检索问题
用科普语言解释睡眠不足为什么会影响代谢和体重
睡眠不足对代谢和体重的影响是一个复杂但日益受到关注的健康问题，尤其是在现代社会，许多人面临睡眠时间不足和作息不规律的挑战。研究表明，睡眠不足和生物钟紊乱是导致肥胖和代谢综合征的重要风险因素，传统观念中认为的能量摄入过多和缺乏体育锻炼并不能完全解释这些疾病的高发率。
什么是睡眠不足和生物钟紊乱？
- 睡眠不足：通常定义为睡眠时间少于推荐的健康时长。这意味着身体没有得到足够的休息来完成其重要的生理修复和调节过程。
- 生物钟紊乱（Circadian Misalignment）：指的是清醒和进食活动发生在体内生物钟系统促进睡眠的时候。这可能发生在夜间使用电子屏幕、倒班工作或夜间社交活动等情境下，这些行为与自然的生理节律不符。
睡眠不足如何影响代谢和体重？
睡眠不足和生物钟紊乱通过多种机制影响身体的能量平衡、食欲、葡萄糖代谢和整体代谢健康。
1. 对食欲激素的调节失衡
睡眠不足最显著的影响之一是导致食欲调节激素的失衡。这主要涉及瘦素（leptin）和胃饥饿素（ghrelin）这两种关键激素。
- 胃饥饿素（Ghrelin）：这是一种“饥饿激素”，由胃分泌，能刺激食欲。睡眠不足会导致胃饥饿素水平升高，使人感到更饥饿，从而增加进食量。
- 瘦素（Leptin）：这是一种“饱腹激素”，由脂肪细胞分泌，能抑制食欲并向大脑发出信号，表明身体有足够的能量储存。睡眠不足会导致瘦素水平降低，使得饱腹感减弱，从而更容易过度进食。
这种胃饥饿素升高和瘦素降低的双重作用，会增加主观饥饿感和食欲，促使人们摄入更多的食物，尤其偏爱高脂肪和高碳水化合物的食物，这直接导致能量摄入增加，从而促进体重增加和肥胖。
此外，其他胃肠道激素也参与食欲调节。例如，胰高血糖素样肽-1（GLP-1）、葡萄糖依赖性促胰岛素多肽（GIP）、胆囊收缩素（CCK）、餐后肽YY（PYY）和催产素（OXM）是抑制食欲的激素，而胃饥饿素则是刺激食欲的激素。睡眠不足可能会影响这些激素的平衡，进一步影响食欲和能量摄入。
2. 对能量消耗的影响
虽然一些早期研究认为，短睡眠时间对总日常能量消耗没有显著影响，也缺乏足够证据表明对静息代谢率、身体活动、饮食诱导的产热或底物利用有有意义的影响，但更新的研究提供了不同的视角。
- 静息代谢率（Resting Metabolic Rate, RMR）：一项研究发现，睡眠限制会导致健康成年人早晨的静息代谢率下降2.6% 。静息代谢率是能量消耗的最大组成部分，其下降表明睡眠不足可能导致身体进入一种节约能量的状态。这可能意味着身体在睡眠不足时，会倾向于储存能量而不是消耗能量，从而影响体重的维持。
- 底物利用：短睡眠持续时间对底物利用（例如，身体是燃烧脂肪还是碳水化合物来获取能量）的影响目前尚无定论。然而，有迹象表明，其他可能影响能量代谢的因素可能会受到影响，例如甲状腺激素和糖皮质激素的调节以及散热增加，尤其是在完全或严重睡眠不足之后。
虽然还需要更多研究来明确睡眠不足在现实生活条件下对能量代谢的精确影响，但初步证据表明，睡眠限制可能通过降低能量消耗来促进体重增加。
3. 对食物选择和摄入量的影响
睡眠不足会影响人们的饮食习惯和食物选择。研究显示，睡眠紊乱会导致能量摄入增加，部分原因是过度零食，主要是高脂肪和高碳水化合物的食物。这种对“垃圾食品”的偏好增加，加上食欲激素的失衡，会进一步加剧体重增加的风险。
4. 对葡萄糖代谢和胰岛素敏感性的影响
睡眠不足和生物钟紊乱与2型糖尿病（T2D）的风险增加密切相关，这主要是通过影响葡萄糖代谢和胰岛素敏感性来实现的。
- 胰岛素敏感性下降：胰岛素是调节血糖的关键激素。当胰岛素敏感性下降时，身体细胞对胰岛素的反应不那么灵敏，需要分泌更多的胰岛素才能将血糖维持在正常水平。长期睡眠不足，即使是轻度睡眠限制（如每晚6.2小时睡眠，持续6周），也会损害女性的胰岛素敏感性，且这种影响独立于体脂变化。在绝经后女性中，这种对胰岛素抵抗的影响更为明显。
- 血糖水平升高：胰岛素敏感性下降会导致空腹胰岛素和HOMA-IR（胰岛素抵抗的稳态模型评估）值升高。这意味着身体在没有进食的情况下，血糖也可能偏高，或需要更高的胰岛素水平才能控制血糖。
- β细胞功能障碍：实验研究表明，睡眠限制与能量稳态、胰岛素抵抗和β细胞功能（胰岛素分泌细胞）的变化相关。长期的胰岛素抵抗会使胰腺的β细胞过度劳累，最终可能导致其功能衰竭，从而引发2型糖尿病。
- 急性夜间血糖波动：饮食和膳食构成对血糖控制有急性和慢性影响，并且餐后夜间血糖和外周血糖水平可能会影响睡眠质量。夜间血糖的急性波动可能导致睡眠碎片化，形成一个恶性循环。
因此，睡眠不足被认为是胰岛素抵抗的一个可修改的风险因素，可以作为糖尿病预防工作的目标。
5. 对炎症和自主神经系统的影响
肥胖和睡眠障碍之间存在双向关系，两者通过行为、生理和激素机制相互加剧。
- 炎症：睡眠不足会加剧代谢综合征的组成部分，包括胰岛素抵抗和血脂异常，进一步促进体重增加。同样，肥胖引起的睡眠障碍会导致促炎状态、血管功能障碍和交感神经过度激活，从而增加心血管代谢风险。
- 自主神经系统失调：睡眠紊乱还可能影响自主神经系统的调节，导致交感神经系统过度活跃，这与代谢异常和心血管风险有关。
6. 生物钟系统的关键作用
昼夜节律系统产生大约24小时的内源性节律，其同步对于健康的身体功能至关重要。许多生理过程，包括葡萄糖代谢的时间，都由昼夜节律系统协调。昼夜节律紊乱或这些节律的失调会导致不良健康结果。
- 时钟基因与代谢：昼夜节律基因网络存在于从细菌到人类的大多数生物中，大多数细胞和组织都表达自主时钟，并且时钟基因的破坏会导致代谢失调。这揭示了代谢和昼夜节律在神经、分子和细胞层面的相互作用。
- 昼夜节律对葡萄糖代谢的调节：昼夜节律系统在调节葡萄糖代谢方面发挥着关键作用。当生物钟系统与外界环境（如光照、进食时间）不同步时，就会发生昼夜节律紊乱，例如倒班工作、不规律的进食时间或夜间暴露于光线。这种紊乱已被证明会损害葡萄糖控制，并增加2型糖尿病的风险。
总结与展望
全球肥胖和2型糖尿病的发病率正在上升，与此同时，睡眠不足和睡眠障碍的患病率也在增加。短睡眠时间是导致肥胖和2型糖尿病发生的风险因素。
睡眠不足通过以下途径对代谢和体重产生负面影响：
- 扰乱食欲激素平衡：增加胃饥饿素，降低瘦素，导致食欲增加，偏好高热量食物。
- 降低能量消耗：可能通过降低静息代谢率来促进能量储存。
- 损害葡萄糖代谢：导致胰岛素敏感性下降和血糖控制受损，增加2型糖尿病风险。
- 加剧炎症和自主神经失调：增加代谢综合征和心血管疾病的风险。
- 生物钟紊乱：使生理过程与自然节律脱节，进一步影响代谢健康。
鉴于这些证据，睡眠不足被认为是一个重要且可改变的代谢综合征、糖尿病和肥胖的风险因素。在过去50年里，平均睡眠时间的显著减少与肥胖患病率的增加相吻合，这提示了反复部分睡眠剥夺对代谢和激素过程的不利影响可能对公众健康产生重要影响。
因此，将睡眠评估和管理纳入肥胖治疗策略至关重要。通过解决睡眠与肥胖之间的双向关系，可以减轻心血管代谢并发症的进展，并改善整体健康结果。避免睡眠不足可能有助于预防肥胖的发生，特别是在儿童中。延长短睡眠者的睡眠时间应该作为一种新的行为干预措施进行探索，以预防体重增加或促进体重减轻。同时，研究人员也在探索通过协同营养策略（特别是碳水化合物的质量、数量和可用性以及碳水化合物与蛋白质的比例）来改善睡眠质量的方法。
References
1The role of insufficient sleep and circadian misalignment in obesity.PubMed
Jean-Philippe Chaput, Andrew W McHill, Rebecca C Cox, et al.
Traditional risk factors for obesity and the metabolic syndrome, such as excess energy intake and lack of physical activity, cannot fully explain the high prevalence of these conditions. Insufficient sleep and circadian misalignment predispose individuals to poor metabolic health and promote weight gain and have received increased research attention in the past 10 years. Insufficient sleep is defined as sleeping less than recommended for health benefits, whereas circadian misalignment is defined as wakefulness and food intake occurring when the internal circadian system is promoting sleep. This Review discusses the impact of insufficient sleep and circadian misalignment in humans on appetite hormones (focusing on ghrelin, leptin and peptide-YY), energy expenditure, food intake and choice, and risk of obesity. Some potential strategies to reduce the adverse effects of sleep disruption on metabolic health are provided and future research priorities are highlighted. Millions of individuals worldwide do not obtain sufficient sleep for healthy metabolic functions. Furthermore, modern working patterns, lifestyles and technologies are often not conducive to adequate sleep at times when the internal physiological clock is promoting it (for example, late-night screen time, shift work and nocturnal social activities). Efforts are needed to highlight the importance of optimal sleep and circadian health in the maintenance of metabolic health and body weight regulation.
2The interrelationship between sleep, diet, and glucose metabolism.PubMed
Marie-Pierre St-Onge, Anna Cherta-Murillo, Christian Darimont, et al.
Obesity and type 2 diabetes (T2D) are increasingly common worldwide. While these disorders have increased in prevalence over the past several decades, there has been a concomitant reduction in sleep duration. Short sleep duration has been associated with higher rates of obesity and T2D, and the causality of these associations and their directionality, continue to necessitate evaluation. In this review we consider the evidence that sleep is an intrinsic factor in the development of obesity and chronic metabolic disorders, such as insulin resistance and T2D, while evaluating a potential bi-directional association. We consider the evidence that diet and meal composition, which are known to impact glycemic control, may have both chronic and acute impact upon sleep. Moreover, we consider that postprandial nocturnal metabolism and peripheral glycemia may affect sleep quality. We propose putative mechanisms whereby acute effects of nighttime glucose excursions may lead to increased sleep fragmentation. We conclude that dietary manipulations, particularly with respect to carbohydrate quality, may confer sleep benefits. Future research may seek to evaluate the effectiveness of synergistic nutrient strategies to promote sleep quality, with particular attention to carbohydrate quality, quantity, and availability as well as carbohydrate to protein ratio.
3Short sleep duration and its association with energy metabolism.PubMed
L Klingenberg, A Sjödin, U Holmbäck, et al.
A growing body of observational evidence suggests that short sleep duration is a risk factor for the development of obesity. Although increased energy intake is the most prevailing causal explanation for this association, we should also consider possible effects on energy metabolism to understand fully the potential impact of short sleep duration on the regulation of energy balance. We performed a search of the literature from 1970 to 2011, including original papers, investigating the relation between short sleep and energy metabolism in animals and humans. Although the limited number of experimental studies in humans precludes any definitive conclusions about causality, short sleep duration does not seem to substantially affect total daily energy expenditure, nor is there sufficient evidence in support of any meaningful effect of restricted sleep on the specific components of energy metabolism (i.e. resting metabolic rate, intentional as well as unintentional physical activity, diet-induced thermogenesis, and substrate utilization). As studies on rats suggest that other factors that can potentially influence energy metabolism could be affected (i.e. hormonal systems and thermoregulation), we included these factors in our literature search and found some indications in support of an up-regulation of thyroid hormones and glucocorticoids as well as increased heat dissipation following total or severe sleep deficit. Although we found some evidence also in humans that suggests a possible effect on energy metabolism, the limitations of the studies make it difficult to draw conclusions on the effect of short sleep on energy metabolism under relevant free living conditions. To explore this area further, more studies using suitable methodology under relevant conditions to mimic real-life situations are needed.
4Sleep Deprivation: Effects on Weight Loss and Weight Loss Maintenance.PubMed
Evangelia Papatriantafyllou, Dimitris Efthymiou, Evangelos Zoumbaneas, et al.
This narrative review presents the findings from intervention studies on the effects of sleep deprivation on eating habits, metabolic rate, and the hormones regulating metabolism, and discusses their relevance to weight loss efforts. Disturbed sleeping patterns lead to increased energy intake, partly from excessive snacking, mainly on foods high in fat and carbohydrates. The studies focused mainly on the effects of sleep duration, but also of sleep quality, on dietary intake during weight loss trials, and on weight loss maintenance. It is important to explore sleep routines that could enhance the efforts of obese and overweight people to lose weight, maintain their weight loss, and improve their overall health.
5Impact of circadian disruption on glucose metabolism: implications for type 2 diabetes.PubMed
Ivy C Mason, Jingyi Qian, Gail K Adler, et al.
The circadian system generates endogenous rhythms of approximately 24 h, the synchronisation of which are vital for healthy bodily function. The timing of many physiological processes, including glucose metabolism, are coordinated by the circadian system, and circadian disruptions that desynchronise or misalign these rhythms can result in adverse health outcomes. In this review, we cover the role of the circadian system and its disruption in glucose metabolism in healthy individuals and individuals with type 2 diabetes mellitus. We begin by defining circadian rhythms and circadian disruption and then we provide an overview of circadian regulation of glucose metabolism. We next discuss the impact of circadian disruptions on glucose control and type 2 diabetes. Given the concurrent high prevalence of type 2 diabetes and circadian disruption, understanding the mechanisms underlying the impact of circadian disruption on glucose metabolism may aid in improving glycaemic control.
6Sleep Deprivation and Central Appetite Regulation.PubMed
Shuailing Liu, Xiya Wang, Qian Zheng, et al.
Research shows that reduced sleep duration is related to an increased risk of obesity. The relationship between sleep deprivation and obesity, type 2 diabetes, and other chronic diseases may be related to the imbalance of appetite regulation. To comprehensively illustrate the specific relationship between sleep deprivation and appetite regulation, this review introduces the pathophysiology of sleep deprivation, the research cutting edge of animal models, and the central regulatory mechanism of appetite under sleep deprivation. This paper summarizes the changes in appetite-related hormones orexin, ghrelin, leptin, and insulin secretion caused by long-term sleep deprivation based on the epidemiology data and animal studies that have established sleep deprivation models. Moreover, this review analyzes the potential mechanism of associations between appetite regulation and sleep deprivation, providing more clues on further studies and new strategies to access obesity and metabolic disease.
7Resting metabolic rate varies by race and by sleep duration.PubMed
Andrea M Spaeth, David F Dinges, Namni Goel
OBJECTIVE: Short sleep duration is a significant risk factor for weight gain, particularly in African Americans and men. Increased caloric intake underlies this relationship, but it remains unclear whether decreased energy expenditure is a contributory factor. The current study assessed the impact of sleep restriction and recovery sleep on energy expenditure in African American and Caucasian men and women. METHODS: Healthy adults participated in a controlled laboratory study. After two baseline sleep nights, subjects were randomized to an experimental (n = 36; 4 h sleep/night for five nights followed by one night with 12 h recovery sleep) or control condition (n = 11; 10 h sleep/night). Resting metabolic rate and respiratory quotient were measured using indirect calorimetry in the morning after overnight fasting. RESULTS: Resting metabolic rate-the largest component of energy expenditure-decreased after sleep restriction (-2.6%, P = 0.032) and returned to baseline levels after recovery sleep. No changes in resting metabolic rate were observed in control subjects. Relative to Caucasians (n = 14), African Americans (n = 22) exhibited comparable daily caloric intake but a lower resting metabolic rate (P = 0.043) and higher respiratory quotient (P = 0.013) regardless of sleep duration. CONCLUSIONS: Sleep restriction decreased morning resting metabolic rate in healthy adults, suggesting that sleep loss leads to metabolic changes aimed at conserving energy.
8Chronic Insufficient Sleep in Women Impairs Insulin Sensitivity Independent of Adiposity Changes: Results of a Randomized Trial.PubMed
Faris M Zuraikat, Blandine Laferrère, Bin Cheng, et al.
OBJECTIVE: Insufficient sleep is associated with type 2 diabetes, yet the causal impact of chronic insufficient sleep on glucose metabolism in women is unknown. We investigated whether prolonged mild sleep restriction (SR), resembling real-world short sleep, impairs glucose metabolism in women. RESEARCH DESIGN AND METHODS: Women (aged 20-75 years) without cardiometabolic diseases and with actigraphy-confirmed habitual total sleep time (TST) of 7-9 h/night were recruited to participate in this randomized, crossover study with two 6-week phases: maintenance of adequate sleep (AS) and 1.5 h/night SR. Outcomes included plasma glucose and insulin levels, HOMA of insulin resistance (HOMA-IR) values based on fasting blood samples, as well as total area under the curve for glucose and insulin, the Matsuda index, and the disposition index from an oral glucose tolerance test. RESULTS: Our sample included 38 women (n = 11 postmenopausal women). Values are reported with ±SEM. Linear models adjusted for baseline outcome values demonstrated that TST was reduced by 1.34 ± 0.04 h/night with SR versus AS (P < 0.0001). Fasting insulin (β = 6.8 ± 2.8 pmol/L; P = 0.016) and HOMA-IR (β = 0.30 ± 0.12; P = 0.016) values were increased with SR versus AS, with effects on HOMA-IR more pronounced in postmenopausal women compared with premenopausal women (β = 0.45 ± 0.25 vs. β = 0.27 ± 0.13, respectively; P for interaction = 0.042). Change in adiposity did not mediate the effects of SR on glucose metabolism or change results in the full sample when included as a covariate. CONCLUSIONS: Curtailing sleep duration to 6.2 h/night, reflecting the median sleep duration of U.S. adults with short sleep, for 6 weeks impairs insulin sensitivity, independent of adiposity. Findings highlight insufficient sleep as a modifiable risk factor for insulin resistance in women to be targeted in diabetes prevention efforts.
9Sleep Apnea, Obesity, and Diabetes - an Intertwined Trio.PubMed
Soumya Kurnool, Karen C McCowen, Nicole A Bernstein, et al.
PURPOSE OF REVIEW: To synthesize the existing literature regarding the complex interplay between sleep disturbance, obesity, and diabetes. The review emphasizes the three pillars of health being diet, exercise, and sleep, with the notion that if one is ignored, then the other two could suffer. RECENT FINDINGS: Sleep deprivation is associated with incident obesity, perhaps mediated by dysregulation in leptin and ghrelin - hormones important in regulation of appetite. Sleep apnea is very common particularly among obese people with type 2 diabetes mellitus. Treatment of sleep apnea has clear symptomatic benefits although its impact on long-term cardiometabolic health is less clear. Sleep disturbance may be an important modifiable risk for patients at risk of cardiometabolic disease. An assessment of sleep health may be an important component of the comprehensive care of patients with obesity and diabetes mellitus.
10Circadian rhythms, sleep, and metabolism.PubMed
Wenyu Huang, Kathryn Moynihan Ramsey, Biliana Marcheva, et al.
The discovery of the genetic basis for circadian rhythms has expanded our knowledge of the temporal organization of behavior and physiology. The observations that the circadian gene network is present in most living organisms from eubacteria to humans, that most cells and tissues express autonomous clocks, and that disruption of clock genes results in metabolic dysregulation have revealed interactions between metabolism and circadian rhythms at neural, molecular, and cellular levels. A major challenge remains in understanding the interplay between brain and peripheral clocks and in determining how these interactions promote energy homeostasis across the sleep-wake cycle. In this Review, we evaluate how investigation of molecular timing may create new opportunities to understand and develop therapies for obesity and diabetes.
11Obesity and sleep disorders: A bidirectional relationship.PubMed
Michela Figorilli, Fernanda Velluzzi, Stefania Redolfi
AIMS: Obesity and sleep disorders are highly prevalent conditions with profound implications for public health. Emerging evidence highlights a bidirectional relationship between these two conditions, with each exacerbating the other in a complex interplay of behavioral, physiological, and hormonal mechanisms. Sleep deprivation and poor sleep quality contribute to energy imbalance through dysregulation of appetite hormones (e.g., leptin and ghrelin), increased caloric intake, and reduced physical activity. Conversely, sleep disorders such as obstructive sleep apnea syndrome (OSAS), insomnia, and restless leg syndrome (RLS) are significantly more common in individuals with obesity. DATA SYNTHESIS: This review explores the pathophysiological mechanisms underlying this relationship, including the roles of inflammation, autonomic dysregulation, and neuroendocrine pathways. Sleep loss exacerbates metabolic syndrome components, including insulin resistance and dyslipidemia, further perpetuating weight gain. Similarly, obesity-induced sleep disorders lead to pro-inflammatory states, vascular dysfunction, and sympathetic overactivation, compounding cardiometabolic risks. Specific conditions like OSA and RLS are examined as models of this interdependence, emphasizing their shared pathways and clinical implications. CONCLUSIONS: The bidirectional link between obesity and sleep disorders underscores the importance of integrating sleep assessment and management into obesity treatment strategies. Addressing this relationship could mitigate the progression of cardiometabolic comorbidities and improve overall health outcomes. Moreover, the intertwined dynamics between obesity, sleep disorders, and mental health-mediated by inflammatory pathways, hormonal dysregulation, and neurobehavioral factors-highlight the critical need for integrated treatment approaches targeting physical, psychological, and sleep-related dimensions to enhance health and quality of life.
12Metabolic consequences of sleep and sleep loss.PubMed
Eve Van Cauter, Karine Spiegel, Esra Tasali, et al.
Reduced sleep duration and quality appear to be endemic in modern society. Curtailment of the bedtime period to minimum tolerability is thought to be efficient and harmless by many. It has been known for several decades that sleep is a major modulator of hormonal release, glucose regulation and cardiovascular function. In particular, slow wave sleep (SWS), thought to be the most restorative sleep stage, is associated with decreased heart rate, blood pressure, sympathetic nervous activity and cerebral glucose utilization, compared with wakefulness. During SWS, the anabolic growth hormone is released while the stress hormone cortisol is inhibited. In recent years, laboratory and epidemiologic evidence have converged to indicate that sleep loss may be a novel risk factor for obesity and type 2 diabetes. The increased risk of obesity is possibly linked to the effect of sleep loss on hormones that play a major role in the central control of appetite and energy expenditure, such as leptin and ghrelin. Reduced leptin and increased ghrelin levels correlate with increases in subjective hunger when individuals are sleep restricted rather than well rested. Given the evidence, sleep curtailment appears to be an important, yet modifiable, risk factor for the metabolic syndrome, diabetes and obesity. The marked decrease in average sleep duration in the last 50 years coinciding with the increased prevalence of obesity, together with the observed adverse effects of recurrent partial sleep deprivation on metabolism and hormonal processes, may have important implications for public health.
13The links between sleep duration, obesity and type 2 diabetes mellitus.PubMed
Christina Antza, Georgios Kostopoulos, Samiul Mostafa, et al.
Global rates of obesity and type 2 diabetes mellitus (T2DM) are increasing globally concomitant with a rising prevalence of sleep deprivation and sleep disorders. Understanding the links between sleep, obesity and T2DM might offer an opportunity to develop better prevention and treatment strategies for these epidemics. Experimental studies have shown that sleep restriction is associated with changes in energy homeostasis, insulin resistance and β-cell function. Epidemiological cohort studies established short sleep duration as a risk factor for developing obesity and T2DM. In addition, small studies suggested that short sleep duration was associated with less weight loss following lifestyle interventions or bariatric surgery. In this article, we review the epidemiological evidence linking sleep duration to obesity and T2DM and plausible mechanisms. In addition, we review the impact of changes in sleep duration on obesity and T2DM.
14Gut hormones and appetite regulation.PubMed
So-Hyeon Hong, Kyung Mook Choi
PURPOSE OF REVIEW: Various gut hormones interact with the brain through delicate communication, thereby influencing appetite and subsequent changes in body weight. This review summarizes the effects of gut hormones on appetite, with a focus on recent research. RECENT FINDINGS: Ghrelin is known as an orexigenic hormone, whereas glucagon-like peptide-1 (GLP-1), glucose-dependent insulinotropic polypeptide (GIP), cholecystokinin (CCK), postprandial peptide YY (PYY), and oxyntomodulin (OXM) are known as anorexigenic hormones. Recent human studies have revealed that gut hormones act differently in various systems, including adipose tissue, beyond appetite and energy intake, and even involve in high-order thinking. Environmental factors including meal schedule, food contents and quality, type of exercise, and sleep deprivation also play a role in the influence of gut hormone on appetite, weight change, and obesity. Recently published studies have shown that retatrutide, a triple-agonist of GLP-1, GIP, and glucagon receptor, and orforglipron, a GLP-1 receptor partial agonist, are effective in weight loss and improving various metabolic parameters associated with obesity. SUMMARY: Various gut hormones influence appetite, and several drugs targeting these receptors have been reported to exert positive effects on weight loss in humans. Given that diverse dietary and environmental factors affect the actions of gut hormones and appetite, there is a need for integrated and largescale long-term studies in this field.
15Role of sleep and sleep loss in hormonal release and metabolism.PubMed
Rachel Leproult, Eve Van Cauter
Compared to a few decades ago, adults, as well as children, sleep less. Sleeping as little as possible is often seen as an admirable behavior in contemporary society. However, sleep plays a major role in neuroendocrine function and glucose metabolism. Evidence that the curtailment of sleep duration may have adverse health effects has emerged in the past 10 years. Accumulating evidence from both epidemiologic studies and well-controlled laboratory studies indicates that chronic partial sleep loss may increase the risk of obesity and weight gain. The present chapter reviews epidemiologic studies in adults and children and laboratory studies in young adults indicating that sleep restriction results in metabolic and endocrine alterations, including decreased glucose tolerance, decreased insulin sensitivity, increased evening concentrations of cortisol, increased levels of ghrelin, decreased levels of leptin and increased hunger and appetite. Altogether, the evidence points to a possible role of decreased sleep duration in the current epidemic of obesity. Bedtime extension in short sleepers should be explored as a novel behavioral intervention that may prevent weight gain or facilitate weight loss. Avoiding sleep deprivation may help to prevent the development of obesity, particularly in children.
16Physiological adaptations to weight loss and factors favouring weight regain.PubMed
F L Greenway
Obesity is a major global health problem and predisposes individuals to several comorbidities that can affect life expectancy. Interventions based on lifestyle modification (for example, improved diet and exercise) are integral components in the management of obesity. However, although weight loss can be achieved through dietary restriction and/or increased physical activity, over the long term many individuals regain weight. The aim of this article is to review the research into the processes and mechanisms that underpin weight regain after weight loss and comment on future strategies to address them. Maintenance of body weight is regulated by the interaction of a number of processes, encompassing homoeostatic, environmental and behavioural factors. In homoeostatic regulation, the hypothalamus has a central role in integrating signals regarding food intake, energy balance and body weight, while an 'obesogenic' environment and behavioural patterns exert effects on the amount and type of food intake and physical activity. The roles of other environmental factors are also now being considered, including sleep debt and iatrogenic effects of medications, many of which warrant further investigation. Unfortunately, physiological adaptations to weight loss favour weight regain. These changes include perturbations in the levels of circulating appetite-related hormones and energy homoeostasis, in addition to alterations in nutrient metabolism and subjective appetite. To maintain weight loss, individuals must adhere to behaviours that counteract physiological adaptations and other factors favouring weight regain. It is difficult to overcome physiology with behaviour. Weight loss medications and surgery change the physiology of body weight regulation and are the best chance for long-term success. An increased understanding of the physiology of weight loss and regain will underpin the development of future strategies to support overweight and obese individuals in their efforts to achieve and maintain weight loss.