to total daily energy requirements produces a negative energy balance which can lead to a fall in RQ, accompanied by a decrease in resting energy expenditure (REE). However, the net change in body weight does not usually match predicted weight change due to intraindividual metabolic adaptations. Our aim is to determine the effectiveness of utilising EE information from indirect calorimetry during weight loss intervention.Methods and analysisWe will undertake an assessor-blinded, parallel-group randomised controlled trial of 105 adults with obesity randomised in 1:1 ratio to receive either standard weight management care (SC) or EE information plus SC (INT) during a 24-week multicomponent weight management programme. The primary outcome is difference in weight loss between INT and SC group at 24 weeks. Secondary outcomes include: change in RQ, REE, glycaemic variability, and appetite-relating gut hormones (glucagon-like peptide 1, gastric inhibitory polypeptide, peptide YY). Generalised linear mixed models (intention to treat) will assess outcomes for treatment (INT vs SC), time (baseline, 24 weeks) and the treatment-by-time interaction. This will be the first study to evaluate impact of utilising measured REE and RQ on the lifestyle-based intensive intervention programme.Ethics and disseminationEthics approval was obtained from the Health Research Authority and the North West Research Ethics Committee (18/NW/0645). Results from this trial will be disseminated through publication in peer-reviewed journals, national and international presentations.Trial registration numbersNCT03638895; UoL001379.


2011 ◽  
Vol 301 (2) ◽  
pp. E409-E415 ◽  
Author(s):  
Brenna R. Hill ◽  
Mary Jane De Souza ◽  
Nancy I. Williams

PYY may play a role in modulating satiety and energy expenditure; increasing PYY postprandially has been studied largely in single-meal responses. The diurnal rhythm of PYY and its role in energy balance have not been fully characterized. The purpose of our study was to characterize features of the diurnal rhythm of PYY and determine its role in regulating energy balance. This study was a cross-sectional analysis of 11 subjects in whom 24-h repeated blood sampling was conducted at baseline of a larger prospective study. Breakfast (B), lunch (L), dinner (D), and a snack (S) occurred between 0900 and 1900. Total PYY was assayed every hour from 0800 to 1000, every 20 min from 1000 to 2000, and every hour from 2000 to 0800. PYY variables included total AUC, postprandial peaks, and 24-h mean. Energy balance variables included energy intake, RMR, RQ, and NEAT. PYY postprandial peaks were significantly higher than fasting ( P < 0.05). Twenty-four-hour peak PYY occurred after L and was significantly higher than all other peaks ( P < 0.05). A cubic curve function accounted for most of the variance in PYY ( r2 = 69.9%, P < 0.01). Fasting PYY (0800) correlated with postprandial peaks at B ( r = 0.77, P = 0.01), L ( r = 0.71, P = 0.01), and D ( r = 0.65, P = 0.03). The only significant association between PYY and energy expenditure was that RMR (kcal/24 h) correlated with 24-h mean PYY ( r = 0.71, P = 0.013) and total AUC ( r = 0.69, P = 0.019). We conclude that PYY displays a meal-driven diurnal rhythm and is correlated to RMR, a major contributor to energy expenditure. Thus, PYY varies in accordance with energy content and RMR, supporting a role for PYY in energy balance modulation.


2019 ◽  
Vol 121 (8) ◽  
pp. 945-954 ◽  
Author(s):  
Kevin Deighton ◽  
Andy J. King ◽  
Jamie Matu ◽  
Oliver M. Shannon ◽  
Oliver Whiteman ◽  
...  

AbstractDiscrete episodes of overconsumption may induce a positive energy balance and impair metabolic control. However, the effects of an ecologically relevant, single day of balanced macronutrient overfeeding are unknown. Twelve healthy men (of age 22 (sd 2) years, BMI 26·1 (sd 4·2) kg/m2) completed two 28 h, single-blind experimental trials. In a counterbalanced repeated measures design, participants either consumed their calculated daily energy requirements (energy balance trial (EB): 10 755 (sd 593) kJ) or were overfed by 50 % (overfeed trial (OF): 16 132 (sd 889) kJ) under laboratory supervision. Participants returned to the laboratory the next day, after an overnight fast, to complete a mixed-meal tolerance test (MTT). Appetite was not different between trials during day 1 (P>0·211) or during the MTT in the fasted or postprandial state (P>0·507). Accordingly, plasma acylated ghrelin, total glucagon-like peptide-1 and total peptide YY concentrations did not differ between trials during the MTT (all P>0·335). Ad libitum energy intake, assessed upon completion of the MTT, did not differ between trials (EB 6081 (sd 2260) kJ; OF 6182 (sd 1960) kJ; P=0·781). Plasma glucose and insulin concentrations were not different between trials (P>0·715). Fasted NEFA concentrations were lower in OF compared with EB (P=0·005), and TAG concentrations increased to a greater extent on OF than on EB during the MTT (P=0·009). The absence of compensatory changes in appetite-related variables after 1 d of mixed macronutrient overfeeding highlights the limited physiological response to defend against excess energy intake. This supports the concept that repeated discrete episodes of overconsumption may promote weight gain, while elevations in postprandial lipaemia may increase CVD risk.


1994 ◽  
Vol 144 ◽  
pp. 315-321 ◽  
Author(s):  
M. G. Rovira ◽  
J. M. Fontenla ◽  
J.-C. Vial ◽  
P. Gouttebroze

AbstractWe have improved previous model calculations of the prominence-corona transition region including the effect of the ambipolar diffusion in the statistical equilibrium and energy balance equations. We show its influence on the different parameters that characterize the resulting prominence theoretical structure. We take into account the effect of the partial frequency redistribution (PRD) in the line profiles and total intensities calculations.


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