Metabolic, endocrine and mood responses to nocturnal eating in men are affected by sources of dietary energy

Holmbäck, Ulf

doi:10.3109/2000-1967-124

Cited by 6 publications

(4 citation statements)

References 111 publications

(202 reference statements)

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“…The suppression of circadian melatonin production by ocular exposure to bright white light at night, leading to augmented nocturnal tumor uptake of dietary linoleic acid and its conversion to mitogenically active 13-HODE, can now be afforded serious consideration as a new risk factor for human breast cancer (4, 5) and a significant public health issue (55). The high nocturnal dietary intake of fat, particularly linoleic acid, reported for night shift workers (56,57), coupled with melatonin suppression by exposure to light at night provide a firm mechanistic basis upon which to explain, in part, the increased risk of breast cancer in some women who work night shifts for many years (9)(10)(11). Thus, strategies to preserve the integrity of the circadian melatonin signal (i.e., avoidance of bright light at night, intelligent lighting design, circadian-timed physiologic melatonin supplementation) coupled with modifications in nocturnal dietary fat intake may offer a unique approach to the prevention of breast cancer, and perhaps other melatonin-sensitive cancers, in our increasingly 24-hour society.…”

Section: Discussionmentioning

confidence: 99%

Melatonin-Depleted Blood from Premenopausal Women Exposed to Light at Night Stimulates Growth of Human Breast Cancer Xenografts in Nude Rats

et al. 2005

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The increased breast cancer risk in female night shift workers has been postulated to result from the suppression of pineal melatonin production by exposure to light at night. Exposure of rats bearing rat hepatomas or human breast cancer xenografts to increasing intensities of white fluorescent light during each 12-hour dark phase (0-345 MW/cm 2 ) resulted in a dose-dependent suppression of nocturnal melatonin blood levels and a stimulation of tumor growth and linoleic acid uptake/metabolism to the mitogenic molecule 13-hydroxyoctadecadienoic acid. Venous blood samples were collected from healthy, premenopausal female volunteers during either the daytime, nighttime, or nighttime following 90 minutes of ocular bright, white fluorescent light exposure at 580 MW/cm 2 (i.e., 2,800 lx). Compared with tumors perfused with daytimecollected melatonin-deficient blood, human breast cancer xenografts and rat hepatomas perfused in situ, with nocturnal, physiologically melatonin-rich blood collected during the night, exhibited markedly suppressed proliferative activity and linoleic acid uptake/metabolism. Tumors perfused with melatonin-deficient blood collected following ocular exposure to light at night exhibited the daytime pattern of high tumor proliferative activity. These results are the first to show that the tumor growth response to exposure to light during darkness is intensity dependent and that the human nocturnal, circadian melatonin signal not only inhibits human breast cancer growth but that this effect is extinguished by short-term ocular exposure to bright, white light at night. These mechanistic studies are the first to provide a rational biological explanation for the increased breast cancer risk in female night shift workers. (Cancer Res 2005; 65(23): 11174-84)

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Section: Discussionmentioning

confidence: 99%

Melatonin-Depleted Blood from Premenopausal Women Exposed to Light at Night Stimulates Growth of Human Breast Cancer Xenografts in Nude Rats

et al. 2005

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“…The serum levels of glucocorticoids and melatonin, factors with potent adipogenic properties, exhibit circadian oscillations (Hirota and Fukada 2004;Lowrey and Takahashi 2004). Eating during periods of darkness (Holmback et al 2002(Holmback et al , 2003Spiegel et al 2004) and antipsychotic drugs influencing circadian rhythms such as lithium chloride and valproic acid (Baptista et al 1995;Elmslie et al 2001;Atmaca et al 2002;Chengappa et al 2002;Fagiolini et al 2002Fagiolini et al , 2003Iwahana et al 2004) have been associated with an increased incidence of obesity. The serum levels of multiple adipose-derived proteins, including adiponectin, interleukin-6, leptin, lipoprotein lipase, PAI-1, and tumor necrosis factor-α, display a diurnal profile characterized by a distinct amplitude, zenith (peak), and nadir (trough) (Kotlar and Borensztajn 1977;Goubern and Portet 1981;Saad et al 1998;Ahmad et al 2001;Arasaradnam et al 2002;Mastronardi et al 2002;Gavrila et al 2003;Calvani et al 2004;Ruge et al 2004;Yildiz et al 2004).…”

Section: Introductionmentioning

confidence: 99%

Biological aging alters circadian mechanisms in murine adipose tissue depots

Sutton

Ptitsyn

Floyd

et al. 2012

AGE

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Biological aging alters the metabolism and volume of adipose tissue depots. Recent evidence suggests that circadian mechanisms play a role in promoting adipogenesis, obesity, and lipodystrophy.The current study compared cohorts of younger (5-9 months) and older (24-28 months) C57BL/6 mice as a function of biological age and circadian time. Advanced age significantly reduced the weight of the AGE (2013) 35:533-547 DOI 10.1007 Electronic supplementary material The online version of this article (doi:10.1007/s11357-012-9389-7) contains supplementary material, which is available to authorized users. brown, epididymal, inguinal, and retroperitoneal adipose depots but not total body weight. The older mice reduced their physical activity by >50% and delayed their activity initiation after light offset. The expressed transcriptome in brown and white adipose depots and liver of both cohorts displayed evidence of circadian rhythmicity; however, the oscillating mRNAs differed significantly between age groups and across tissues. The amplitude of Cry1, a component of the negative arm of the circadian apparatus, and downstream regulators such as Rev-erbα were elevated in the older relative to the younger cohorts as a function of circadian time. Overall, transcript levels differed significantly for 557 (inguinal adipose), 1,016 (liver), and 1,021 (brown adipose) expressed sequences between the cohorts as a function of age. These included transcripts encoding proteins within the canonical and non-canonical Wnt pathways. Since the Wnt pathway regulates adipose stem cell differentiation and shares a critical enzyme, glycogen synthase kinase 3β, with the circadian mechanism, the intersection between these two fundamental regulatory mechanisms merits further investigation with respect to biological aging of adipose tissues.

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“…Circadian misalignment is common in shiftwork. More than 20% of adults in the United States work nontraditional hours (8) and eat some of their meals during the biological night (9), which can increase blood glucose and triacylglycerol levels in response to a high-carbohydrate versus high-fat diet (10) and increase low-density lipoprotein cholesterol levels (11). Further, shiftwork is associated with increased risk for obesity (12), metabolic syndrome (13), and diabetes (14).…”

mentioning

confidence: 99%

Impact of circadian misalignment on energy metabolism during simulated nightshift work

McHill

Melanson

Higgins

et al. 2014

Proc. Natl. Acad. Sci. U.S.A.

280

238

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Eating at a time when the internal circadian clock promotes sleep is a novel risk factor for weight gain and obesity, yet little is known about mechanisms by which circadian misalignment leads to metabolic dysregulation in humans. We studied 14 adults in a 6-d inpatient simulated shiftwork protocol and quantified changes in energy expenditure, macronutrient utilization, appetitive hormones, sleep, and circadian phase during day versus nightshift work. We found that total daily energy expenditure increased by ∼4% on the transition day to the first nightshift, which consisted of an afternoon nap and extended wakefulness, whereas total daily energy expenditure decreased by ∼3% on each of the second and third nightshift days, which consisted of daytime sleep followed by afternoon and nighttime wakefulness. Contrary to expectations, energy expenditure decreased by ∼12-16% during scheduled daytime sleep opportunities despite disturbed sleep. The thermic effect of feeding also decreased in response to a late dinner on the first nightshift. Total daily fat utilization increased on the first and second nightshift days, contrary to expectations, and carbohydrate and protein utilization were reduced on the second nightshift day. Ratings of hunger were decreased during nightshift days despite decreases in 24-h levels of the satiety hormones leptin and peptide-YY. Findings suggest that reduced total daily energy expenditure during nightshift schedules and reduced energy expenditure in response to dinner represent contributing mechanisms by which humans working and eating during the biological night, when the circadian clock is promoting sleep, may increase the risk of weight gain and obesity.insufficient sleep | melatonin | diet-induced thermogenesis | eating at night | appetite E merging evidence from nonhuman animal models indicates a fundamental interplay between circadian and metabolic physiology (1, 2) with implications for health and disease (3-5). Eating at inappropriate circadian times (e.g., at night) is considered a novel risk factor for weight gain and obesity, yet little research has been conducted in humans on this topic. The circadian time-keeping system in humans modulates energy metabolism so that wakefulness, activity, and food intake are promoted during the solar day and sleep, inactivity, and fasting occur during the solar night (2). With the widespread use of electrical lighting, however, work and social activities are capable of being extended further into the night (6, 7). Being awake during the biological night leads to disturbed physiology and behavior, because it creates a state of desynchrony between the circadian clock and wakefulness-sleep cycle known as circadian misalignment. Circadian misalignment is common in shiftwork. More than 20% of adults in the United States work nontraditional hours (8) and eat some of their meals during the biological night (9), which can increase blood glucose and triacylglycerol levels in response to a high-carbohydrate versus high-fat diet (10) and increase low-dens...

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Metabolic, endocrine and mood responses to nocturnal eating in men are affected by sources of dietary energy

Cited by 6 publications

References 111 publications

Melatonin-Depleted Blood from Premenopausal Women Exposed to Light at Night Stimulates Growth of Human Breast Cancer Xenografts in Nude Rats

Melatonin-Depleted Blood from Premenopausal Women Exposed to Light at Night Stimulates Growth of Human Breast Cancer Xenografts in Nude Rats

Biological aging alters circadian mechanisms in murine adipose tissue depots

Impact of circadian misalignment on energy metabolism during simulated nightshift work

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