Intense exercise and food restriction cause similar hypothalamic neuropeptide Y increases in rats

1993 ◽  
Vol 264 (2) ◽  
pp. E279-E284 ◽  
Author(s):  
D. E. Lewis ◽  
L. Shellard ◽  
D. G. Koeslag ◽  
D. E. Boer ◽  
H. D. McCarthy ◽  
...  

Neuropeptide Y (NPY) is a potent central appetite stimulant whose concentrations rise markedly in hypothalamic appetite-regulating regions in food-deprived rats. To determine whether increased energy expenditure also affects hypothalamic NPY, we studied the effects of intense physical exercise in rats (n = 10) running voluntarily on a large-diameter exercise wheel. Running was initiated by restricting food intake but stabilized at an average of 8 km/day when food intake was matched to that in 11 nonexercised, freely fed controls [23.9 +/- 1.9 (SE) g/day vs. 24.7 +/- 1.3 g/day; P > 0.5]. Running expended approximately 40% of daily energy intake, and weight gain was significantly inhibited. A separate group (n = 10) of nonexercised rats was food restricted (approximately 15 g/day) to match the weights of the exercised rats. The rats were killed after 40 days, when both experimental groups weighed 30% less than controls (P < 0.01). Hypothalamic NPY concentrations showed significant (P < 0.01) increases of 30–70% in specific regions (arcuate and dorsomedial nuclei and medial preoptic and lateral hypothalamic areas) in both the running and food-restricted groups, compared with controls. There were no significant differences between the two experimental groups in NPY concentrations in any hypothalamic region. These findings suggest that negative energy balance, whether caused by reduced energy intake or increased expenditure, increases hypothalamic NPYergic activity. As NPY acts on the hypothalamus to increase body weight, these data support the postulated homeostatic role of NPY in maintaining nutritional state.

2000 ◽  
Vol 83 (1) ◽  
pp. 7-14 ◽  
Author(s):  
A. M. Johnstone ◽  
E. Shannon ◽  
S. Whybrow ◽  
C. A. Reid ◽  
R. J. Stubbs

The objectives of the present study were to examine the effects of (1) ingesting mandatory snacks v. no snacks and (2) the composition of isoenergetically-dense snacks high in protein, fat or carbohydrate, on food intake and energy intake (EI) in eight men with ad libitum access to a diet of fixed composition. Subjects were each studied four times in a 9 d protocol per treatment. On days 1–2, subjects were given a medium-fat maintenance diet estimated at 1·6 × resting metabolic rate (RMR). On days 3–9, subjects consumed three mandatory isoenergetic, isoenergetically dense (380 kJ/100 g) snacks at fixed time intervals (11.30, 15.30 and 19.30 hours). Total snack intake comprised 30 % of the subjects' estimated daily energy requirements. The treatments were high protein (HP), high carbohydrate (HC), high fat (HF) and no snack (NS). The order was randomized across subjects in a counterbalanced, Latin-square design. During the remainder of the day, subjects had ad libitum (meal size and frequency) access to a covertly manipulated medium-fat diet of fixed composition (fat: carbohydrate: protein, 40:47:13 by energy), energy density 550 kJ/100 g. All foods eaten were investigator-weighed before ingestion and left-overs were weighed after ingestion. Subjective hunger and satiety feelings were tracked hourly during waking hours using visual analogue scales. Ad libitum EI amounted to 13·9 MJ/d on the NS treatment compared with 11·7, 11·7 and 12·2 MJ/d on the HP, HC and HF diets respectively (F(3,21) 5·35; P = 0·007, sed 0·66). Total EI values were not significantly different at 14·6, 14·5, 15·0 and 14·2 MJ/d respectively. Snack composition did not differentially affect total daily food intake or EI. Average daily hunger was unaffected by the composition of the snacks. Only at 12.00 hours did subjects feel significantly more hungry during the NS condition, relative to the other dietary treatments (F(3,18) 4·42; P = 0·017). Body weight was unaffected by dietary treatment. In conclusion, snacking per se led to compensatory adjustments in feeding behaviour in lean men. Snack composition (with energy density controlled) did not affect the amount eaten of a diet of fixed composition. Results may differ in real life where subjects can alter both composition and amount of food they eat and energy density is not controlled.


2011 ◽  
Vol 107 (3) ◽  
pp. 445-449 ◽  
Author(s):  
John E. Blundell ◽  
Phillipa Caudwell ◽  
Catherine Gibbons ◽  
Mark Hopkins ◽  
Erik Näslund ◽  
...  

The idea of body weight regulation implies that a biological mechanism exerts control over energy expenditure and food intake. This is a central tenet of energy homeostasis. However, the source and identity of the controlling mechanism have not been identified, although it is often presumed to be some long-acting signal related to body fat, such as leptin. Using a comprehensive experimental platform, we have investigated the relationship between biological and behavioural variables in two separate studies over a 12-week intervention period in obese adults (totaln92). All variables have been measured objectively and with a similar degree of scientific control and precision, including anthropometric factors, body composition, RMR and accumulative energy consumed at individual meals across the whole day. Results showed that meal size and daily energy intake (EI) were significantly correlated with fat-free mass (FFM,Pvalues < 0·02–0·05) but not with fat mass (FM) or BMI (Pvalues 0·11–0·45) (study 1,n58). In study 2 (n34), FFM (but not FM or BMI) predicted meal size and daily EI under two distinct dietary conditions (high-fat and low-fat). These data appear to indicate that, under these circumstances, some signal associated with lean mass (but not FM) exerts a determining effect over self-selected food consumption. This signal may be postulated to interact with a separate class of signals generated by FM. This finding may have implications for investigations of the molecular control of food intake and body weight and for the management of obesity.


Nutrients ◽  
2019 ◽  
Vol 11 (7) ◽  
pp. 1517 ◽  
Author(s):  
Jia Jiet Lim ◽  
Sally D. Poppitt

Developing novel foods to suppress energy intake and promote negative energy balance and weight loss has been a long-term but commonly unsuccessful challenge. Targeting regulation of appetite is of interest to public health researchers and industry in the quest to develop ‘functional’ foods, but poor understanding of the underpinning mechanisms regulating food intake has hampered progress. The gastrointestinal (GI) or ‘satiety’ peptides including cholecystokinin (CCK), glucagon-like peptide 1 (GLP-1) and peptide YY (PYY) secreted following a meal, have long been purported as predictive biomarkers of appetite response, including food intake. Whilst peptide infusion drives a clear change in hunger/fullness and eating behaviour, inducing GI-peptide secretion through diet may not, possibly due to modest effects of single meals on peptide levels. We conducted a review of 70 dietary preload (DIET) and peptide infusion (INFUSION) studies in lean healthy adults that reported outcomes of CCK, GLP-1 and PYY. DIET studies were acute preload interventions. INFUSION studies showed that minimum increase required to suppress ad libitum energy intake for CCK, GLP-1 and PYY was 3.6-, 4.0- and 3.1-fold, respectively, achieved through DIET in only 29%, 0% and 8% of interventions. Whether circulating ‘thresholds’ of peptide concentration likely required for behavioural change can be achieved through diet is questionable. As yet, no individual or group of peptides can be measured in blood to reliably predict feelings of hunger and food intake. Developing foods that successfully target enhanced secretion of GI-origin ‘satiety’ peptides for weight loss remains a significant challenge.


2015 ◽  
Vol 100 (8) ◽  
pp. 758-762 ◽  
Author(s):  
Hayley Syrad ◽  
Cornelia H M van Jaarsveld ◽  
Jane Wardle ◽  
Clare H Llewellyn

ObjectiveParental decision-making around extended formula feeding (12 months+) has not been explored previously. This study tested the hypotheses that extended formula milk use (i) is associated with poorer appetite and (ii) supplements lower food intake.MethodsAppetite was assessed with the Child Eating Behaviour Questionnaire (CEBQ) in 3854 twin children aged 16 months. Diet was assessed from 3-day diaries in 2714 children at 21 months. Parents reported their children's weight at 24 months. Associations between formula feeding and (1) appetite, (2) energy intake and (3) weight were examined. 35 mothers were interviewed when the children were 7 years old to explore retrospectively their reasons for extended formula feeding.ResultsFormula consumers (13% of the sample) scored significantly differently than non-formula consumers on five of the six CEBQ subscales, indicating lower appetite avidity: ‘food responsiveness’ (2.02 vs 2.22, respectively),‘enjoyment of food’ (3.99 vs 4.20), ‘satiety responsiveness’ (2.89 vs 2.65), ‘slowness in eating’ (2.63 vs 2.46) and ‘food fussiness’ (2.34 vs 2.14). Formula consumers had a significantly lower percentage of daily energy intake from food (70% vs 74%); however, total daily energy intake did not differ significantly from non-consumers (4315 vs 4373 kJ). At interview, mothers reported supplementing their child's diet with formula because of ‘picky eating’ and concerns about inadequate food intake.ConclusionsHigh formula milk intake is associated with picky-eating behaviours, but seems to act as a substitute for rather than a supplement to solid food. Prospective and intervention studies are needed to determine whether extended formula feeding has an enduring impact on weight trajectories, eating behaviours or health.


Nutrients ◽  
2020 ◽  
Vol 12 (11) ◽  
pp. 3484
Author(s):  
Christina Sonne Mogensen ◽  
Kristine Færch ◽  
Lea Bruhn ◽  
Hanan Amadid ◽  
Inge Tetens ◽  
...  

Knowledge on how energy intake and macronutrients are distributed during the day and the role of daily eating patterns in body composition among adults with overweight/obesity and prediabetes is lacking. Therefore, we evaluated the diurnal dietary intake and studied the associations of daily eating patterns with body fat percentage. A total of 119 adults with prediabetes were included (mean (SD) HbA1c 41 (2.3) mmol/mol, BMI 31.5 (5.0) kg/m2, age 57.8 (9.3) years, 44% men). Information on dietary intake was obtained from self-reported food records for three consecutive days. All foods and beverages (except water) were registered with information on time of ingestion. Body fat was measured by dual-energy X-ray absorptiometry. A total of 60.5% of the participants reported a daily eating window of 12 or more hours/day, and almost half of the daily total energy intake was reported in the evening. In analyses adjusted for age, gender, and total daily energy intake, having the first daily energy intake one hour later was associated with slightly higher body fat percentage (0.64% per hour, 95% CI: 0.28; 1.01; p < 0.001), whereas higher meal frequency was associated with slightly lower body fat percentage (0.49% per extra daily meal, 95% CI: −0.81; −0.18; p = 0.002). Prospective studies are warranted to address the clinical implications of daily eating patterns on body fat and cardiometabolic health.


1999 ◽  
Vol 24 ◽  
pp. 171-175 ◽  
Author(s):  
B. L. Collard ◽  
P. J. Boettcher ◽  
J. C. M. Dekkers ◽  
L. R. Schaeffer ◽  
D. Petitclerc

AbstractData were records of daily food intake and milk production, periodic measures of milk composition and all health and reproductive information from 140 multiparous Holstein cows involved in various experiments at the Agriculture Canada dairy research station in Lennoxville, Quebec. Energy concentrations of the total mixed rations were also available. Daily energy balance was calculated by multiplying the food intake by the concentration of energy in the diet and then subtracting from this quantity the expected (National Research Council) amount of energy required for maintenance (based on parity and body weight) and for milk production (based on yield and concentrations of fat, protein and lactose). Four energy balance traits were defined: (1) average daily energy balance within the first 10 to 100 days of lactation, (2) minimum daily energy balance, (3) days in negative energy balance and (4) total energy deficit during the period of negative energy balance. Health traits were the numbers of incidences of each of the following: (1) all udder problems, (2) mastitis, (3) all locomotive problems, (4) laminitis, (5) digestive problems and (6) reproductive problems. Reproductive traits were the number of days to first observed oestrous and number of inseminations. Phenotypic relationships between energy balance and health were investigated by regressing the energy balance traits on each health trait. Parity and treatment (according to the research trial that the cow was involved with) were also included in the model. Genetic parameters were estimated with restricted maximum likelihood and a model that included effects of parity, treatment and animal. Phenotypically, several significant (P<0.10) relationships between energy balance and health were observed. Cows with longer periods of negative energy balance had increased digestive problems. Cows with greater total energy deficit had more digestive problems and laminitis. Estimates of heritabilities for energy intake and milk energy were 0.42 and 0.12, respectively but estimates of heritability for all energy balance traits were zero. The low estimates for these traits may have been due to (1) low true additive genetic variance, (2) small amount of data, or (3) relatively few genetic ties among cows.


1998 ◽  
Vol 274 (5) ◽  
pp. R1500-R1504 ◽  
Author(s):  
A. Ishihara ◽  
T. Tanaka ◽  
A. Kanatani ◽  
T. Fukami ◽  
M. Ihara ◽  
...  

Neuropeptide Y (NPY) is one of the most potent orexigenic substances known. 1229U91 was found to be a potent and selective NPY antagonist. To elucidate a physiological role of NPY in hyperphagia in obese animals, we studied the effect of 1229U91 on spontaneous food intake in obese and lean Zucker rats. The food intake of Zucker rats was suppressed by intracerebroventricular administration of 1229U91 more potently in obese than in lean animals without abnormal behavior (31.7 and 67.3% inhibition at doses of 10 and 30 μg, respectively, in Zucker fatty rats and 22.2% inhibition at 30 μg in lean rats). This compound markedly suppressed NPY-induced food intake at 30 μg but did not affect galanin-induced food intake, suggesting that the feeding suppression seen in Zucker fatty and lean rats is pharmacologically and behaviorally specific. These results suggest that NPY is involved in feeding behavior in Zucker fatty rats and that NPY contributes to feeding to a greater degree in Zucker fatty than in lean rats. The hyperphagia in Zucker fatty rats may be due to the abnormal overactivation of the NPYergic system.


1987 ◽  
Vol 252 (3) ◽  
pp. R599-R609 ◽  
Author(s):  
J. E. Morley ◽  
A. S. Levine ◽  
B. A. Gosnell ◽  
J. Kneip ◽  
M. Grace

Neuropeptide Y (NPY) is a potent stimulator of food and water intake in rats. NPY still increases food intake even after a 2-h delay in access to food after central injection. When two injections of NPY are given 2 h apart, the second injection produced a substantial increase in food intake. This suggests that tolerance to the NPY effect does not develop after a single injection of NPY. NPY increases moving and exploration in the absence of food when rats are in their home environment but not when tested in a novel environment. Following administration of NPY, rats preferred a high-carbohydrate diet over a high-fat or high-protein diet. Microinjections of NPY showed that active sites included the anterior ventromedial nucleus, paraventricular nucleus of the hypothalamus, and the posterior lateral hypothalamus. NPY was neither additive nor synergistic when coadministered with norepinephrine. Whereas norepinephrine-induced feeding was inhibited by adrenalectomy and vagotomy, these maneuvers had no effect on NPY-induced food intake. This provides further evidence that NPY does not exert its effects on food intake through an alpha-adrenergic mechanism. The effects of NPY on food intake were attenuated by peripherally administered bombesin and centrally administered corticotropin-releasing factor and calcitonin. Cholecystokinin failed to inhibit NPY-induced feeding. NPY did not alter circulating glucose levels. These studies provide further insights into the role of NPY as a stimulator of ingestive behaviors.


1999 ◽  
Vol 84 (10) ◽  
pp. 3781-3791
Author(s):  
P. J. Larsen ◽  
M. Tang-Christensen ◽  
C. E. Stidsen ◽  
K. Madsen ◽  
M. S. Smith ◽  
...  

Abstract The orexigenic role of central neuropeptide Y (NPY) in nonhuman primates has been questioned. Therefore, we have studied the effect of central NPY on feeding in ad libitum-fed male rhesus macaques. NPY dose-dependently increased food intake, with the maximal effect obtained by 50 μg (960 min food intake ± sem, 104 ± 5 to 188 ± 11 g; vehicle vs. NPY; n = 6). Blood glucose levels were unaffected by intracerebroventricular administration of NPY, but animals receiving either 20 or 50 μg displayed increased plasma levels of insulin and cortisol at few time points. To assess the pharmacological specificity of this response, a novel Y1 antagonist,[ (Ile,Glu,Pro,Daba,Tyr, Arg,Leu,Arg,Tyr-NH2)2 cyclic (2,4′),(2′,4)-diamide] (Y1ANT), was synthesized. Receptor binding experiments demonstrated that Y1ANT preferentially binds to Y1 and Y4 receptors (pKi 10.12 ± 0.06 and 9.11 ± 0.05 nmol/L, respectively). Functional analysis revealed that Y1ANT is a Y1 antagonist and a partial Y4 agonist. Central administration of Y1ANT blocked NPY-induced feeding. In food-deprived monkeys, Y1ANT attenuated the feeding response. However, Y1ANT had no effect on food intake in satiated monkeys. Thus, endogenous NPY is likely to be involved in the regulation of food intake in the nonhuman primate, and this effect is at least partially mediated via Y1-like receptors.


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