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      Carbohydrate-rich breakfast attenuates glycaemic, insulinaemic and ghrelin response to ad libitum lunch relative to morning fasting in lean adults

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          Abstract

          Breakfast omission is associated with obesity and CVD/diabetes, but the acute effects of extended morning fasting upon subsequent energy intake and metabolic/hormonal responses have received less attention. In a randomised cross-over design, thirty-five lean men ( n 14) and women ( n 21) extended their overnight fast or ingested a typical carbohydrate-rich breakfast in quantities relative to RMR (i.e. 1963 ( sd 238) kJ), before an ad libitum lunch 3 h later. Blood samples were obtained hourly throughout the day until 3 h post-lunch, with subjective appetite measures assessed. Lunch intake was greater following extended fasting (640 ( sd 1042) kJ, P< 0·01) but incompletely compensated for the omitted breakfast, with total intake lower than the breakfast trial (3887 ( sd 1326) v. 5213 ( sd 1590) kJ, P< 0·001). Systemic concentrations of peptide tyrosine–tyrosine and leptin were greater during the afternoon following breakfast (both P< 0·05) but neither acylated/total ghrelin concentrations were suppressed by the ad libitum lunch in the breakfast trial, remaining greater than the morning fasting trial throughout the afternoon (all P< 0·05). Insulin concentrations were greater during the afternoon in the morning fasting trial (all P< 0·01). There were no differences between trials in subjective appetite during the afternoon. In conclusion, morning fasting caused incomplete energy compensation at an ad libitum lunch. Breakfast increased some anorectic hormones during the afternoon but paradoxically abolished ghrelin suppression by the second meal. Extending morning fasting until lunch altered subsequent metabolic and hormonal responses but without greater appetite during the afternoon. The present study clarifies the impact of acute breakfast omission and adds novel insights into second-meal metabolism.

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          Most cited references37

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          Using confidence intervals in within-subject designs.

          We argue that to best comprehend many data sets, plotting judiciously selected sample statistics with associated confidence intervals can usefully supplement, or even replace, standard hypothesis-testing procedures. We note that most social science statistics textbooks limit discussion of confidence intervals to their use in between-subject designs. Our central purpose in this article is to describe how to compute an analogous confidence interval that can be used in within-subject designs. This confidence interval rests on the reasoning that because between-subject variance typically plays no role in statistical analyses of within-subject designs, it can legitimately be ignored; hence, an appropriate confidence interval can be based on the standard within-subject error term-that is, on the variability due to the subject × condition interaction. Computation of such a confidence interval is simple and is embodied in Equation 2 on p. 482 of this article. This confidence interval has two useful properties. First, it is based on the same error term as is the corresponding analysis of variance, and hence leads to comparable conclusions. Second, it is related by a known factor (√2) to a confidence interval of the difference between sample means; accordingly, it can be used to infer the faith one can put in some pattern of sample means as a reflection of the underlying pattern of population means. These two properties correspond to analogous properties of the more widely used between-subject confidence interval.
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            Human distribution and release of a putative new gut hormone, peptide YY.

            A radioimmunoassay has been developed for the new intestinal hormonal peptide tyrosine tyrosine [peptide YY (PYY)]. Peptide YY concentrations were measured in separated layers of the human gastrointestinal tract, where PYY was found exclusively in the mucosal epithelium which contained the endocrine cells. Peptide YY was found throughout the small intestine, in very low concentrations (5 pmol/g) in duodenum (6 pmol/g) and jejunum (5 pmol/g), but in higher concentrations in the terminal ileum (84 pmol/g). High concentrations were found throughout the colon (ascending 82 pmol/g, sigmoid 196 pmol/g), being maximum in the rectum (480 pmol/g). The major molecular form of PYY-like immunoreactivity in human intestine appeared to be identical to pure porcine hormone, both as judged by gel permeation chromatography and by reverse-phase high-pressure liquid chromatography. Basal plasma concentrations of PYY were low but rose in response to food, remaining elevated for several hours postprandially. The known potent biologic actions of PYY, its high concentrations in gut endocrine cells, and its release into the circulation after a normal meal suggest that this peptide may function physiologically as a circulating gut hormone.
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              Gut hormone PYY(3-36) physiologically inhibits food intake.

              Food intake is regulated by the hypothalamus, including the melanocortin and neuropeptide Y (NPY) systems in the arcuate nucleus. The NPY Y2 receptor (Y2R), a putative inhibitory presynaptic receptor, is highly expressed on NPY neurons in the arcuate nucleus, which is accessible to peripheral hormones. Peptide YY(3-36) (PYY(3-36)), a Y2R agonist, is released from the gastrointestinal tract postprandially in proportion to the calorie content of a meal. Here we show that peripheral injection of PYY(3-36) in rats inhibits food intake and reduces weight gain. PYY(3-36) also inhibits food intake in mice but not in Y2r-null mice, which suggests that the anorectic effect requires the Y2R. Peripheral administration of PYY(3-36) increases c-Fos immunoreactivity in the arcuate nucleus and decreases hypothalamic Npy messenger RNA. Intra-arcuate injection of PYY(3-36) inhibits food intake. PYY(3-36) also inhibits electrical activity of NPY nerve terminals, thus activating adjacent pro-opiomelanocortin (POMC) neurons. In humans, infusion of normal postprandial concentrations of PYY(3-36) significantly decreases appetite and reduces food intake by 33% over 24 h. Thus, postprandial elevation of PYY(3-36) may act through the arcuate nucleus Y2R to inhibit feeding in a gut-hypothalamic pathway.
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                Author and article information

                Journal
                Br J Nutr
                Br. J. Nutr
                BJN
                The British Journal of Nutrition
                Cambridge University Press (Cambridge, UK )
                0007-1145
                1475-2662
                14 July 2015
                25 May 2015
                : 114
                : 1
                : 98-107
                Affiliations
                [ 1 ]Department for Health, University of Bath , BathBA2 7AY, UK
                [ 2 ]School of Life Sciences, Queen's Medical Centre, University of Nottingham , Nottingham, UK
                Author notes
                [* ] Corresponding author: Dr J. A. Betts, fax +44 1225 383833, email j.betts@ 123456bath.ac.uk
                Article
                S0007114515001506 00150
                10.1017/S0007114515001506
                4530602
                26004166
                1c407947-d848-4031-b990-bac0bffbaf04
                © The Authors 2015

                This is an Open Access article, distributed under the terms of the Creative Commons Attribution licence ( http://creativecommons.org/licenses/by/3.0/), which permits unrestricted re-use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                : 29 January 2015
                : 27 March 2015
                : 09 April 2015
                Categories
                Full Papers
                Human and Clinical Nutrition

                Nutrition & Dietetics
                breakfast skipping,appetite hormones,insulin sensitivity,second-meal effect,energy intake

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