2012
DOI: 10.1159/000336500
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Food Cues Do Not Modulate the Neuroendocrine Response to a Prolonged Fast in Healthy Men

Abstract: Introduction: Dietary restriction benefits health and increases lifespan in several species. Food odorants restrain the beneficial effects of dietary restriction in Drosophila melanogaster. We hypothesized that the presence of visual and odorous food stimuli during a prolonged fast modifies the neuroendocrine and metabolic response to fasting in humans. Subjects and Methods: In this randomized, crossover intervention study,healthy young men (n = 12) fasted twice for 60 h; once in the presence and once in the a… Show more

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Cited by 7 publications
(3 citation statements)
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“…They demonstrated increased glucose and insulin concentrations in response to an oral glucose tolerance test due to the prolonged fasting period, but these effects were not modified by food cues (Snel, et al, 2012). Nevertheless, the very long period of fasting might have provoked a ceiling effect that could have masked any stimulatory effects of food cues.…”
Section: Discussionmentioning
confidence: 99%
“…They demonstrated increased glucose and insulin concentrations in response to an oral glucose tolerance test due to the prolonged fasting period, but these effects were not modified by food cues (Snel, et al, 2012). Nevertheless, the very long period of fasting might have provoked a ceiling effect that could have masked any stimulatory effects of food cues.…”
Section: Discussionmentioning
confidence: 99%
“…Larger randomized trials such as the DIRECT study (NCT02126449) are now ongoing to evaluate the impact of STF on tolerance to and efficacy of neoadjuvant chemotherapy in women with stage II or III BC. Because it is likely that the positive effects of STF will be enhanced if the period of fasting is prolonged [ 37 , 49 ], a very low calorie, low protein fasting mimicking diet (FMD) is used to ease the burden of prolonged fasting [ 50 ]. Prophylactic dexamethasone will be omitted in the FMD arm during the first 4 chemotherapy cycles to reduce its potentially counteractive metabolic effects.…”
Section: Discussionmentioning
confidence: 99%
“…IGF-1 and insulin stimulate proliferation and growth and inhibit apoptosis in response to calorie and protein availability through signalling via the IGF-1 receptor (IGF-1R) and insulin receptor isoform A (IR-A), respectively [50–53]. Serum IGF-1 levels decrease during STF [5456], because low insulin levels cause growth hormone (GH) resistance of the liver, which inhibits hepatic IGF-1 production [54, 57, 58]. Both insulin and IGF-1 activate the Ras/mitogen-activated protein kinase (MAPK) and phosphatidylinositol-3-kinase (PI3K)/Akt pathways.…”
Section: Differential Stress Resistance and Sensitization In Responsementioning
confidence: 99%