See discussions, stats, and author profiles for this publication at: https://www.researchgate.

net/publication/223986215

Short sleep duration and obesity: Mechanisms and future perspectives

Article  in  Cell Biochemistry and Function · August 2012

DOI: 10.1002/cbf.2832 · Source: PubMed

CITATIONS READS

34 744

8 authors, including:

Ioná Zalcman Zimberg Ana Dâmaso

Universidade Federal de São Paulo Universidade Federal de São Paulo
49 PUBLICATIONS   455 CITATIONS    170 PUBLICATIONS   2,535 CITATIONS   

SEE PROFILE SEE PROFILE

Aline Millani-Carneiro Helton De Sá Souza

Universidade Federal de São Paulo Universidade Federal de São Paulo
6 PUBLICATIONS   44 CITATIONS    28 PUBLICATIONS   209 CITATIONS   

SEE PROFILE SEE PROFILE

Some of the authors of this publication are also working on these related projects:

Repercussions of adipose tissue remodeling during cachexia in patients with gastrointestinal cancer View project

HIIT and immunometabolic response View project

All content following this page was uploaded by Ioná Zalcman Zimberg on 07 December 2017.

The user has requested enhancement of the downloaded file.

cell biochemistry and function
Cell Biochem Funct 2012; 30: 524–529.
Published online 4 April 2012 in Wiley Online Library
(wileyonlinelibrary.com) DOI: 10.1002/cbf.2832

Short sleep duration and obesity: mechanisms and future perspectives

Ioná Zalcman Zimberg1,2, Ana Dâmaso2,3, Mariana Del Re1,2, Aline Millani Carneiro2, Helton de Sá Souza2,
Fábio Santos de Lira1,2,4, Sergio Tufik1 and Marco Túlio de Mello1,2*
1
Departamento de Psicobiologia, Universidade Federal de São Paulo, São Paulo, Brazil
2
Centro de Estudos em Psicobiologia e Exercício (CEPE), São Paulo, Brazil
3
Departamento de Biociências, Universidade Federal de São Paulo, Santos, Brazil
4
Laboratório de Fisiologia e Bioquímica do Exercício, Universidade do Extremo Sul Catarinense, Criciúma, SC, Brazil

A reduction of sleep time has become common over the last century, and growing evidence from both epidemiological and laboratory-based
studies suggests sleep curtailment is a new risk factor for the development of obesity. On this basis, the present review examines the role of
sleep curtailment in the metabolic and endocrine alterations, including decreased glucose tolerance and insulin sensitivity, increased evening
concentrations of cortisol, increased levels of ghrelin, decreased levels of leptin and increased hunger and appetite. It will be discussed how
sleep restriction may lead to increase in food intake and result in greater fatigue, which may favour decreased energy expenditure. Altogether,
evidences point to a possible role of decreased sleep duration in the current epidemic of obesity and therefore present literature highlights the
importance of getting enough good sleep for metabolic health. Many aspects still need to be clarified and intervention studies also need to be
conducted. Copyright © 2012 John Wiley & Sons, Ltd.

key words—sleep; obesity; diabetes; nutrition; hormones

INTRODUCTION SLEEP LOSS AND OBESITY

The worldwide prevalence of obesity is increasing rapidly,
representing one of today’s most important contemporary
health problems. A recent report from the World Health
Organization estimated that in 2008, 1
5 billion adults were
overweight, and over 200 million men and nearly 300
million women were obese.1
Obesity is a chronic disease that involves social,
behavioural, environmental, cultural, psychological, metabolic
and genetic factors. Although changes in the balance between
energy intake and expenditure are clearly responsible for the
current epidemic of obesity,2 factors that can lead to a positive
energy balance are still inconclusive. In the past few years, a
large body of evidence has shown that short sleep duration
may affect both sides of the energy balance equation (energy
intake and expenditure), resulting in obesity.3
Even though the mechanisms involved in modifications
in eating habits are not completely understood, it is known
that alterations in sleep patterns and sleep efficiency
induced by alterations in the sleep–wake schedule can
significantly alter appetite, satiety4, food intake5,6 and energy
balance4,7 that, consequently, could have important implica-
tions in the increase of obesity.8–10
*Correspondence to: M. T. de Mello, Departamento de Psicobiologia,
Universidade Federal de São Paulo, Rua Professor Francisco de Castro,
93. Vila Clementino, São Paulo, SP, Brazil, CEP 04020–050. E-mail:
tmello@demello.net.br
A reduction of sleep time has become common in recent
years, prompted by the demands and opportunities of
modern society.7 Over the last 40 years, self-reported sleep
duration has decreased by 1
5–2 h in the USA. In 2009, a poll
conducted by the National Sleep Foundation demonstrated
that American adults sleep an average of 6 h and 40 min on
weekdays and 7 h and 7 min during the weekend. By com-
parison, in 1960, the average sleep duration was 8
5 h.11
The proportion of young adults with a period of sleep shorter
than 7 h per day has increased from 15
6% in 1960 to 43% in
2009.12 In Brazil, self-reported sleep duration has decreased
approximately 0
3 h between 1987 and 2007.13,14
Sleep research has mainly focused on the cognitive conse-
quences of sleep loss in the belief that sleep is essential only
for the brain. In the past few years, however, there has been
a shift in concern about the consequences of sleep loss for
other organs and physiological systems.
Over the past 6 years, much attention has been focused
on the relationship between sleep duration and obesity.
Cross-sectional studies have confirmed the association
between sleep duration and body mass index (BMI) in
both children and adults, and prospective studies have
tested the hypothesis that short sleep duration at baseline
predicted weight gain or increased incidence of obesity
over the follow-up period.15–27
Epidemiological and laboratory studies of partial sleep
restriction have provided increasing evidence that short

Received 12 December 2011

Revised 29 February 2012
Copyright © 2012 John Wiley & Sons, Ltd. Accepted 20 March 2012
 SLEEP AND OBESITY
sleep duration results in metabolic changes that may con-
tribute to the development of obesity, insulin resistance,
diabetes and cardiovascular disease.3,4,17,19,28–30 Cappuc-
cio et al.,31 in a meta-analysis, demonstrated that a
reduction of 1 h of sleep per day was associated with a
0
35 kg m 2 increase in BMI.
Taheri3 suggested some hypotheses regarding the
mechanism that relates sleep restriction and obesity.
According to the author, greater awake time, besides pro-
moting hormonal changes capable of increasing caloric
intake, may provide more opportunity for food intake
and result in greater fatigue, which tends to decrease
the level of physical activity and decreases basal meta-
bolic rate. Significant weight gain may, in turn, result
in insulin resistance, which is a condition that may pro-
mote further adiposity.
NEUROENDOCRINE CHANGES ASSOCIATED
WITH REDUCED SLEEP
Sleep curtailment is associated with two parallel endo-
crine modifications that can significantly alter food
intake: decreased secretion of the anorexigenic hormone
leptin7,18,32 and increased secretion of the orexigenic
hormone ghrelin,4,7,18,33 thus resulting in increased
hunger and food intake.4
In the experiment conducted by Spiegel et al.,4 two
consecutive nights of sleep restriction (4 h of sleep per
night) in young men was associated with a 28% increase
in ghrelin level and an 18% reduction in leptin level
during the day. The researchers found that sleep restric-
tion was significantly associated with increase in hunger
(24%) and appetite (23%) as measured by visual
analogue scales.
Spiegel and colleagues7,30 also demonstrated that six
consecutive nights of sleep restriction (4 h of sleep per
night) was associated with increases in sympathetic
nervous system activity, evening cortisol level and growth
hormone level and reductions in thyroid-stimulating hor-
mone. Magee et al.34 observed that two consecutive nights
of 5 h of sleep led to a significant reduction in peptide YY
level and a corresponding decrease in satiety. Moreover,
sleep restriction has been found to promote an inflamma-
tory response with increases in serum pro-inflammatory
C-reactive protein, IL-6, and TNF-a.35
The effects of sleep restriction in circulating levels of
cytokines are particularly controversial. Studies have
demonstrated that the cytokines can be elevated,36
decreased37 or not measurably changed after sleep
deprivation.38 Our group recently found that paradoxical
sleep deprivation of 96 h decrease fat mass and may
modulate the cytokine content in different depots of adi-
pose tissue.39 It was found an increased IL-6 levels and
decreased TNF-a protein concentration in adipose tissue
with increased levels of corticosterone in serum.
Increased levels of IL-6 in adipose tissue cause an in-
crease lipolysis, decrease lipase lipoprotein activity and
Copyright © 2012 John Wiley & Sons, Ltd.
525
increase mobilization of fatty acids, leading to a state
of increase metabolic demands.
Chronic elevation of cytokine levels in the adipose tissue
and systemic may progress to low-grade inflammation, a
similar state found in obesity.40 Probably the link between
short sleep and development of obesity may have start in
the persistence of elevated levels of cytokines.
Many studies have described a significant impairment
of glucose control in individuals who have decreased
sleep duration.41,42,30 Spiegel et al.30 found that six con-
secutive nights of sleep restriction (4 h of sleep per night)
was associated with a decrease of 30% of glucose effect-
iveness and 30% of acute insulin response to glucose.
This difference in glucose effectiveness was nearly
identical to that reported between groups of patients
with non-insulin-dependent diabetes and normoglycemic
white men.43 The mechanism involved in impaired
glucose metabolism following changes in the sleep-wake
rhythm seems to be the decreased efficacy of the negative-
feedback regulation of the hypothalamus-pituitary-adrenal
axis.41
The results of these and other studies11,17,18,32,33 suggest
that modification of sleep duration can lead to endocrine
dysregulations that promote obesity (Figure 1).
Insulin resistance may also be promoted by the mainten-
ance of higher levels of glucose and fatty acids generated
by the increased food intake during sleep restriction. Several
studies have showed that hyperglycemic and hyperlipidemic
conditions contribute to the development of insulin resist-
ance in obese individuals.44–46 Some studies with animals
have demonstrated that consumption of high fat and/or high
carbohydrate diet leads to insulin resistance in several
tissues because of inflammatory and disrupted insulin
pathways.47–50
INCREASED FOOD INTAKE RESULTING FROM
SLEEP RESTRICTION
Sleep deprivation seems to increase not only appetite but
also preference for foods containing more energy.18,51
Spiegel et al.4 showed that the appetite for energy-rich foods
with high carbohydrate content, including sweets, salty
snacks and starchy foods, increased from 33% to 45%
after sleep restriction, although the appetite for fruits,
vegetables and high-protein foods was less affected.
This preference for such foods is concerning because in
addition to presenting a hormone pattern that predisposes
to increased energy intake,4 individuals with sleep loss
tend to meet this need with foods of low nutritional
quality (Figure 2).42–56
In a protocol of 14 consecutive days of sleep restriction
(5
5 h of sleep per night) with ad libitum food intake,
Nedeltcheva et al.57 indicated that sleep restriction led to
an increase in calorie consumption that was attributed to
snacking, particularly during the night when the individual
would normally be sleeping. This greater opportunity to
eat during the evening, which is a time of the day when
Cell Biochem Funct 2012; 30: 524–529.
526
Figure 1. Metabolic alterations caused by sleep debt. PYY, peptide YY; GH, growth hormone
Figure 2. Effect of sleep restriction on food intake
people become less satisfied by a given amount of food
intake and may be more vulnerable to overeating, could pro-
mote a higher susceptibility to weight gain.58,59
EFFECT OF SLEEP RESTRICTION ON ENERGY
EXPENDITURE
Another plausible pathway linking chronic sleep restriction
to obesity regards energy expenditure. Individuals who get
insufficient sleep are more likely to experience fatigue and
excessive daytime sleepiness, which could make them less
likely to engage in daytime physical activity and more likely
to engage in sedentary behaviours such as television view-
ing (Figure 3).3,19,60,61
Cross-sectional studies have shown that sleep disturbance
or wakefulness during nighttime is associated with
lower daytime physical activity and more obesity-related
Copyright © 2012 John Wiley & Sons, Ltd.
i. z. zimberg ET AL.
behaviours in both children and adults.19,61,21,62 In a large
sample of adolescents, Knutson et al.8 found that about
40% of 12–16 year olds reported waking up tired, which
could have an adverse effect on daily physical activity. In
a cross-sectional sample of adolescents, Gupta et al.19
observed that for each hour decrease in sleep, the odds of
obesity increased by 80%, and daytime physical activity
diminished by 3% for every hour of increased sleep disturb-
ance. Ortega et al.,61 in a large sample of adolescents,
observed that short sleep duration was associated with
excessive TV watching, which may confer risk for reduced
energy expenditure and increased caloric intake.63 These
reductions in physical activity could promote a positive
energy balance and may partially account for the association
between chronic sleep restriction and obesity.
On the other hand, Nedeltcheva et al.57 reported no differ-
ences in total energy expenditure after measuring ten
subjects, who spent either 5
5 or 8
5 h time in bed, with
Cell Biochem Funct 2012; 30: 524–529.
 SLEEP AND OBESITY
Figure 3. Effect of sleep restriction on energy expenditure
doubly labelled water for 14 d during caloric restriction.
They found decreased resting metabolic rate after only
5
5 h in bed compared with 8
5 h, which may be an effect
of a decrease in sleeping metabolic rate because of fewer
sleeping hours.
Jung et al.64 recently design protocol with seven healthy
men, who lived for 3 days in a whole-room indirect calorim-
eter, and were submitted to 24 h normal sleep (8 h), followed
by 40 h sleep deprivation and 8 h scheduled recovery sleep.
The authors demonstrated that 24 h energy expenditure dur-
ing sleep deprivation was significantly increased by ~7%
(~134  2
1 kcal) and was significantly decreased by ~5%
during recovery (~96  25 kcal). This indicates that main-
taining wakefulness under bed-rest conditions is energetic-
ally costly, and human metabolic physiology has the
capacity to make adjustments to respond to the energetic
cost of sleep deprivation.
Several human studies have demonstrated reduced levels
of leptin after sleep loss,4,7,18 then it is possible that the
reduction in leptin is associated with a reduction in energy
expenditure. Still, the increase in ghrelin during sleep
restriction could also be associated with a decrease in non-
exercise activity thermogenesis. Indeed, in rodent models,
there is good evidence to indicate that leptin and ghrelin
have opposite effects on energy expenditure. Leptin
possibly increases energy expenditure via increased thermo-
genesis in brown adipose tissue,65 whereas central ghrelin
administration has been reported to decrease locomotor
activity in rats.61,76
EFFECT OF CIRCADIAN DISRUPTION
Modification of sleep schedule has been pointed as a factor
that can lead to changes of circadian rhythms.66 Mullignton
et al.32 verified in a study of 88 h of sleep deprivation that
the diurnal amplitude of leptin was reduced and returned
toward normal during the period of recovery sleep.
Likewise, in the experiment conducted by Spiegel et al.,7
6 days of 4-h bedtimes was associated with a decline in
leptin and thyroid-stimulating hormone diurnal amplitude
and acrophase and a slower rate of decline of cortisol across
the day time. The inverse relationship between leptin and
cortisol 24 h profile was disrupted after sleep restriction as
leptin levels stopped rising in the early evening, when
Copyright © 2012 John Wiley & Sons, Ltd.
527
cortisol concentrations were still declining, and the curtail-
ment of the leptin elevation was quantitatively associated
with an elevation of evening cortisol levels.
Continuous disruption of circadian rhythms as well as
nocturnal eating, as seen in human shift workers, has been
associated with body weight gain, metabolic disturbances,
type 2 diabetes and cardiovascular diseases,67–72 in a forced
desynchrony protocol with ten subjects, found that short-
term circadian misalignment—similar to what occurs chron-
ically with shift work—results in systematic increases in
postprandial glucose, insulin and mean arterial pressure,
systematic decreases in 24 h leptin and the complete inver-
sion of the cortisol profile (increased cortisol at the end of
the wake episode and beginning of the sleep episode).
Alterations in the sleep–wake schedule affect intracellular
circadian clocks—molecular mechanisms that enable the
cell, tissue or organism to anticipate diurnal variations in
the environment. The environment (of cells and tissues)
may include circulating levels of nutrients (for example,
glucose, fatty acids and triacylglycerol) and various
hormones (for example, insulin, leptin, ghrelin and gluco-
corticoids). As such, alterations in the timing mechanism
are likely to induce nutritional changes that may potentiate
disrupted metabolism73 and influence appetite, satiety and,
therefore, food intake.4 It is believed also that problems in
adjustment of the biological clock, so impairing the duration
and quality of sleep, can also modify food intake.74,75
CONSIDERATIONS AND FUTURE PERSPECTIVES
Although laboratory studies have been conducted in adults
only, a large number of epidemiologic studies in paediatric
and adolescent populations have demonstrated associations
between short sleep and adiposity. There is still no conclu-
sive position on the relationship between short sleep
duration and obesity in the elderly population. Further
research should be conducted to explore the relationship of
short sleep duration and neuroendocrine release and meta-
bolic function in different populations, such as with obesity,
diabetes, sleep disorders (e.g. obstructive sleep apnea,
insomnia), shift workers, among others.
Intervention studies with manipulations of sleep duration
are important to determine the role of sleep duration in
weight gain and weight loss. In addition, other hormones
Cell Biochem Funct 2012; 30: 524–529.
528 i. z. zimberg
that affect appetite, such as orexins, resistin, GLP-1 and
obestatin, should be investigated to better address the role
of sleep duration in weight gain and metabolic disturbances.
Lastly, studies carrying out nonpharmacology strategies as
exercise training and nutrition intervention are needed to
evaluate how sleep restriction damages could be prevented
and/or restored.
CONFLICT OF INTEREST
The authors have declared that there is no conflict of
interest.
ACKNOWLEDGEMENTS
The authors thank Thaiene Campos, Luciana Caxa, Marcos
Monico Neto, Paula Amaral Brandão de Souza, the
Associação Fundo de Incentivo à Pesquisa (AFIP), Centro
de Estudos em Psicobiologia e Exercicio (CEPE), Centro de
Estudo Multidisciplinar em Sonolencia e Acidentes (CEMSA),
CEPID/SONO-FAPESP (1998/14303-3), CNPq, CAPES,
FAPESP (2009/05657-2, 2008/09565-2, 2008/53069-0, 2006/
00684-3), UNIFESP, FADA, and FADA/UNIFESP.
REFERENCES
1. World Health Organization (WHO). Obesity and Overweight. Fact
sheet n.311 URL: http://www.who.int/mediacentre/factsheets/fs311/
en/index.html [Accessed July 2011]
2. World Health Organization (WHO). Obesity: Preventing and
managing the global epidemic. World Health Organization, WHO
Technical Report Series, No. 894, Geneva, 2000.
3. Taheri S. The link between short sleep duration and obesity: we should
recommend more sleep to prevent obesity. Arch Dis Child 2006; 9: 81–4.
4. Spiegel K, Tasali E, Penev P, Van Cauter E. Brief communication:
Sleep curtailment in healthy young men is associated with decreased
leptin levels, elevated ghrelin levels, and increased hunger and
appetite. Ann Intern Med 2004; 141: 846–50.
5. Rechtschaffen A, Gilliland MA, Bergmann BM, Winter JB.
Physiological correlates of prolonged sleep deprivation in rats. Science
1983; 221: 182–4.
6. Rechtschaffen A, Bergmann BM. Sleep deprivation in the rat by the
disk-over-water method. Behav Brain Res 1995; 69: 55–63.
7. Spiegel K, Leproult R, L’hermite-Baleriaux M, Copinschi G, Penev PD,
Van Cauter E. Leptin levels are dependent on sleep duration: relation-
ships with sympathovagal balance, carbohydrate regulation, cortisol,
and thyrotropin. J Clin Endocrinol Metab 2004; 89: 5762–71.
8. Knutson K. Impact of sleep and sleep loss on glucose homeostasis and
appetite regulation. Sleep Med Clin 2007; 2: 187–97.
9. Scheen AJ. Does chronic sleep deprivation predispose to metabolic
syndrome? Rev Med Liege 1999; 54: 898–900.
10. Nakamura K, Shimai S, Kikuchi S, et al. Shift work and risk factors for
coronary heart disease in Japanese blue-collar workers: serum lipids
and anthropometric characteristics. Occup Med 1997; 47: 142–6.
11. Kripke DF, Simons RN, Garfinkel L, Hammond EC. Short and long
sleep and sleeping pills. Is increased mortality associated? Arch Gen
Psychiatry 1979; 36: 103–16.
12. National Sleep Foundation: Sleep in America Poll. Washington, 2009.
13. Pires MLN, Benedito-Silva AA, Mello MT, Del Giglio S, Pompeia C,
Tufik S. Sleep habits and complaints of adults in the city of
São Paulo, Brazil, in 1987 and 1995. Braz J Med Biol Res 2007;
40: 1505–15.
Copyright © 2012 John Wiley & Sons, Ltd.
ET AL.
14. Santos-Silva R, Bittencourt LR, Pires ML, et al. Increasing trends of sleep
complaints in the city of Sao Paulo, Brazil. Sleep Med 2010; 11: 520–4.
15. Kohatsu ND, Tsai R, Young T, Vangilder R, Burmeister LF,
Stromquist AM. Sleep duration and body mass index in a rural
population. Arch Intern Med 2006; 166: 1701–5.
16. Vorona R, Winn M, Babineau T, Eng B, Feldman H, Ware J. Overweight
and obese patients in a primary care population report less sleep than
patients with a normal body mass index. Arch Inter Med 2005; 165: 25–30.
17. Hasler G, Buysse DJ, Klaghofer R, Gamma A, Ajdacic V, Eich D. The
association between short sleep duration and obesity in young adults: a
13-year prospective study. Sleep 2004; 27: 661–6.
18. Taheri S, Lin L, Austin D, Young T, Mignot E. Short sleep duration is
associated with reduced leptin, elevated ghrelin and increased body
mass index. PLoS Med 2004; 1: 210–7.
19. Gupta NK, Mueller WH, Chan W, Meininger JC. Is obesity associated
with poor sleep quality in adolescents? Am J Hum Biol 2002; 14: 762–8.
20. Kripke DF, Garfinkel L, Wingard DL, Klauber MR, Marler MR.
Mortality associated with sleep duration and insomnia. Arch Gen
Psychiatry 2002; 59: 131–6.
21. Sekine M, Yamagami T, Handa K, et al. A dose–response relationship
between short sleeping hours and childhood obesity: results of the
Toyama Birth Cohort Study. Child Care Health Dev 2002; 28: 163–70.
22. Vioque J, Torres A, Quiles J. Time spent watching television, sleep
duration and obesity in adults living in Valencia, Spain. Int J Obes
Relat Metab Disord 2000; 24: 1683–8.
23. Stranges S, Cappuccio FP, Kandala NB, et al. Cross-sectional versus
prospective associations of sleep duration with changes in relative
weight and body fat distribution: the Whitehall II Study. Am J Epide-
miol 2008; 167: 321–9.
24. López-García E, Faubel R, León-Muñoz L, Zuluaga MC, Banegas JR,
Rodríguez-Artalejo F. Sleep duration, general and abdominal obesity,
and weight change among the older adult population of Spain. Am J
Clin Nutr 2008; 87: 310–316.
25. Rontoyanni VG, Baic S, Cooper AR. Association between nocturnal
sleep duration, body fatness, and dietary intake in Greek women.
Nutrition 2007; 23: 773–7.
26. Bjorvatn B, Sagen IM, yane N, et al. The association between sleep
duration, body mass index and metabolic measures in the Hordaland
Health Study. J Sleep Res 2007; 16: 66–76.
27. Chaput JP, Després JP, Bouchard C, Tremblay A. The association
between sleep duration and weight gain in adults: a 6-year prospective
study from the Quebec Family Study. Sleep 2008; 31: 517–23.
28. Tasali E, Leproult R, Ehrmann DA, Cauter EV. Slow-wave sleep and
the risk of type 2 diabetes in humans. Proc Natl Acad Sci U S A
2008; 105: 1044–49.
29. Gottlieb DJ, Punjabi NM, Newman AB, et al. Association of sleep
time with diabetes mellitus and impaired glucose tolerance. Arch
Intern Med 2005; 165: 863–7.
30. Spiegel K, Leproult R, Van Cauter E. Impact of sleep debt on meta-
bolic and endocrine function. Lancet 1999; 354: 1435–9.
31. Cappuccio FP, Taggart FM, Kandala NB, et al. Meta-analysis of
short sleep duration and obesity in children and adults. Sleep
2008; 3: 619–626.
32. Mullington JM, Chan JL, Van Dongen HP, et al. Sleep loss reduces
diurnal rhythm amplitude of leptin in healthy men. J Neuroendocrinol
2003; 15: 851–4.
33. Bodosi B, Gardi J, Hajdu I, Szentirmai E, Obal F, Jr, Krueger JM.
Rhythms of ghrelin, leptin, and sleep in rats: effects of the normal
diurnal cycle, restricted feeding, and sleep deprivation. Am J Physiol
Regul Integr Comp Physiol 2004; 287: R1071–9.
34. Magee CA, Huang X, Iverson DC, Caputi P. Acute sleep restriction
alters neuroendocrine hormones and appetite in healthy male adults.
Sleep Biol Rhythms 2009; 7: 125–127.
35. Vgontzas AN, Zoumakis E, Bixler EO, et al. Adverse effects of modest
sleep restriction on sleepiness, performance, and inflammatory
cytokines. J Clin Endocrinol Metab 2004; 89: 2119–26.
36. Shearer WT, Reuben JM, Mullington JM, et al. Soluble TNF-alpha
receptor 1 and IL-6 plasma levels in humans subjected to the sleep
deprivation model of spaceflight. J Allergy Clin Immunol 2001;
107: 165–70.
Cell Biochem Funct 2012; 30: 524–529.
 SLEEP AND OBESITY
37. Frey DJ, Fleshner M, Wright KP, Jr. The effects of 40 hours of total
sleep deprivation on inflammatory markers in healthy young adults.
Brain Behav Immun 2007; 21: 1050–7.
38. Dinges DF. An overview of sleepiness and accidents. J Sleep Res
1995; 4: 4–14.
39. Rosa Neto JC, Lira FS, Venancio DP, et al. Sleep deprivation affects
inflammatory marker expression in adipose tissue. Lipids Health Dis
2010; 9: 125.
40. Calder PC, Ahluwalia N, Brouns F, Buetler T, Clement K,
Cunningham K. Dietary factors and low-grade inflammation in relation
to overweight and obesity. Br J Nutr 2011; 106: S5–78.
41. Spiegel K, Knutson K, Leproult R, Tasali E, Van Cauter E. Sleep loss:
a novel risk factor for insulin resistance and type 2 diabetes. J Appl
Physiol 2005; 99: 2008–2019.
42. Van Cauter E, Blackman JD, Roland D, Spire JP, Refetoff S, Polonsky
KS. Modulation of glucose regulation and insulin secretion by circa-
dian rhythmicity and sleep. J Clin Invest 1991; 88: 934–942.
43. Bergman RN. Lilly lecture 1989. Toward physiological understanding
of glucose tolerance. Minimal-model approach. Diabetes 1989;
38: 1512–1527.
44. Obarzanek E, Schreiber GB, Crawford PB, et al. Energy intake and
physical activity in relation to indexes of body fat: the National Heart,
Lung, and Blood Institute Growth and Health Study. Am J Clin Nutr
1994 Jul; 60: 15–22.
45. Hirabara SM, Silveira LR, Abdulkader F, Carvalho CR, Procopio J,
Curi R. Time-dependent effects of fatty acids on skeletal muscle me-
tabolism. J Cell Physiol 2007 Jan; 210: 7–15.
46. Matthews VL, Wien M, Sabaté J. The risk of child and adolescent over-
weight is related to types of food consumed. Nutr J 2011; 24: 10–71.
47. Carvalho CR, Bueno AA, Mattos AM, et al. Fructose alters adiponec-
tin, haptoglobin and angiotensinogen gene expression in 3T3-L1
adipocytes. Nutr Res 2010 Sep; 30: 644–9.
48. Motoyama CS, Pinto MJ, Lira FS, Ribeiro EB, do Nascimento CM,
Oyama LM. Gum Guar fiber associated with fructose reduces serum
triacylglycerol but did not improve the glucose tolerance in rats.
Diabetol Metab Syndr 2010; 27: 2–61.
49. Estadella D, Oyama LM, Bueno AA, et al. A palatable hyperlipidic
diet causes obesity and affects brain glucose metabolism in rats. Lipids
Health Dis 2011; 23: 10–168.
50. Pimentel GD, Lira FS, Rosa JC, et al. Intake of trans fatty acids during
gestation and lactation leads to hypothalamic inflammation via TLR4/
NFkBp65 signaling in adult offspring. J Nutr Biochem 2012; 23: 265–71.
51. Naitoh P. Sleep deprivation in human subjects: A reappraisal. Waking
Sleeping 1976; 1: 53–60.
52. Sudo N, Ohtsuka R. Nutrient intake among female shift workers in a
computer factory in Japan. Int J Food Sci Nutr 2001; 52: 367–78.
53. Armstrong S. A chronometric approach to the study of feeding behav-
iour. Neurosci Biobehav Rev 1980; 4: 27–53.
54. Adams CE, Morgan KJ. Periodicity of eating: implications for human
food consumption. Nutr Res 1981; 1: 525–50.
55. Verboeket-van de Venne WP, Westerterp KR. Influence of the feeding
frequency on nutrient utilization in man: consequences for energy
metabolism. Eur J Clin Nutr 1991; 45: 161–9.
56. Moore JG. Chronobiology of the gastrointestinal system. In Biological
Rhythms in Clinical and Laboratory Medicine. Touitou Y, Haus E
(eds). Springer-Verlag: Berlin, 1992; 410–7.
Copyright © 2012 John Wiley & Sons, Ltd.
View publication stats
529
57. Nedeltcheva AV, Kilkus JM, Imperial J, Schoeller DA, Penev PD.
Insufficient sleep undermines dietary efforts to reduce adiposity. Ann
Intern Med 2010; 153: 435–41.
58. Dattilo M, Crispim CA, Zimberg IZ, Tufik S, de Mello MT. Meal dis-
tribution across the day and its relationship with body composition.
Biol Rhythm Res 2010; 42: 119–129.
59. De Castro JM. The time of day of food intake influences overall intake
in humans. J Nutr 2004; 134: 104–11.
60. Knutson KL. Sex differences in the association between sleep and
body mass index in adolescents. J Pediatr 2005; 147: 830–4.
61. Ortega FB, Chillón P, Ruiz JR, et al. Sleep patterns in Spanish adoles-
cents: associations with TV watching and leisure-time physical activ-
ity. Eur J Appl Physiol 2010; 110: 563–73.
62. Singh M, Drake CL, Roehrs T, Hudgel DW, Roth T. The association
between obesity and short sleep duration: a population based study.
J Clin Sleep Med 2005; 1: 357–63.
63. Robinson TN. Reducing children’s television viewing to prevent obes-
ity: randomized controlled trial. JAMA 1999; 282: 1561–7.
64. Jung CM, Melanson EL, Frydendall EJ, Perreault L, Eckel RH, Wright
KP. Energy expenditure during sleep, sleep deprivation and sleep follow-
ing sleep deprivation in adult humans. J Physiol 2011; 589(Pt 1): 235–44.
65. Scarpace PJ. Thermoregulation with age: role of beta-adrenergic signal
transduction. Ann N Y Acad Sci 1997; 15: 111–6.
66. Froy O. Metabolism and Circadian Rhythms—Implications for Obes-
ity. Endocrine Rev 2010; 31: 11–24.
67. Van Drongelen A, Boot CRL, Merkus SL, Smid T, van der Beek AJ.
The effects of shift work on body weight change – a systematic review
of longitudinal studies. Scand J Work Environ Health 2011; 37: 263–275.
68. Crispim CA, Waterhouse J, Dâmaso AR, et al. Hormonal appetite
control is altered by shift work: a preliminary study. Metabolism 2011;
60: 1726–35.
69. Padilha HG, Crispim CA, Zimberg IZ, Folkard S, Tufik S, De Mello
MT. Metabolic Responses on the Early Shift. Chronobiol Int 2010;
27: 1–13.
70. Morikawa Y, Nakagawa H, Miura K. Shift work and the risk of
diabetes mellitus among Japanese male factory workers. Scand J Work
Environ Health 2005; 31: 179–183.
71. Suwazono Y, Dochi M, Sakata K, et al. A longitudinal study on the
effect of shift work on weight gain in male Japanese workers. Obesity
2008; 16: 1887–1893.
72. Scheer FA, Hilton MF, Mantzoros CS, Shea SA. Adverse metabolic
and cardiovascular consequences of circadian misalignment. Proc Natl
Acad Sci U S A 2009; 106: 4453–4458.
73. Bray MS, Young ME. Circadian rhythms in the development of obes-
ity: potential role for the circadian clock within the adipocyte. Obes
Rev 2007; 8: 169–181.
74. Lennernäs M, Akerstedt T, Hambraeus L. Nocturnal eating and serum
cholesterol of three-shift workers. Scand J Work Environ Health 1994;
20: 401–6.
75. Waterhouse J, Minors D, Redfern P. Some comments on the measure-
ment of circadian rhythms after time-zone transitions and during night
work. Chronobiol Int 1997; 14: 125–132.
76. Tang-Christensen M, Vrang N, Ortmann S, Bidlingmaier M, Horvath
TL, Tschöp M. Central administration of ghrelin and agouti-related
protein (83–132) increases food intake and decreases spontaneous
locomotor activity in rats. Endocrinology 2004; 145: 4645–52.
Cell Biochem Funct 2012; 30: 524–529.