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An acute bout of cycling does not induce compensatory responses in pre-menopausal women not using hormonal contraceptives.
Rocha, J, Paxman, JR, Dalton, CF, Hopkins, M, Broom, DR
Appetite. 2018;:87-94
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Abstract
There is a clear need to improve understanding of the effects of physical activity and exercise on appetite control. Therefore, the acute and short-term effects (three days) of a single bout of cycling on energy intake and energy expenditure were examined in women not using hormonal contraceptives. Sixteen active (n = 8) and inactive (n = 8) healthy pre-menopausal women completed a randomised crossover design study with two conditions (exercise and control). The exercise day involved cycling for 1 h (50% of maximum oxygen uptake) and resting for 2 h, whilst the control day comprised 3 h of rest. On each experimental day participants arrived at the laboratory fasted, consumed a standardised breakfast and an ad libitum pasta lunch. Food diaries and combined heart rate-accelerometer monitors were used to assess free-living food intake and energy expenditure, respectively, over the subsequent three days. There were no main effects or condition (exercise vs control) by group (active vs inactive) interaction for absolute energy intake (P > 0.05) at the ad libitum laboratory lunch meal, but there was a condition effect for relative energy intake (P = 0.004, ηp2 = 0.46) that was lower in the exercise condition (1417 ± 926 kJ vs. 2120 ± 923 kJ). Furthermore, post-breakfast satiety was higher in the active than in the inactive group (P = 0.005, ηp2 = 0.44). There were no main effects or interactions (P > 0.05) for mean daily energy intake, but both active and inactive groups consumed less energy from protein (14 ± 3% vs. 16 ± 4%, P = 0.016, ηp2 = 0.37) and more from carbohydrate (53 ± 5% vs. 49 ± 7%, P = 0.031, ηp2 = 0.31) following the exercise condition. This study suggests that an acute bout of cycling does not induce compensatory responses in active and inactive women not using hormonal contraceptives, while the stronger satiety response to the standardised breakfast meal in active individuals adds to the growing literature that physical activity helps improve the sensitivity of short-term appetite control.
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The effect of L-rhamnose on intestinal transit time, short chain fatty acids and appetite regulation: a pilot human study using combined 13CO2/H2 breath tests.
Byrne, CS, Preston, T, Brignardello, J, Garcia-Perez, I, Holmes, E, Frost, GS, Morrison, DJ
Journal of breath research. 2018;(4):046006
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Abstract
BACKGROUND The appetite-regulating effects of non-digestible carbohydrates (NDC) have in part previously been attributed to their effects on intestinal transit rates as well as microbial production of short chain fatty acids (SCFA). Increased colonic production of the SCFA propionate has been shown to reduce energy intake and stimulate gut hormone secretion acutely in humans. OBJECTIVE We investigated the effect of the propiogenic NDC, L-rhamnose, on gastrointestinal transit times using a combined 13CO2/H2 breath test. We hypothesised that L-rhamnose would increase plasma propionate leading to a reduction in appetite, independent of changes in gastrointestinal transit times. DESIGN We used a dual 13C-octanoic acid/lactose 13C-ureide breath test combined with breath H2 to measure intestinal transit times following the consumption of 25 g d-1 L-rhamnose, compared with inulin and cellulose, in 10 healthy humans in a randomised cross-over design pilot study. Gastric emptying (GE) and oro-caecal transit times (OCTTs) were derived from the breath 13C data and compared with breath H2. Plasma SCFA and peptide YY (PYY) were also measured alongside subjective measures of appetite. RESULTS L-rhamnose significantly slowed GE rates (by 19.5 min) but there was no difference in OCTT between treatments. However, breath H2 indicated fermentation of L-rhamnose before it reached the caecum. OCTT was highly correlated with breath H2 for inulin but not for L-rhamnose or cellulose. L-rhamnose consumption significantly increased plasma propionate and PYY but did not significantly reduce subjective appetite measures. CONCLUSIONS The NDCs tested had a minimal effect on intestinal transit time. Our data suggest that L-rhamnose is partially fermented in the small intestine and that breath H2 reflects the site of gastrointestinal fermentation and is only a reliable marker of OCTT for certain NDCs (e.g. inulin). Future studies should focus on investigating the appetite-suppressing potential of L-rhamnose and verifying the findings in a larger cohort.
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The gut-brain axis in health neuroscience: implications for functional gastrointestinal disorders and appetite regulation.
Weltens, N, Iven, J, Van Oudenhove, L, Kano, M
Annals of the New York Academy of Sciences. 2018;(1):129-150
Abstract
Over the past few years, scientific interest in the gut-brain axis (i.e., the bidirectional communication system between the gastrointestinal tract and the brain) has exploded, mostly due to the identification of the gut microbiota as a novel key player in this communication. However, important progress has also been made in other aspects of gut-brain axis research, which has been relatively underemphasized in the review literature. Therefore, in this review, we provide a comprehensive, although not exhaustive, overview of recent research on the functional neuroanatomy of the gut-brain axis and its relevance toward the multidisciplinary field of health neuroscience, excluding studies on the role of the gut microbiota. More specifically, we first focus on irritable bowel syndrome, after which we outline recent findings on the role of the gut-brain axis in appetite and feeding regulation, primarily focusing on the impact of subliminal nutrient-related gut-brain signals. We conclude by providing future perspectives to facilitate translation of the findings from gut-brain axis neuroscientific research to clinical applications in these domains.
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Homeostatic and non-homeostatic appetite control along the spectrum of physical activity levels: An updated perspective.
Beaulieu, K, Hopkins, M, Blundell, J, Finlayson, G
Physiology & behavior. 2018;:23-29
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The current obesogenic environment promotes physical inactivity and food consumption in excess of energy requirements, two important modifiable risk factors influencing energy balance. Habitual physical activity has been shown to impact not only energy expenditure, but also energy intake through mechanisms of appetite control. This review summarizes recent theory and evidence underpinning the role of physical activity in the homeostatic and non-homeostatic mechanisms controlling appetite. Energy intake along the spectrum of physical activity levels (inactive to highly active) appears to be J-shaped, with low levels of physical activity leading to dysregulated appetite and a mismatch between energy intake and expenditure. At higher levels, habitual physical activity influences homeostatic appetite control in a dual-process action by increasing the drive to eat through greater energy expenditure, but also by enhancing post-meal satiety, allowing energy intake to better match energy expenditure in response to hunger and satiety signals. There is clear presumptive evidence that physical activity energy expenditure can act as a drive (determinant) of energy intake. The influence of physical activity level on non-homeostatic appetite control is less clear, but low levels of physical activity may amplify hedonic states and behavioural traits favouring overconsumption indirectly through increased body fat. More evidence is required to understand the interaction between physical activity, appetite control and diet composition on passive overconsumption and energy balance. Furthermore, potential moderators of appetite control along the spectrum of physical activity, such as body composition, sex, and type, intensity and timing of physical activity, remain to be fully understood.
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Cholecystokinin responsiveness varies across the population dependent on metabolic phenotype.
Desai, AJ, Dong, M, Langlais, BT, Dueck, AC, Miller, LJ
The American journal of clinical nutrition. 2017;(2):447-456
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Background: Cholecystokinin (CCK) is an important satiety factor, acting at type 1 receptors (CCK1Rs) on vagal afferent neurons; however, CCK agonists have failed clinical trials for obesity. We postulated that CCK1R function might be defective in such patients due to abnormal membrane composition, such as that observed in cholesterol gallstone disease.Objective: Due to the challenges in directly studying CCK1Rs relevant to appetite control, our goal was to develop and apply a method to determine the impact of a patient's own cellular environment on CCK stimulus-activity coupling and to determine whether CCK sensitivity correlated with the metabolic phenotype of a high-risk population.Design: Wild-type CCK1Rs were expressed on leukocytes from 112 Hispanic patients by using adenoviral transduction and 24-h culture, with quantitation of cholesterol composition and intracellular calcium responses to CCK. Results were correlated with clinical, biochemical, and morphometric characteristics.Results: Broad ranges of cellular cholesterol and CCK responsiveness were observed, with elevated cholesterol correlated with reduced CCK sensitivity. This was prominent with increasing degrees of obesity and the presence of diabetes, particularly when poorly controlled. No single standard clinical metric correlated directly with CCK responsiveness. Reduced CCK sensitivity best correlated with elevated serum triglycerides in normal-weight participants and with low HDL concentrations and elevated glycated hemoglobin in obese and diabetic patients.Conclusions: CCK responsiveness varies widely across the population, with reduced signaling in patients with obesity and diabetes. This could explain the failure of CCK agonists in previous clinical trials and supports the rationale to develop corrective modulators to reverse this defective servomechanism for appetite control. This trial was registered at www.clinicaltrials.gov as NCT03121755.
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Obesity is associated with altered mid-insula functional connectivity to limbic regions underlying appetitive responses to foods.
Avery, JA, Powell, JN, Breslin, FJ, Lepping, RJ, Martin, LE, Patrician, TM, Donnelly, JE, Savage, CR, Simmons, WK
Journal of psychopharmacology (Oxford, England). 2017;(11):1475-1484
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Obesity is fundamentally a disorder of energy balance. In obese individuals, more energy is consumed than is expended, leading to excessive weight gain through the accumulation of adipose tissue. Complications arising from obesity, including cardiovascular disease, elevated peripheral inflammation, and the development of Type II diabetes, make obesity one of the leading preventable causes of morbidity and mortality. Thus, it is of paramount importance to both individual and public health that we understand the neural circuitry underlying the behavioral regulation of energy balance. To this end, we sought to examine obesity-related differences in the resting state functional connectivity of the dorsal mid-insula, a region of gustatory and interoceptive cortex associated with homeostatically sensitive responses to food stimuli. Within the present study, obese and healthy weight individuals completed resting fMRI scans during varying interoceptive states, both while fasting and after a standardized meal. We examined group differences in the pre- versus post-meal functional connectivity of the mid-insula, and how those differences were related to differences in self-reported hunger ratings and ratings of meal pleasantness. Obese and healthy weight individuals exhibited opposing patterns of eating-related functional connectivity between the dorsal mid-insula and multiple brain regions involved in reward, valuation, and satiety, including the medial orbitofrontal cortex, the dorsal striatum, and the ventral striatum. In particular, healthy weight participants exhibited a significant positive relationship between changes in hunger and changes in medial orbitofrontal functional connectivity, while obese participants exhibited a complementary negative relationship between hunger and ventral striatum connectivity to the mid-insula. These obesity-related alterations in dorsal mid-insula functional connectivity patterns may signify a fundamental difference in the experience of food motivation in obese individuals, wherein approach behavior toward food is guided more by reward-seeking than by homeostatically relevant interoceptive information from the body.
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Psychological and neural contributions to appetite self-regulation.
Stoeckel, LE, Birch, LL, Heatherton, T, Mann, T, Hunter, C, Czajkowski, S, Onken, L, Berger, PK, Savage, CR
Obesity (Silver Spring, Md.). 2017;(Suppl 1):S17-S25
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OBJECTIVE This paper reviews the state of the science on psychological and neural contributions to appetite self-regulation in the context of obesity. METHODS Three content areas (neural systems and cognitive functions; parenting and early childhood development; and goal setting and goal striving) served to illustrate different perspectives on the psychological and neural factors that contribute to appetite dysregulation in the context of obesity. Talks were initially delivered at an NIH workshop consisting of experts in these three content areas, and then content areas were further developed through a review of the literature. RESULTS Self-regulation of appetite involves a complex interaction between multiple domains, including cognitive, neural, social, and goal-directed behaviors and decision-making. Self-regulation failures can arise from any of these factors, and the resulting implications for obesity should be considered in light of each domain. In some cases, self-regulation is amenable to intervention; however, this does not appear to be universally true, which has implications for both prevention and intervention efforts. CONCLUSIONS Appetite regulation is a complex, multifactorial construct. When considering its role in the obesity epidemic, it is advisable to consider its various dimensions together to best inform prevention and treatment efforts.
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A high fat breakfast attenuates the suppression of appetite and acylated ghrelin during exercise at simulated altitude.
Matu, J, Deighton, K, Ispoglou, T, Shannon, OM, Duckworth, L
Physiology & behavior. 2017;:353-360
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High-altitude exposure induces a negative energy balance by increasing resting energy expenditure and decreasing energy intake. This diminished energy intake is likely caused by altitude-induced anorexia and can have detrimental effects for those travelling to high-altitude. We aimed to investigate whether altering the macronutrient composition of breakfast could attenuate altitude-induced anorexia and augment energy intake at high-altitude. Twelve healthy men (aged 26 (8) years, body mass index 23.9 (2.7) kg·m-2) completed two, 305min experimental trials at 4300m simulated altitude (~11.7% O2). After an overnight fast, participants entered a normobaric hypoxic chamber and rested for one hour, before receiving either a high fat (HF; 60% fat, 25% carbohydrate) or an isocaloric high carbohydrate (HC; 60% carbohydrate, 25% fat) breakfast. One hour after breakfast, participants performed 60min of treadmill walking at 50% of relative V̇O2max. An ad-libitum buffet meal was consumed 1h 30min after exercise. Appetite perceptions, blood samples and substrate oxidation rates were measured throughout. A significantly higher area under the curve for composite appetite score was observed during exercise in HF (40 (12) mm·h-1) compared with HC (30 (17) mm·h-1, P=0.036). During exercise, lower insulin concentrations (P=0.013) and elevated acylated ghrelin concentrations (P=0.048) were observed in HF compared with HC. After exercise there was no significant difference in composite appetite score (P=0.356), acylated ghrelin (P=0.229) or insulin (P=0.513) between conditions. Energy intake at the buffet did not significantly differ between conditions (P=0.384). A HF breakfast attenuated appetite suppression during exercise at 4300m simulated altitude, however ad-libitum energy intake did not increase.
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Appetite self-regulation: Environmental and policy influences on eating behaviors.
Schwartz, MB, Just, DR, Chriqui, JF, Ammerman, AS
Obesity (Silver Spring, Md.). 2017;:S26-S38
Abstract
OBJECTIVE Appetite regulation is influenced by the environment, and the environment is shaped by food-related policies. This review summarizes the environment and policy research portion of an NIH Workshop (Bethesda, MD, 2015) titled "Self-Regulation of Appetite-It's Complicated." METHODS In this paper, we begin by making the case for why policy is an important tool in efforts to improve nutrition, and we introduce an ecological framework that illustrates the multiple layers that influence what people eat. We describe the state of the science on how policies influence behavior in several key areas: the federal food programs, schools, child care, food and beverage pricing, marketing to youth, behavioral economics, and changing defaults. Next, we propose novel approaches for multidisciplinary prevention and intervention strategies to promote breastfeeding, and examine interactions between psychology and the environment. RESULTS Policy and environmental change are the most distal influences on individual-level appetite regulation, yet these strategies can reach many people at once by changing the environment in which food choices are made. We note the need for more research to understand compensatory behavior, reactance, and how to effectively change social norms. CONCLUSIONS To move forward, we need a more sophisticated understanding of how individual psychological and biological factors interact with the environment and policy influences.
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Effects of small intestinal glucose on glycaemia, insulinaemia and incretin hormone release are load-dependent in obese subjects.
Trahair, LG, Marathe, CS, Standfield, S, Rayner, CK, Feinle-Bisset, C, Horowitz, M, Jones, KL
International journal of obesity (2005). 2017;(2):225-232
Abstract
BACKGROUND/OBJECTIVES Studies concerning the glycaemic response to oral glucose, or meals in obesity have usually failed to account for gastric emptying. It has been suggested that the incretin effect may be diminished in obesity as a result of a reduction in glucagon-like peptide-1 (GLP-1) secretion. We sought to determine the effect of two different rates of intraduodenal glucose infusions on glycaemic, insulinaemic and incretin hormone responses in lean and obese subjects and compare the effects of oral and intraduodenal glucose in obese subjects. SUBJECTS/METHODS Eleven obese subjects (age 37.5±4.1 years, body mass index (BMI) 35.7±1.4 kg m-2) and 12 controls (age 34.7±4.0 years, BMI 23.9±0.7 kg m-2) received intraduodenal infusions of glucose at 1 or 3 kcal min-1, or saline for 60 min (t=0-60 min), followed by intraduodenal saline (t=60-120 min). In obese subjects, an oral glucose tolerance test was performed. Blood glucose, serum insulin, plasma total GLP-1 and total gastric inhibitory polypeptide (GIP) were measured. RESULTS In both the groups (P<0.001), the incremental areas under the curve (iAUC)0-60 min for glucose was greater with the 3 kcal min-1 than the 1 kcal min-1 infusion; the iAUC0-120 min for glucose during 3 kcal min-1 was greater (P<0.05), in the obese. Insulin responses to 1 kcal min-1 and, particularly, 3 kcal min-1 were greater (P<0.001) in the obese. Stimulation of GLP-1 and GIP were greater (P<0.001) in response to 3 kcal min-1, compared with 1 kcal min-1 and saline, without any difference between the groups. In the obese, glycaemic, insulinaemic and GIP, but not GLP-1, responses to oral and intraduodenal glucose were related (P<0.05). CONCLUSIONS The rate of duodenal glucose delivery is a major determinant of glycaemia, insulinaemia and incretin hormone release in obese subjects. Obesity is not apparently associated with impaired GLP-1 secretion.