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Energy homeostasis

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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.
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hypothalamus and other brain areas 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 content. ... 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.
236:, first introduced in 1953, postulated that each body has a preprogrammed fixed weight, with regulatory mechanisms to compensate. This theory was quickly adopted and used to explain failures in developing effective and sustained weight loss procedures. A 2019 systematic review of multiple weight change interventions on humans, including 240:, exercise and overeating, found systematic "energetic errors", the non-compensated loss or gain of calories, for all these procedures. This shows that the body cannot precisely compensate for errors in energy/calorie intake, contrary to what the Set-Point Theory hypothesizes, and potentially explaining both 475:
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
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to below normal values have beneficial effects, and even though they are showing positive indications in nonhuman primates it is still not certain if calorie restriction has a positive effect on longevity for humans and other primates. Calorie restriction may be viewed as attaining energy balance at
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The first law of thermodynamics states that energy can be neither created nor destroyed. But energy can be converted from one form of energy to another. So, when a calorie of food energy is consumed, one of three particular effects occur within the body: a portion of that calorie may be stored as
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However, in normal individuals, body weight and body fat content are typically quite stable over time 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
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Levitsky, DA; Sewall, A; Zhong, Y; Barre, L; Shoen, S; Agaronnik, N; LeClair, JL; Zhuo, W; Pacanowski, C (1 February 2019). "Quantifying the imprecision of energy intake of humans to compensate for imposed energetic errors: A challenge to the physiological control of human food intake".
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a lower intake and expenditure, and is, in this sense, not generally an energy imbalance, except for an initial imbalance where decreased expenditure hasn't yet matched the decreased intake.
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by integrating a number of biochemical signals that transmit information about energy balance. Fifty percent of the energy from glucose metabolism is immediately converted to heat.
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Energy intake is measured by the amount of calories consumed from food and fluids. Energy intake is modulated by hunger, which is primarily regulated by the
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with a capital C (i.e. a kilocalorie), which equals the energy needed to increase the temperature of 1 kilogram of water by 1 Â°C (about 4.18 k
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A negative balance is a result of energy intake being less than what is consumed in external work and other bodily means of energy expenditure.
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Energy expenditure is mainly a sum of internal heat produced and external work. The internal heat produced is, in turn, mainly a sum of
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David Halliday, Robert Resnick, Jearl Walker, Fundamentals of physics, 9th edition,John Wiley & Sons, Inc., 2011, p. 485
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There has been controversy over energy-balance messages that downplay energy intake being promoted by food industry groups.
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has compiled a detailed report on human energy requirements. An older but commonly used and fairly accurate method is the
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Kevin G. Murphy & Stephen R. Bloom (December 14, 2006). "Gut hormones and the regulation of energy homeostasis".
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Energy intake (from food and fluids) = Energy expended (through work and heat generated) + Change in stored energy (
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Field JB (1989). "Exercise and deficient carbohydrate storage and intake as causes of hypoglycemia".
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Weingarten HP (1985). "Stimulus control of eating: implications for a two-factor theory of hunger".
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Normal energy requirement, and therefore normal energy intake, depends mainly on age, sex and
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Rezzi S, Martin FP, Shanmuganayagam D, Colman RJ, Nicholson JK, Weindruch R (May 2009).
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than what is consumed in external work and other bodily means of energy expenditure.
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of eating behavior. Hunger is regulated in part by the action of certain
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Molecular Neuropharmacology: A Foundation for Clinical Neuroscience
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Malenka RC, Nestler EJ, Hyman SE (2009). Sydor A, Brown RY (ed.).
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Ziauddeen H, Alonso-Alonso M, Hill JO, Kelley M, Khan NA (2015).
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In the US, biological energy is expressed using the energy unit
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Human energy requirements (Rome, 17–24 October 2001)
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A positive balance results in energy being stored as
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Anderson RM, Shanmuganayagam D, Weindruch R (2009).
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Yet, there are currently ongoing studies to show if
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External work may be estimated by measuring the 591: 589: 1068:Diagram of regulation of fat stores and hunger 986: 984: 88:, can be measured with the following equation: 46:regulation of food intake (energy inflow) and 1094: 934: 932: 415: 413: 411: 409: 407: 405: 61:Energy homeostasis is an important aspect of 8: 304:may develop, with resultant complications. 1152: 1101: 1087: 1079: 1016: 964: 893: 800: 716: 569: 516: 426:Metabolic Regulation: A Human Perspective 127:) or related compounds, or dissipated as 491:Morton GJ, Meek TH, Schwartz MW (2014). 401: 274:, resulting in increased energy intake 544:Farr OM, Li CS, Mantzoros CS (2016). 36:homeostatic control of energy balance 7: 1074:Daily energy requirement calculator 319:due to a medical condition such as 256:A positive balance is a result of 25: 658:Endocrinol. Metab. Clin. North Am 349:Food and Agriculture Organization 267:The main preventable causes are: 802:10.1111/j.1467-789X.2006.00270.x 1040:O’Connor, Anahad (2015-08-09). 42:that involves the coordinated 1: 754:10.1016/S0195-6663(85)80006-4 670:10.1016/S0889-8529(18)30394-3 562:10.1016/j.metabol.2016.02.002 876:Harris, RB (December 1990). 1176:Wernicke–Korsakoff syndrome 1009:10.1016/j.exger.2009.02.008 895:10.1096/fasebj.4.15.2253845 847:10.1016/j.appet.2018.11.017 1554: 225: 199: 1181:Wernicke's encephalopathy 957:10.1177/0192623308329476 357:Harris-Benedict equation 244:and weight gain such as 84:Energy balance, through 18:Total energy expenditure 345:physical activity level 216:physical activity level 188:, among others) in the 390:Earth's energy balance 212:thermic effect of food 158:classical conditioning 121:adenosine triphosphate 86:biosynthetic reactions 1357:Electrolyte imbalance 1225:Pyridoxine deficiency 1199:Riboflavin deficiency 709:10.3945/an.115.008268 385:Dynamic energy budget 335:can also be a cause. 226:Further information: 200:Further information: 1335:Vitamin K deficiency 1329:Vitamin E deficiency 1306:Vitamin D deficiency 1287:Vitamin A deficiency 1186:Korsakoff's syndrome 208:basal metabolic rate 154:operant conditioning 27:A biological process 618:10.1038/nature05484 610:2006Natur.444..854M 371:Society and culture 364:calorie restriction 278:Sedentary lifestyle 1349:Mineral deficiency 1148:Vitamin deficiency 497:Nat. Rev. Neurosci 321:decreased appetite 315:The main cause is 228:Nutrition disorder 202:Energy expenditure 48:energy expenditure 40:biological process 32:energy homeostasis 1515: 1514: 1464:Failure to thrive 1459:Delayed milestone 1343: 1342: 1321:Harrison's groove 1251:Folate deficiency 1238:Biotin deficiency 604:(7121): 854–859. 420:Frayn KN (2013). 329:digestive disease 162:cognitive control 16:(Redirected from 1545: 1153: 1103: 1096: 1089: 1080: 1056: 1055: 1053: 1052: 1037: 1031: 1030: 1020: 988: 979: 978: 968: 936: 927: 922: 916: 915: 897: 873: 867: 866: 829: 823: 822: 804: 780: 774: 773: 737: 731: 730: 720: 688: 682: 681: 653: 647: 644: 638: 637: 593: 584: 583: 573: 550:Metab. Clin. 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Index

Total energy expenditure
biological process
homeostatic
energy expenditure
hypothalamus
hunger
bioenergetics
Calorie
J
biosynthetic reactions
body fat
glycogen
body fat
triglycerides
glycogen
adenosine triphosphate
coenzyme
heat
hypothalamus
stimulus control
operant conditioning
classical conditioning
cognitive control
peptide hormones
neuropeptides
insulin
leptin
ghrelin
neuropeptide Y
hypothalamus

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