scholarly journals Acute effects of pharmacological modifications of fatty acid metabolism on human satiety

2008 ◽  
Vol 101 (12) ◽  
pp. 1867-1877 ◽  
Author(s):  
Blandine Gatta ◽  
Christine Zuberbuehler ◽  
Myrtha Arnold ◽  
Roberte Aubert ◽  
Wolfgang Langhans ◽  
...  

The role of NEFA in eating behaviour is still poorly known. Our objective was to examine whether etomoxir (ETO), an inhibitor of NEFA oxidation, or ( − )-hydroxycitrate (HCA), an inhibitor of lipogenesis which may indirectly stimulate NEFA oxidation, alters satiety. Post-lunch satiety was measured in eight normal-weight male subjects who were deprived of time cues and received on three occasions either ETO (320 mg), HCA (2 g) or placebo (PLA) in random order. Between lunch and dinner, blood was withdrawn continuously and collected every 10 min for measures of plasma concentrations of glucose, insulin, lactate, TAG, NEFA, β-hydroxybutyrate (BHB), leptin and ghrelin. Results showed that HCA began to decrease hunger and desire to eat compared to PLA and ETO 210 min after lunch and increased satiety duration compared to PLA by 70 (se23) min (P < 0·05), but did not modify energy intake at dinner. ETO did not affect any variable of satiety. HCA increased NEFA concentrations during the pre-dinner period, whereas ETO increased and decreased plasma concentrations of NEFA and BHB, respectively. Mean differences in plasma NEFA concentrations between HCA and PLA were predictive of the differences in satiety duration between treatments (r20·71,P < 0·01). Among treatments, plasma leptin concentration at dinner onset was the only blood variable correlated with energy intake at this meal (r− 0·75,P < 0·0005). In healthy, normal-weight men, acute HCA increased the intensity and duration of satiety possibly via increased NEFA disposal for oxidation.

2015 ◽  
Vol 115 (2) ◽  
pp. 262-270 ◽  
Author(s):  
Sarah Heap ◽  
Jessica Ingram ◽  
Marron Law ◽  
Amy J. Tucker ◽  
Amanda J. Wright

AbstractIncreasing feelings of satiety may reduce appetite and energy intake. The role of inulin consumption in impacting satiety is unclear. A randomised double-blind controlled crossover trial aimed to determine the effects of inulin+yogurt on satiety after 1 and 8-d consumption. The preload breakfast included 100 g vanilla yogurt with (yogurt-inulin (YI)) and without (yogurt-control (YC)) 6 g inulin. A total of nineteen healthy females (22·8 (sd 2·7) years) with non-restrained eating behaviour and taking hormonal contraceptives participated in the study. Day 1 and 8 visual analogue scale (VAS) ratings of Hunger, Fullness, Desire to Eat and Prospective Food Consumption (PFC) were collected at fasting and every 30 min for 180 min. Energy intake was calculated from a weighed ad libitum lunch and remainder of day food records. Total AUC was calculated for each VAS. Day 1 (VAS only) and 8 (VAS and energy intakes) data were compared between YI and YC using ANCOVA, and ANOVA was used to compare energy intakes on Day 1. There were no significant differences between Day 1 YI and YC AUC appetite ratings or energy intakes. However, 8-d consumption of YI v. YC was associated with lower Desire to Eat and PFC ratings but similar lunch and total day energy intakes. Therefore, the addition of 6 g inulin to a commercially available yogurt affected feelings of appetite, but not energy intake, after repeated consumption. These results suggest that inulin may be a suitable ingredient to increase dietary fibre consumption, with potential to impact appetite.


1998 ◽  
Vol 30 (Supplement) ◽  
pp. 185
Author(s):  
M. S. Hickey ◽  
K. P. Davy ◽  
J. A. Houmard ◽  
R. G. Israel

2009 ◽  
Vol 102 (6) ◽  
pp. 929-937 ◽  
Author(s):  
Natalie D. Luscombe-Marsh ◽  
Astrid J. P. G. Smeets ◽  
Margriet S. Westerterp-Plantenga

In a fed and orally stimulated state, whether the addition of monosodium glutamate (MSG) (alone or in combination with inosine monophosphate-5 (IMP-5)) to a high-protein (HP) meal leads to early satiety and a difference in energy intake at a second course was investigated. Ten men and twelve women consumed, in random order, a first-course meal consisting of: (1) water (control); (2) a HP meal with 0·6 % MSG and 0·25 % IMP-5; (3) a HP meal with no additives; (4) a HP meal with MSG only; (5) a sham-fed meal 2 (oral-stimulation). Appetite perceptions, plasma concentrations of glucagon-like peptide 1 (GLP-1), glucose and insulin, and energy intake at a buffet (i.e. a second course) were measured before and after each condition. Changes in appetite, and in GLP-1, glucose and insulin, were similar for the three fed HP conditions and all were greater (post hoc all P < 0·01) than the control and sham conditions. Energy intake was not different following the HP+MSG+IMP (1·86 (sem 0·3) MJ) as compared with the HP+MSG-only (2·24 (sem 0·28) MJ) condition (P = 0·08), or for the HP+MSG+IMP compared with the HP no-additives condition (1·60 (sem 0·29) MJ) (P = 0·21). Following the HP+MSG-only condition, 0·64 (sem 0·20) MJ more energy was consumed compared with the HP no-additives condition (P = 0·005). We conclude that the addition of MSG to a HP meal does not influence perceptions of satiety and it may increase energy intake at a second course. Cephalic responses after the sham condition were of similar magnitude to the control and therefore just tasting food is not enough to influence appetite and energy intake.


1989 ◽  
Vol 61 (2) ◽  
pp. 201-208 ◽  
Author(s):  
A. V. Kurpad ◽  
R. N. Kulkarni ◽  
M. L. Sheela ◽  
P. S. Shetty

1. Seventeen male subjects with an energy intake of 10.6 (sd 1.7) MJ/d and ten male undernourished labourers with an energy intake of 8.0 (sd 1.2) MJ/d were studied. The controls were subdivided into ten underweight controls with a body mass index (weight/height2; BMI) < 18 (17.2 (sd 0.9)) and seven normal-weight controls with a BMI > 20 (21.3 (sd 1.6)), while the undernourished labourers had a BMI < 18 (16.8 (sd 1.2)).2. Comparison of thermogenic responses to increasing doses of noradrenaline showed no overall significant inter-group differences when subjected to a nested analysis of variance (ANOVA). For the initial doses of 0.05 and 0.1 μg noradrenaline, significantly lower responses were seen in the undernourished subjects, while the highest dose showed comparable responses in all three groups. Thermogenic responses to the initial two doses, when corrected for fat-free mass (FFM) differences, were 40 % lower in the undernourished group when compared with the underweight group with similar BMI and FFM values. However, this finding was not statistically significant.3. The basal oxygen consumption of the undernourished group, expressed per unit FFM, was significantly higher than that of the controls.


1983 ◽  
Vol 102 (2) ◽  
pp. 271-276 ◽  
Author(s):  
Judith A. Whitworth ◽  
Aldona Butkus ◽  
J. P. Coghlan ◽  
D. A. Denton ◽  
Dianne Saines ◽  
...  

Abstract. Investigation of the mechanisms involved in ACTH induced hypertension in sheep led to delineation of the major role of 4-pregnene-17α,20α-diol-3-one (17α,20α-OHP) in ovine adrenal venous blood. It has been shown in this model of steroid induced hypertension that 17α,20α-OHP is 'hypertensinogenic' i.e. capable of raising blood pressue when infused concurrently with the major mineralocorticoid and glucocorticoid steroid hormones, but in itself it has no significant blood pressure elevating effect and no significant glucocorticoid or mineralocorticoid activity. The present study examines the regulation of 17α,20α-OHP and 17α-hydroxyprogesterone (17-OHP) in man. The plasma concentration of 17α,20α-OHP in normal ambulant subjects (n = 29) bled at 08.00 to 10.00 h was 14.5 ± 0.8 nmol/l compared with 17-OHP 7.8 ± 0.6 nmol/l. Administration of ACTH (20 μg/kg/day) to normotensive male subjects (n = 6) produced after 5 days of rise in 17α,20α-OHP from 16.6 ± 2.2 to 48.9 ± 7.9 nmol/l and in 17-OHP from 10.9 ± 1.12 to 29.3 ± 4.2 nmol/l. In normal subjects, 17α,20α-OHP had a diurnal rhythm similar to that of cortisol but of lower amplitude. Plasma concentrations of both steroids rose with stepped 30 min ACTH infusions and were suppressed by dexamethasone administration. Angiotensin II infusion, dietary sodium restriction and 9α-fluorocortisol administration had no effect on plasma 17α,20α-OHP. There was no change in 17α,20α-OHP throughout the menstrual cycle but 17-OHP increased during the luteal phase of the cycle. 17-OHP was lower in women on oral contraceptives than in control women, but values for 17α,20α-OHP were unchanged. The mean plasma clearance rate for 17α,20α-OHP in 3 normal subjects was 30.2 l/day/kg, similar to that for aldosterone (31.2 l/day/kg). Unlike the sheep there was no in vitro conversion of 17-OHP to 17α,20α-OHP in human blood. These studies show that 17α,20α-OHP is present in human plasma in higher concentration than 17-OHP. The secretion of 17α,20α-OHP appears to be primarily under the control of ACTH.


2000 ◽  
Vol 88 (2) ◽  
pp. 599-610 ◽  
Author(s):  
Wulf Hildebrandt ◽  
Andy Ottenbacher ◽  
Markus Schuster ◽  
Erik R. Swenson ◽  
Peter Bärtsch

We studied the contributions of hypoxemia, hypocapnia, and hyperpnea to the acute hypoxic diuretic response (HDR) in humans and evaluated the role of peripheral O2 chemosensitivity and renal hormones in HDR. Thirteen healthy male subjects (age 19–38 yr) were examined after sodium equilibration (intake: 120 mmol/day) during 90 min of normoxia (NO), poikilocapnic hypoxia (PH), and isocapnic hypoxia (IH) ( days 1–3, random order, double blind), as well as normoxic voluntary hyperpnea (HP; day 4), matching ventilation during IH. O2 saturation during PH and IH was kept equal to a mean level measured between 30 and 90 min of breathing 12% O2 in a pretest. Urine flow during PH and IH (1.81 ± 0.92 and 1.94 ± 1.03 ml/min, respectively) but not during HP (1.64 ± 0.96 ml/min) significantly exceeded that during NO (control, 1.38 ± 0.71 ml/min). Urine flow increases vs. each test day's baseline were significant with PH, IH, and HP. Differences in glomerular filtration rate, fractional sodium clearance, urodilatin, systemic blood pressure, or leg venous compliance were excluded as factors of HDR. However, slight increases in plasma and urinary endothelin-1 and epinephrine with PH and IH could play a role. In conclusion, the early HDR in humans is mainly due to hypoxia and hypocapnia. It occurs without natriuresis and is unrelated to O2 chemosensitivity (hypoxic ventilatory response).


2012 ◽  
Vol 112 (4) ◽  
pp. 552-559 ◽  
Author(s):  
Lucy K. Wasse ◽  
Caroline Sunderland ◽  
James A. King ◽  
Rachel L. Batterham ◽  
David J. Stensel

The reason for high altitude anorexia is unclear but could involve alterations in the appetite hormones ghrelin and peptide YY (PYY). This study examined the effect of resting and exercising in hypoxia (12.7% O2; ∼4,000 m) on appetite, energy intake, and plasma concentrations of acylated ghrelin and PYY. Ten healthy males completed four, 7-h trials in an environmental chamber in a random order. The four trials were control-normoxia, control-hypoxia, exercise-normoxia, and exercise-hypoxia. During exercise trials, participants ran for 60 min at 70% of altitude-specific maximal oxygen consumption (V̇o2max) and then rested. Participants rested throughout control trials. A standardized meal was consumed at 2 h and an ad libitum buffet meal at 5.5 h. Area under the curve values for hunger (assessed using visual analog scales) tended to be lower during hypoxic trials than normoxic trials (repeated-measures ANOVA, P = 0.07). Ad libitum energy intake was lower ( P = 0.001) in hypoxia (5,291 ± 2,189 kJ) than normoxia (7,718 ± 2,356 kJ; means ± SD). Mean plasma acylated ghrelin concentrations were lower in hypoxia than normoxia (82 ± 66 vs. 100 ± 69 pg/ml; P = 0.005) while PYY concentrations tended to be higher in normoxia (32 ± 4 vs. 30 ± 3 pmol/l; P = 0.059). Exercise suppressed hunger and acylated ghrelin and increased PYY but did not influence ad libitum energy intake. These findings confirm that hypoxia suppresses hunger and food intake. Further research is required to determine if decreased concentrations of acylated ghrelin orchestrate this suppression.


2002 ◽  
Vol 5 (5) ◽  
pp. 683-690 ◽  
Author(s):  
I Asbeck ◽  
M Mast ◽  
A Bierwag ◽  
J Westenhöfer ◽  
KJ Acheson ◽  
...  

AbstractObjective:To assess the influence of different standards and restrained eating on underreporting in healthy, non-obese, weight-stable young subjects.Design and subjects:Eighty-three young adults (20–38 years, 55 women, 28 men) were assessed under weight-stable conditions with a 7-day dietary record and the three-factor eating questionnaire by Stunkard and Messick. Resting energy expenditure (REE; indirect calorimetry) plus data derived from physical activity records (PA) (Standard 1) or REE times an activity factor (AF) (Standard 2) was used as standard for total energy expenditure (TEE). For comparison, doubly labelled water (DLW) was used to measure TEE in a subgroup of subjects.Results:There was an association between self-reported energy intake and Standard 2 (r = 0.72) but not with Standard 1. When compared with DLW both calculated standards were inaccurate, but Standard 2 avoided high levels of overreporting. Using Standard 2 to identify ‘severe’ underreporting (SU; as defined by a deviation of energy intake (EI) and TEE of >20%), SU was seen in 37% of all subjects. It was more frequently found in women than in men (49% of women, 14.3% of men, P < 0.05). Underreporting subjects had a reduced EI (P < 0.01) but there were no significant differences in nutritional status (body weight and height, body mass index, fat mass and fat-free mass), energy expenditure and the proportion of energy from macronutrients between normal and underreporting subjects. However, high restraint was associated with a higher degree of underreporting in the total group, whereas disinhibition had an influence only in men.Conclusions:A high prevalence of SU is seen in non-obese subjects. Characteristics of eating behaviour (restraint and disinhibition) were associated with underreporting but seemed to have a different influence in men and women.


Nutrients ◽  
2020 ◽  
Vol 12 (10) ◽  
pp. 3133
Author(s):  
Kerstin Schweiger ◽  
Verena Grüneis ◽  
Julia Treml ◽  
Claudia Galassi ◽  
Corinna M. Karl ◽  
...  

Knowledge regarding the involvement of sweetness perception on energy intake is scarce. Here, the impact of glucose and sucrose sweetness, beyond their caloric load, on subsequent food intake and biomarkers of satiation was evaluated by co-administration of the sweet taste receptor inhibitor lactisole. A total of 27 healthy, male subjects received solutions of either 10% glucose w/o 60 ppm lactisole or 10% sucrose w/o 60 ppm lactisole. Subsequent food intake from a standardized breakfast was evaluated 2 h after receiving the respective test solution. Changes in postprandial plasma concentrations of cholecystokinin, ghrelin, and serotonin were determined over a period of 120 min, as was the body temperature. Administration of lactisole to the sucrose solution increased the energy intake from the subsequent standardized breakfast by 12.9 ± 5.8% (p = 0.04), led to a decreased Δ AUC of the body core temperature by 46 ± 20% (p = 0.01), and time-dependently reduced Δ serotonin plasma concentrations (−16.9 ± 6.06 ng/mL vs. −0.56 ± 3.7 ng/mL after sucrose administration, p = 0.03). The present study shows that lactisole increases energy intake and decreases plasma serotonin concentrations as well as body core temperature induced by sucrose, but not glucose. This finding may be associated with the different binding affinities of sucrose and glucose to the sweet taste receptor.


1972 ◽  
Vol 42 (1) ◽  
pp. 91-104 ◽  
Author(s):  
G. W. Boyd ◽  
A. R. Adamson ◽  
Marion Arnold ◽  
V. H. T. James ◽  
W. S. Peart

1. The relationship between circulating plasma angiotensin II and plasma aldosterone in man during sodium deficiency has been investigated in normal male subjects by comparing the amounts of the two hormones: (a) after 5 days of sodium restriction with an injection of frusemide on the third day, (b) during intravenous infusions of angiotensin II given in normal sodium balance. 2. The results show that aldosterone and angiotensin II plasma concentrations were both increased by sodium deficiency, but the increase in aldosterone was much greater than was found when angiotensin II was infused during normal sodium balance so as to equal or even exceed the plasma angiotensin II concentrations of sodium deficiency. 3. Other factors capable of increasing aldosterone secretion (plasma Na+, K+ and ACTH) seemed unlikely to account for the discrepancy, nor was there evidence of sufficient increase in adrenal sensitivity during Na+ deficiency. 4. It is suggested that some other unknown factor or factors are necessary to account for the full aldosterone response to this stimulus in man.


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