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能量穩態

維基百科，自由的百科全書

能量穩態（英文：Energy homeostasis）或能量平衡的穩態控制，在生物學中，是一個生物過程，涉及食物攝入（能量流入）和能量消耗（能量流出）的協調穩態調節。[1][2][3]人腦，尤其是下丘腦會通過整合許多傳遞能量平衡信息的生化信號，在調節能量穩態和產生飢餓感方面發揮着核心作用。[2][3][4]50%的葡萄糖代謝能量立即轉化為熱量。[5]

能量穩態是生物能量學的一個重要方面。

定義

在美國，生物能量用大寫C（即千卡）的能量單位卡路里表示。它等於將1公斤水的溫度升高1°C所需的能量（約4.18kJ）。[6]

通過生物合成反應的能量平衡可以用以下等式測量：[1]

能量攝入（來自食物和液體）= 能量消耗（通過做功和產生的熱量）+ 儲存能量的變化（身體脂肪和糖原儲存）

熱力學第一定律指出，能量既不能被創造也不能被摧毀。但是能量可以從一種形式的能量轉換為另一種形式的能量。因此，當攝入一卡路里的食物能量時，體內會出現三種特殊效果之一：其中一部分卡路里可能以體脂、三酸甘油酯或糖原的形式儲存起來、一部分卡路里轉移到細胞中並以三磷酸腺苷（ATP，即一種輔因子）或相關化合物的形式轉化為化學能、或者有可能以熱量的形式消散。[1][5][7]

能量

攝入

能量攝入量是通過從食物和液體中攝入的卡路里量來衡量的。[1]能量攝入受飢餓（主要受下丘腦調節[1]）和選擇（由負責刺激控制（英語：Stimulus control）（即操作性條件反射和經典條件反射）和對飲食行為有執行功能的大腦結構集決定）的調節。[8][9]飢餓部分受下丘腦中某些肽激素和神經肽（例如胰島素、瘦素、飢餓素和神經肽Y（英語：Neuropeptide Y）等）的作用調節。[1][10]

消耗

更多資訊：熱量不足（英語：Caloric deficit）

能量消耗主要是內部產生的熱量和外部工作的總和。產生的內部熱量主要是基礎代謝率（BMR）和食物誘導產熱（英語：Specific dynamic action）（SDA或TEF或DIT）的總和。而外部工作可以通過測量身體活動水平（英語：Physical activity level）（PAL）來估算。

失衡

更多資訊：營養不良

設定點理論（英語：Set point theory (body weight)）於1953年首次推出，假設每個身體都有一個預先設定的體重，並具有調節機制來補償。這一理論很快被採用並用於解釋在開發有效和持續的減肥程序方面的失敗。於2019年對人類多種體重變化干預措施（包括節食、鍛煉和暴飲暴食）進行的系統評價發現，所有這些程序都存在系統性「能量錯誤」，即卡路里的無補償損失或增加。這表明身體不能精確地補償能量和卡路里攝入的誤差，這與設定點理論的假設相反，並可能解釋體重減輕和體重增加（如肥胖）。這項審查是針對短期研究進行的，因此從長遠來看，不能排除設定點理論的可能，因為目前缺乏這個時間框架的證據。[11][12]

正平衡

正平衡是能量攝入高於外部工作和其他身體能量消耗的結果。

主要可預防的原因是：

  • 暴飲暴食，導致能量攝入增加。
  • 坐式生活型態，通過外部工作減少能量消耗。

正平衡導致能量以脂肪或肌肉的形式儲存，這會導致體重增加。隨着時間的推移，可能會出現超重和肥胖，從而導致併發症。

負平衡

負平衡是能量攝入少於外部工作和其他身體能量消耗的結果。

主要原因是：

需求

正常的能量需求以及正常的能量攝入主要取決於年齡、性別和體力活動水平（PAL）。聯合國糧食及農業組織（FAO）編制了一份關於人類能源需求的詳細報告。[13]一種較舊但常用且相當準確的方法是哈里斯-本尼迪克特方程。

然而，目前正在進行的研究表明，將卡路里限制在低於正常值是否具有有益效果，即使它們在非靈長類動物中顯示出積極的跡象，[14][15]但仍然不確定卡路里限制是否對人類和其他靈長類動物的壽命有影響。[14][15]卡路里限制可以被視為在較低的攝入量和消耗量下達到能量平衡。從這個意義上說，通常不是能量不平衡，除了最初的不平衡，即減少的消耗尚未與減少的攝入量相匹配。

社會

關於能量平衡信息一直存在爭議，這些信息淡化了食品工業團體所提倡的能量攝入。[16]

參見

參考文獻

  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 , 編. 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 可免費查閱. 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 可免費查閱. 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 可免費查閱. 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]. （原始內容存檔於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 可免費查閱. 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 可免費查閱. 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]. （原始內容存檔於2022-06-25）. 

外部連結

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