Protein PYY and Its Role in Metabolism

Price, Samantha; Bloom, Stephen R.

doi:10.1159/000358343

Cited by 27 publications

(16 citation statements)

References 26 publications

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“…While investigating other hormones that were related to metabolism and obesity, increased PYY serum levels after HFD were observed in adult offspring of maternal swimmers, which is a potential indicator for inhibitory appetite effects [ 39 ]. In accordance, these animals had lower caloric intake suggesting that increased PYY expression led to positive changes in the metabolism.…”

Section: Discussionmentioning

confidence: 99%

Exercise during pregnancy protects adult mouse offspring from diet-induced obesity

et al. 2015

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BackgroundPhysical exercise induces positive alterations in gene expression involved in the metabolism of obesity. Maternal exercise provokes adaptations soon after birth in the offspring. Here, we investigated whether adult mouse offspring of swim-trained mothers is protected against the development of the deleterious effects of high fat diet (HFD).MethodsOur study comprises two parts. First, female C57BL/6 mice were divided into one sedentary and one swim-trained group (before and during pregnancy, n = 18). In the second part, adult offspring (n = 12) of trained and sedentary mothers was challenged to HFD for 16 weeks. Notably, most of the analysis was done in male offspring.ResultsOur results demonstrate that maternal exercise has several beneficial effects on the mouse offspring and protects them from the deleterious effects of HFD in the adult. Specifically, swimming during pregnancy leads to lower birth weight in offspring through 2 months of age. When subjected to HFD for 4 month in the adulthood, our study presents novel data on the male offspring’s metabolism of trained mothers. The offspring gained less weight, which was accompanied by less body fat, and they used more calories during daytime compared with offspring of sedentary mothers. Furthermore, we observed increased adiponectin expression in skeletal muscle, which was accompanied by decreased leptin levels and increased insulin sensitivity. Decreased interleukin-6 expression and increased peptide PYY levels were observed in sera of adult offspring of mothers that swam during pregnancy.ConclusionsOur results point to the conclusion that maternal exercise is beneficial to protect the offspring from developing obesity, which could be important for succeeding generations as well.Electronic supplementary materialThe online version of this article (doi:10.1186/s12986-015-0052-z) contains supplementary material, which is available to authorized users.

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Section: Discussionmentioning

confidence: 99%

Exercise during pregnancy protects adult mouse offspring from diet-induced obesity

et al. 2015

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“…A number of hormones released when food enters the gut also influence food intake and act via effects on the hypothalamus and on brain stem areas such as the nucleus of the solitary tract, which contains a brain stem relay of afferents from the gut. These hormones include glucagon-like peptide-1, cholecystokinin, pancreatic polypeptide, peptide YY, and oxyntomodulin (59,95). The afferents from the gut convey the effects of gastric distension, which is essential for satiety (36,114), and of taste and other receptors in the gut, which probably contribute to satiety.…”

Section: Hormonal Signals Related To Hunger and Satiety And Their Effmentioning

confidence: 99%

“…When food enters the gastrointestinal tract, it activates a wide range of gut receptors, including gut taste receptors, which locally stimulate the release of peptides, such as cholecystokinin, peptide YY, ghrelin, and glucagon-like peptide-1, from endocrine cells (30,66,67,72). These gut endocrine cells play a crucial role in the regulation of food intake (59,91,95). The gut-sensing mechanisms and their role in conditioned appetite are reviewed elsewhere (1,62,154).…”

Section: Postingestive Effects Of Nutrients Including Conditioned Apmentioning

confidence: 99%

“…The fundamental concept this leads to about some of the major causes of obesity is that, over the past 30 years, sensory stimulations produced by the taste, smell, texture, and appearance of food, as well as its availability, have increased dramatically, yet the satiety signals produced by stomach distension, satiety hormones, and so forth (22,59,95) have remained essentially unchanged, so that the effect on the brain's control system for appetite (shown in Figures 1 and 8) is to lead to a net average increase in the reward value and palatability of food that overrides the satiety signals and contributes to the tendency to be overstimulated by food and to overeat.…”

Section: Obesity: Sensory and Cognitive Factors That Make Food Increamentioning

confidence: 99%

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Reward Systems in the Brain and Nutrition

Rolls

2016

Annu. Rev. Nutr.

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The taste cortex in the anterior insula provides separate and combined representations of the taste, temperature, and texture of food in the mouth independently of hunger and thus of reward value and pleasantness. One synapse on, in the orbitofrontal cortex, these sensory inputs are combined by associative learning with olfactory and visual inputs for some neurons, and these neurons encode food reward value in that they respond to food only when hunger is present and in that activations correlate linearly with subjective pleasantness. Cognitive factors, including word-level descriptions and selective attention to affective value, modulate the representation of the reward value of taste, olfactory, and flavor stimuli in the orbitofrontal cortex and a region to which it projects, the anterior cingulate cortex. These food reward representations are important in the control of appetite and food intake. Individual differences in reward representations may contribute to obesity, and there are age-related differences in these reward representations. Implications of how reward systems in the brain operate for understanding, preventing, and treating obesity are described.

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“…Plasma GLP-1 concentrations increased rapidly (within 2 weeks) by DFA III and FOS, and the effect sustained by end of the experimental period, suggesting that cecal fermentation was already modified after 2 weeks of feeding these oligosaccharides. Another anorexic gut hormone, PYY, 43) was significantly elevated by DFA III, but not by FOS, when added to the HFS diet. These results suggest that additive or synergistic effects of increased plasma GLP-1, PYY, and acetate are involved in suppressive effects of DFA III on excess energy intake.…”

Section: After 2 Weeksmentioning

confidence: 89%

Impact of difructose anhydride III, raffinose, and fructooligosaccharides on energy intake, gut hormones, and cecal fermentation in rats fed a high-fat and high-sucrose diet

Hira

Yanagihara

Koga

et al. 2017

Bioscience, Biotechnology, and Biochemistry

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We investigated the effects of dietary supplementation of difructose anhydride III (DFA III), raffinose (Raf), and fructooligosaccharides (FOS) on diet-induced obesity development. Male rats were fed normal or high-fat and high-sucrose (HFS) diet, with or without supplementing (3%) DFA III, Raf, or FOS, for 8 or 5 weeks. Supplementing DFA III to the HFS diet decreased energy intake compared to the non-supplemented HFS diet. Accordingly, body weight gain and fat accumulation reduced in DFA III-fed rats. Cecal acetate production and plasma glucagon-like peptide-1 (GLP-1) and peptide-YY (PYY) were elevated in DFA III-fed rats, while Raf and FOS partially affected these parameters. These results demonstrate that DFA III has suppressive effect on excessive energy intake driven by the palatable obesogenic diet, possibly due to combined effects of increased anorexigenic factors such as cecal acetate production and GLP-1/PYY secretion.

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Protein PYY and Its Role in Metabolism

Cited by 27 publications

References 26 publications

Exercise during pregnancy protects adult mouse offspring from diet-induced obesity

Exercise during pregnancy protects adult mouse offspring from diet-induced obesity

Reward Systems in the Brain and Nutrition

Impact of difructose anhydride III, raffinose, and fructooligosaccharides on energy intake, gut hormones, and cecal fermentation in rats fed a high-fat and high-sucrose diet

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