The Role of Sleep Curtailment on Leptin Levels in Obesity and Diabetes Mellitus
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Review Article
Obes Facts 2021;14:214–221 Received: May 30, 2020
Accepted: December 23, 2020
DOI: 10.1159/000514095 Published online: March 23, 2021
The Role of Sleep Curtailment on Leptin
Levels in Obesity and Diabetes Mellitus
Maryam Mosavat a Mitra Mirsanjari b Diana Arabiat a, c Aisling Smyth a
Lisa Whitehead a
a School
of Nursing and Midwifery, Edith Cowan University, Joondalup, WA, Australia; b Mazandaran University
of Medical Sciences, Emam Khomeini Hospital, Mazandaran, Iran; c Maternal and Child Nursing Department,
The University of Jordan, Amman, Jordan
Keywords Introduction
Short sleep duration · Leptin · Obesity · Diabetes
Sleep is a biological and behavioral process that is fun-
damental for life and optimum health. Sleep is controlled
Abstract by diurnal, homeostatic, and neurohormonal mecha-
Emerging evidence has identified sleep as a significant, but nisms [1]. Existing research acknowledges that sleep is an
modifiable, risk factor for metabolic syndrome, diabetes, and essential modulator of cardiovascular function, glucose
obesity. Leptin, an adipocyte-derived peptide and a regula- regulation, and hormonal release [2]. Sleep duration has
tor of food intake and energy expenditure, has been shown also been shown to have a pivotal function in metabolic
to be associated with a short sleep duration in the patho- hormones and body weight and it has been linked to oth-
physiology of obesity and consequently type 2 diabetes. This er biological mechanisms including inflammation, the
review focuses on the current evidence indicating the effects autonomic nervous system, the coagulation system, en-
of a short sleep duration on the regulation of leptin concen- dothelial function, and metabolic regulation [3, 4]. Sleep
tration in association with obesity and diabetes mellitus. In quality varies in individuals according to factors such as
summary, the evidence suggests that sleep deprivation, by age, gender, occupation, educational level, socioeconom-
affecting leptin regulation, may lead to obesity and conse- ic status, race, family relationships, and pathological con-
quently development of type 2 diabetes through increased ditions including insomnia, depression level, and sleep-
appetite and food intake. However, findings on the role of disordered breathing [5–7]. According to the US Nation-
leptin in diabetes due to sleep deprivation are contradictory, al Sleep Foundation, adequate sleep duration requirements
and further studies with larger sample sizes are needed to vary across lifespans and from person to person, with 7–
confirm previous findings. © 2021 The Author(s) 9 h recommended for adults [8, 9]. In recent decades, the
Published by S. Karger AG, Basel average sleep duration has decreased worldwide, and this
is widely attributed to a modern lifestyle [10]. Based on
National Sleep Foundation criteria, 75% of preadoles-
karger@karger.com © 2021 The Author(s) Maryam Mosavat
www.karger.com/ofa Published by S. Karger AG, Basel School of Nursing and Midwifery, Edith Cowan University
This article is licensed under the Creative Commons Attribution-
270 Joondalup Dr.
NonCommercial-NoDerivatives 4.0 International License (CC BY- Joondalup, WA 6027 (Australia)
NC-ND) (http://www.karger.com/Services/OpenAccessLicense). m.mosavat @ ecu.edu.au
Usage and distribution for commercial purposes as well as any dis-
tribution of modified material requires written permission.cents and 45% of late adolescents experience sleep defi- cardiovascular disease, and downstream targets of leptin
ciency [11]. may have a therapeutic potential role in the management
Insufficient sleep is characterized by either a consider- of diabetes [29, 30]. Furthermore, the adiponectin-leptin
able reduction in sleep time during a certain period due ratio has been found to be significantly correlated with
to 24-h wakefulness or a reduction in sleep time less than the insulin resistance index in diabetes mellitus [31–33].
the optimal level for individual needs. Sleep loss, related Leptin stimulates cytokine activation and immune-cell
to a decreased total sleep time, can be a result of habitual proliferation, which predisposes to inflammatory condi-
behavior or the presence of a pathological condition in- tions [34].
cluding addiction (medications or alcohol), anxiety, de- The evidence suggests a bidirectional relationship be-
pression, idiopathic, somatic and painful diseases, and tween sleep duration and leptin. Leptin has central neural
subjective and psychophysiological insomnia [12]. specific effects beyond modulation of appetite alone [35].
The reports from recent epidemiological studies, me- Leptin concentrations display a circadian pattern, with its
ta-analyses, and systematic reviews have indicated that levels increasing during the first part of the night and then
sleep duration is significantly correlated with several ad- decreasing during the latter part of the night [36]. Fur-
verse health outcomes including diabetes mellitus, car- thermore, leptin has a function in preserving deep sleep
diovascular diseases, coronary heart diseases and stroke, by antagonizing the orexin neuron function in the hypo-
dyslipidemia, hypertension, metabolic disease, obesity, thalamus [37]. The findings of animal studies presented
and mortality [1, 13–20]. Recent evidence proposes that that the orexin (hypocretin) system monitors sleep and
that relationship between a short sleep duration, obesity, wakefulness through interactions with the system that
and diabetes risk may include at least 3 pathways, i.e., regulates energy homeostasis and facilitates adaptive in-
(1) an altered glucose metabolism, (2) up-regulation of tensification of arousal in response to fasting. The orexin
hunger and appetite or dysregulation of appetite/satiety neuron actions are inhibited by leptin, blood glucose, and
hormones, and (3) down-regulation of energy expendi- food intake [37–39]. An animal study in leptin-resistant
ture [21]. (db/db) genetically obese and diabetic mice showed that
Leptin, a metabolic hormone, has a pivotal function in impaired leptin signaling had deleterious impacts on the
balancing appetite and satiety via food intake regulation regulation of sleep duration [40]. This study proposed
and energy homeostasis [22]. Leptin works in synergy that leptin signaling plays an important role in coordina-
with another metabolic hormone, i.e., ghrelin. Whereas tion of sleep-wake states and metabolism. It appears that
leptin suppresses food intake and induces weight loss, sleep-related changes in leptin level promote progression
ghrelin increasing hunger and food intake [22]. Leptin is of metabolic and immune disorders. Leptin’s proinflam-
the product of the ob gene, which has an impact on matory role [24, 41, 42] proposes that increased serum
growth, metabolism, and reproduction [23, 24]. Leptin leptin levels in metabolic syndrome and obesity in a sleep
has several other biological roles in the body [24], includ- deprivation status may be associated with low-grade sys-
ing functions in glucose homeostasis via suppression of temic inflammatory diseases, characterized by increased
insulin production in pancreatic β cells [25]. The regula- proinflammatory cytokine levels including interleukin-6
tion of diurnal blood leptin is controlled by multiple fac- and tumor necrosis factor (TNF)-α. Leptin regulates the
tors such as gender, age, feeding, fasting, sleep, obesity, brain appetite-regulating center with information about
and endocrine disorders [26]. The concentration of se- energy balance [43]. It has been believed that there is an
rum leptin is directly related to fat mass, where increased interaction between leptin and insulin in peripheral tis-
circulating leptin, termed leptin resistance, is related to sues [44, 45]. Leptin inhibits energy storage mechanisms,
obesity [27]. The proposed mechanisms involved in whereas insulin enhances leptin production [46]. Evi-
leptin resistance are comprised of a reduction in the num- dence also indicates that leptin promotes insulin sensitiv-
ber of leptin receptors, impairment of receptor function, ity through enhancement of fatty acid oxidation and de-
a reduction in transport across the blood-brain barrier, clined fat accumulation in non-adipose tissues. Leptin
and a circulating suppressor of leptin function [28]. Since induces fatty acid oxidation in muscle via AMP-activated
a leptin deficit in lipodystrophy is accompanied by dys- protein kinase (AMPK) [47]. Moreover, leptin has a sig-
glycemia and insulin resistance, it is expected that glucose nificant role in increasing the glucose uptake in skeletal
metabolism is affected by leptin resistance [28]. Defects muscle through a β-adrenergic mechanism and the hypo-
or dysfunction in the leptin signaling pathway plays a role thalamic-sympathetic nervous system axis [47].
in the pathophysiology of obesity, diabetes mellitus, and
Sleep Curtailment and Leptin Circulation Obes Facts 2021;14:214–221 215
DOI: 10.1159/000514095As one of the factors affecting leptin level regulation, creased body mass. These researchers suggested that a the effect of sleep has been investigated in several experi- leptin deficiency increases appetite and consequently mental studies. Sleep loss with an effect on appetite hor- may cause obesity. The Child and Adolescent Metabolic mone (leptin) and energy expenditure has been linked to Syndrome cohort studies [55, 56] suggested that a short an increased risk of obesity and diabetes. This review aims sleep duration (
increased hunger [66]. Hayes et al. [65] have examined
the level of leptin in association with a reduced sleep time Sleep curtailment
among adults. They reported that a 1-h decrease in total
sleep duration was associated with a 10% increase in
leptin levels [65]. A study on salivary cortisol and leptin Sympathetic Proinflammatory
↑ Ghrelin ↑ ↑
activity cytokines
in young healthy women showed that a single night of
restricted sleep (3 h) altered the diurnal pattern of cortisol
rhythms (the level of morning cortisol was reduced, and ↑ TSH
↑ cortisol
afternoon/evening cortisol levels were elevated) and in-
creased morning leptin levels in subjects but it did not
have an effect on hunger and craving scores [67]. Bosy- ↑
↓ Leptin Insulin resistance
Westphal et al. [73] found that consecutive nightly de- →
creases in sleep duration significantly increased body
weight, energy intake, glucose-induced thermogenesis, ↑
Appetite &
Obesity Diabetes
leptin/fat mass, free triiodothyronine, and free thyroxine hunger
[73]. Charles et al. [74] showed that both short (8 h) sleep durations were associated with increased
Fig. 1. Role of sleep restriction on leptin regulation in obesity and
leptin levels related to obesity. diabetes.
However, unaffected leptin levels have been reported
in patients with a sleep deficiency [61]. In a study in men
with and without insomnia, circulating levels of leptin
and ghrelin were measured across the night. Serial mea- sequently diabetes mellitus. It was shown by a systematic
surement of appetite hormones showed that ghrelin lev- and meta-analysis study that both short and long sleep
els were significantly lower in insomnia patients, whereas durations in type 2 diabetes patients is significantly associ-
leptin did not differ between the groups. Furthermore, ated with an increase in hemoglobin A1c (HbA1c) levels,
the findings of this study concluded that dysregulation in suggesting poorer glycemic control compared to that with
energy balance in patients with insomnia results in weight a normal sleep duration, with the relationship being U-
gain in this population [61]. A Circadian Locomotor Out- shaped [84]. In another study both a short sleep duration
put Cycles Kaput (CLOCK) gene study showed that a (>5.5 and 5.5–6.4 h) and a long sleep duration (7.5–8.4 h)
shorter sleep duration increased ghrelin levels with no ef- were associated with an increase in the risk of metabolic
fects on leptin values [60]. This study suggested that sleep syndrome, insulin resistance, and high-sensitivity C-reac-
reduction with alterations in ghrelin levels and changes tive protein in diabetic patients compared to those with
in eating behaviors may affect weight and weight loss. 6.5–7.4 h of sleep [85]. These findings also concluded that
Schmid et al. [62], in a study in healthy normal-weight sleep duration has a U-shaped relationship with metabol-
men, reported that feelings of hunger and ghrelin levels ic syndrome and insulin resistance. A recent meta-analy-
were elevated after 1 night of total sleep deprivation, sis confirmed that short sleep (> 6 compared to 7 h) may
whereas morning serum leptin concentrations was unaf- increase the risk of type 2 diabetes by approximately 30%
fected. A large multiethnic study also found no associa- [86]. It has been proposed that sleep deprivation impairs
tion between sleep duration and leptin levels [75]. insulin sensitivity and pancreatic β-cell function and glu-
cose uptake by target cells, increasing insulin resistance
and leading to type 2 diabetes [87–94]. Recent evidence
Sleep Duration, Leptin, and Diabetes suggests that the metabolic hormones leptin and ghrelin
are involved in the relationship between sleep and dys-
Sleep plays a critical role in glucose regulation, and regulation of insulin and glucose and increase the risk of
sleep duration has been shown to have an inverse effect on diabetes [63, 68, 94–97]. Given the effects of sleep defi-
endocrine function and carbohydrate metabolism [2, 76]. ciency on leptin levels and metabolism, a short sleep dura-
The link between sleep and glucose metabolism has been tion may mediate its effects on incident diabetes through
explored in several studies, where it has been proposed weight gain [98, 99] (Fig. 1).
that both short [13, 77–80] and long sleep durations [81– The reviews on the role of sleep restriction in the met-
83] may increase the risk of developing obesity and con- abolic and endocrine alterations propose that a decreased
Sleep Curtailment and Leptin Circulation Obes Facts 2021;14:214–221 217
DOI: 10.1159/000514095sleep duration impairs glucose tolerance and insulin sen- vestigated the role of a short sleep duration on leptin
sitivity, increases evening concentrations of cortisol and regulation; however, the findings regarding the role of
levels of ghrelin, decreases levels of leptin, and increases leptin in diabetes as a consequence of sleep curtailment
appetite and hunger [100, 101]. are conflicting and more studies with a larger sample size
In contrast, a multiethnic study in a population at high are required to confirm the previous findings.
risk for diabetes showed that a short sleep duration (≤5.5
h) was associated with an increase in leptin levels [75]. A
study in diabetic patients showed that an insufficient Strengths and Limitations
sleep duration increased the level of leptin and insulin re-
sistance compared to those with an appropriate sleep du- We reviewed and discussed the probable mechanism
ration [102]. A laboratory-based sleep study showed that underlying the effect of sleep duration on leptin regula-
sleep restriction (5 nights of 4 h in bed) impaired glucose tion as the potential physiological mechanism underlying
homeostasis and increased fasting and insulin levels [63]. obesity and type 2 diabetes. Potential limitations of this
Sleep restriction was associated with an increase in after- work include the conflation of sleep quality and sleep du-
noon cortisol and leptin levels compatible with an in- ration where these were not always reported separately in
creased insulin resistance [63]. It has been reported that the studies included in this review. Furthermore, this re-
a 1-h reduction in sleep duration was associated with a 7% view was conducted as a narrative review and as such a
elevation in leptin levels [65]. Furthermore, a study in ro- quality appraisal of the included papers was not under-
tating-shift-work women reported an inverse association taken. Further work is required to compare the findings
between leptin levels and the risk of type 2 diabetes. How- of both sleep quality and duration on leptin circulation
ever, there was no association between sleep duration, related to obesity and diabetes.
leptin levels, and diabetes [103].
Considering the role of leptin in regulation of energy
consumption, a decrease in the production of leptin due Conflict of Interest Statement
to a lack of sleep may explain the contribution of adjust-
ment of this hormone to obesity, decreased insulin sensi- The authors declare that there is no conflict of interest regard-
ing the publication of this article.
tivity, and increased insulin resistance. It is noteworthy
that elevation of serum leptin levels results in decreased
leptin transport across the blood-brain barrier [104]. It Funding Sources
has been indicated that when leptin reaches its threshold
the blood-brain barrier limits the leptin transport from There were no funding sources for this work.
peripheral blood to the central nervous system, inhibiting
its activity [105]. This condition may explain the eleva-
tion of leptin levels due to sleep restriction, where the ef- Author Contributions
fectiveness of it is attenuated. In this way, leptin resis-
tance, characterized by a decreased response to leptin due Maryam Mosavat drafted this paper. Mitra Mirsanjari, Diana
Arabiat, Aisling Smyth, and Lisa Whitehead reviewed and revised
to a reduced receptor expression, is another possible this work. All authors read and approved the final version of this
mechanism that explains elevated leptin levels in the article.
blood but decreased leptin effects [28]. Thus, in the case
of elevated plasma leptin levels it does not consistently
reflect increased leptin efficacy and function in glucose
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