维基百科

能量稳态

（重定向自能量穩態）

能量稳态（英文：Energy homeostasis）或能量平衡的稳态控制，在生物学中，是一个生物过程，涉及食物摄入（能量流入）和能量消耗（能量流出）的协调稳态调节。[1][2][3]人脑，尤其是下丘脑会通过整合许多传递能量平衡信息的生化信号，在调节能量稳态和产生饥饿感方面发挥着核心作用。[2][3][4]50%的葡萄糖代谢能量立即转化为热量。[5]

能量稳态是生物能量学的一个重要方面。

定义

在美国，生物能量用大写C（即千卡）的能量单位卡路里表示。它等于将1公斤水的温度升高1°C所需的能量（约4.18kJ）。[6]

通过生物合成反应的能量平衡可以用以下等式测量：[1]

能量摄入（来自食物和液体）= 能量消耗（通过做功和产生的热量）+ 储存能量的变化（身体脂肪和糖原储存）

热力学第一定律指出，能量既不能被创造也不能被摧毁。但是能量可以从一种形式的能量转换为另一种形式的能量。因此，当摄入一卡路里的食物能量时，体内会出现三种特殊效果之一：其中一部分卡路里可能以体脂、甘油三酯或糖原的形式储存起来、一部分卡路里转移到细胞中并以三磷酸腺苷（ATP，即一种辅因子）或相关化合物的形式转化为化学能、或者有可能以热量的形式消散。[1][5][7]

能量

摄入

能量摄入量是通过从食物和液体中摄入的卡路里量来衡量的。[1]能量摄入受饥饿（主要受下丘脑调节[1]）和选择（由负责刺激控制（英语：Stimulus control）（即操作性条件反射和经典条件反射）和对饮食行为有执行功能的大脑结构集决定）的调节。[8][9]饥饿部分受下丘脑中某些肽激素和神经肽（例如胰岛素、瘦素、饥饿素和神经肽Y（英语：Neuropeptide Y）等）的作用调节。[1][10]

消耗

更多信息：热量不足（英语：Caloric deficit）

能量消耗主要是内部产生的热量和外部工作的总和。产生的内部热量主要是基础代谢率（BMR）和食物诱导产热（英语：Specific dynamic action）（SDA或TEF或DIT）的总和。而外部工作可以通过测量身体活动水平（英语：Physical activity level）（PAL）来估算。

失衡

更多信息：營養不良

设定点理论（英语：Set point theory (body weight)）于1953年首次推出，假设每个身体都有一个预先设定的体重，并具有调节机制来补偿。这一理论很快被采用并用于解释在开发有效和持续的减肥程序方面的失败。于2019年对人类多种体重变化干预措施（包括节食、锻炼和暴饮暴食）进行的系统评价发现，所有这些程序都存在系统性“能量错误”，即卡路里的无补偿损失或增加。这表明身体不能精确地补偿能量和卡路里摄入的误差，这与设定点理论的假设相反，并可能解释体重减轻和体重增加（如肥胖）。这项审查是针对短期研究进行的，因此从长远来看，不能排除设定点理论的可能，因为目前缺乏这个时间框架的证据。[11][12]

正平衡

正平衡是能量摄入高于外部工作和其他身体能量消耗的结果。

主要可预防的原因是：

  • 暴饮暴食，导致能量摄入增加。
  • 坐式生活型态，通过外部工作减少能量消耗。

正平衡导致能量以脂肪或肌肉的形式储存，这会导致体重增加。随着时间的推移，可能会出现超重和肥胖，从而导致并发症。

负平衡

负平衡是能量摄入少于外部工作和其他身体能量消耗的结果。

主要原因是：

需求

正常的能量需求以及正常的能量摄入主要取决于年龄、性别和体力活动水平（PAL）。联合国粮食及农业组织（FAO）编制了一份关于人类能源需求的详细报告。[13]一种较旧但常用且相当准确的方法是哈里斯-本尼迪克特方程。

然而，目前正在进行的研究表明，将卡路里限制在低于正常值是否具有有益效果，即使它们在非灵长类动物中显示出积极的迹象，[14][15]但仍然不确定卡路里限制是否对人类和其他灵长类动物的寿命有影响。[14][15]卡路里限制可以被视为在较低的摄入量和消耗量下达到能量平衡。从这个意义上说，通常不是能量不平衡，除了最初的不平衡，即减少的消耗尚未与减少的摄入量相匹配。

社会

关于能量平衡信息一直存在争议，这些信息淡化了食品工业团体所提倡的能量摄入。[16]

参见

参考文献

  1. ^ 1.0 1.1 1.2 1.3 1.4 1.5 Frayn KN. Chapter 11: Energy Balance and Body Weight Regulation. Metabolic Regulation: A Human Perspective 3rd. John Wiley & Sons. 2013: 329–349 [9 January 2017]. ISBN 9781118685334. 
  2. ^ 2.0 2.1 Malenka RC, Nestler EJ, Hyman SE. Sydor A, Brown RY , 编. Molecular Neuropharmacology: A Foundation for Clinical Neuroscience 2nd. New York: McGraw-Hill Medical. 2009: 179, 262–263. ISBN 9780071481274. Orexin neurons are regulated by peripheral mediators that carry information about energy balance, including glucose, leptin, and ghrelin. ... Accordingly, orexin plays a role in the regulation of energy homeostasis, reward, and perhaps more generally in emotion. ... The regulation of energy balance involves the exquisite coordination of food intake and energy expenditure. Experiments in the 1940s and 1950s showed that lesions of the lateral hypothalamus (LH) reduced food intake; hence, the normal role of this brain area is to stimulate feeding and decrease energy utilization. In contrast, lesions of the medial hypothalamus, especially the ventromedial nucleus (VMH) but also the PVN and dorsomedial hypothalamic nucleus (DMH), increased food intake; hence, the normal role of these regions is to suppress feeding and increase energy utilization. Yet discovery of the complex networks of neuropeptides and other neurotransmitters acting within the hypothalamus and other brain regions to regulate food intake and energy expenditure began in earnest in 1994 with the cloning of the leptin (ob, for obesity) gene. Indeed, there is now explosive interest in basic feeding mechanisms given the epidemic proportions of obesity in our society, and the increased toll of the eating disorders, anorexia nervosa and bulimia. Unfortunately, despite dramatic advances in the basic neurobiology of feeding, our understanding of the etiology of these conditions and our ability to intervene clinically remain limited. 
  3. ^ 3.0 3.1 Morton GJ, Meek TH, Schwartz MW. Neurobiology of food intake in health and disease. Nat. Rev. Neurosci. 2014, 15 (6): 367–378. PMC 4076116  . PMID 24840801. doi:10.1038/nrn3745. However, in normal individuals, body weight and body fat content are typically quite stable over time2,3 owing to a biological process termed ‘energy homeostasis’ that matches energy intake to expenditure over long periods of time. The energy homeostasis system comprises neurons in the mediobasal hypothalamus and other brain areas4 that are a part of a neurocircuit that regulates food intake in response to input from humoral signals that circulate at concentrations proportionate to body fat content4-6. ... An emerging concept in the neurobiology of food intake is that neurocircuits exist that are normally inhibited, but when activated in response to emergent or stressful stimuli they can override the homeostatic control of energy balance. Understanding how these circuits interact with the energy homeostasis system is fundamental to understanding the control of food intake and may bear on the pathogenesis of disorders at both ends of the body weight spectrum. 
  4. ^ Farr OM, Li CS, Mantzoros CS. Central nervous system regulation of eating: Insights from human brain imaging. Metab. Clin. Exp. 2016, 65 (5): 699–713. PMC 4834455  . PMID 27085777. doi:10.1016/j.metabol.2016.02.002. 
  5. ^ 5.0 5.1 Kevin G. Murphy & Stephen R. Bloom. Gut hormones and the regulation of energy homeostasis. Nature. December 14, 2006, 444 (7121): 854–859. Bibcode:2006Natur.444..854M. PMID 17167473. S2CID 1120344. doi:10.1038/nature05484. 
  6. ^ David Halliday, Robert Resnick, Jearl Walker, Fundamentals of physics, 9th edition,John Wiley & Sons, Inc., 2011, p. 485
  7. ^ Field JB. Exercise and deficient carbohydrate storage and intake as causes of hypoglycemia. Endocrinol. Metab. Clin. North Am. 1989, 18 (1): 155–161. PMID 2645124. doi:10.1016/S0889-8529(18)30394-3. 
  8. ^ Ziauddeen H, Alonso-Alonso M, Hill JO, Kelley M, Khan NA. Obesity and the neurocognitive basis of food reward and the control of intake. Adv Nutr. 2015, 6 (4): 474–86. PMC 4496739  . PMID 26178031. doi:10.3945/an.115.008268. 
  9. ^ Weingarten HP. Stimulus control of eating: implications for a two-factor theory of hunger. Appetite. 1985, 6 (4): 387–401. PMID 3911890. S2CID 21137202. doi:10.1016/S0195-6663(85)80006-4. 
  10. ^ Klok MD, Jakobsdottir S, Drent ML. The role of leptin and ghrelin in the regulation of food intake and body weight in humans: a review. Obes Rev. January 2007, 8 (1): 21–34. PMID 17212793. S2CID 24266123. doi:10.1111/j.1467-789X.2006.00270.x. 
  11. ^ Levitsky, DA; Sewall, A; Zhong, Y; Barre, L; Shoen, S; Agaronnik, N; LeClair, JL; Zhuo, W; Pacanowski, C. Quantifying the imprecision of energy intake of humans to compensate for imposed energetic errors: A challenge to the physiological control of human food intake.. Appetite. 1 February 2019, 133: 337–343. PMID 30476522. S2CID 53712116. doi:10.1016/j.appet.2018.11.017. 
  12. ^ Harris, RB. Role of set-point theory in regulation of body weight.. FASEB Journal. December 1990, 4 (15): 3310–8. PMID 2253845. S2CID 21297643. doi:10.1096/fasebj.4.15.2253845. 
  13. ^ Human energy requirements (Rome, 17–24 October 2001). [2022-11-26]. （原始内容存档于2019-01-31）. 
  14. ^ 14.0 14.1 Anderson RM, Shanmuganayagam D, Weindruch R. Caloric restriction and aging: studies in mice and monkeys. Toxicol Pathol. 2009, 37 (1): 47–51. PMC 3734859  . PMID 19075044. doi:10.1177/0192623308329476. 
  15. ^ 15.0 15.1 Rezzi S, Martin FP, Shanmuganayagam D, Colman RJ, Nicholson JK, Weindruch R. Metabolic shifts due to long-term caloric restriction revealed in nonhuman primates. Exp. Gerontol. May 2009, 44 (5): 356–62. PMC 2822382  . PMID 19264119. doi:10.1016/j.exger.2009.02.008. 
  16. ^ O’Connor, Anahad. Coca-Cola Funds Scientists Who Shift Blame for Obesity Away From Bad Diets. Well. 2015-08-09 [2018-03-24]. （原始内容存档于2022-06-25）. 

外部链接

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