Energy homeostasis

In biology, energy homeostasis, or the homeostatic control of energy balance, is a biological process that involves the coordinated homeostatic regulation of food intake (energy inflow) and energy expenditure (energy outflow).[1][2][3] The human brain, particularly the hypothalamus, plays a central role in regulating energy homeostasis and generating the sense of hunger by integrating a number of biochemical signals that transmit information about energy balance.[2][3][4] Fifty percent of the energy from glucose metabolism is immediately converted to heat.[5]

Energy homeostasis is an important aspect of bioenergetics.

Definition

In the US, biological energy is expressed using the energy unit Calorie with a capital C (i.e. a kilocalorie), which equals the energy needed to increase the temperature of 1 kilogram of water by 1 °C (about 4.18 kJ).[6]

Energy balance, through biosynthetic reactions, can be measured with the following equation:[1]

Energy intake (from food and fluids) = Energy expended (through work and heat generated) + Change in stored energy (body fat and glycogen storage)

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 body fat, triglycerides, or glycogen, transferred to cells and converted to chemical energy in the form of adenosine triphosphate (ATP – a coenzyme) or related compounds, or dissipated as heat.[1][5][7]

Energy

Intake

Energy intake is measured by the amount of calories consumed from food and fluids.[1] Energy intake is modulated by hunger, which is primarily regulated by the hypothalamus,[1] and choice, which is determined by the sets of brain structures that are responsible for stimulus control (i.e., operant conditioning and classical conditioning) and cognitive control of eating behavior.[8][9] Hunger is regulated in part by the action of certain peptide hormones and neuropeptides (e.g., insulin, leptin, ghrelin, and neuropeptide Y, among others) in the hypothalamus.[1][10]

Expenditure
Further information: Caloric deficit

Energy expenditure is mainly a sum of internal heat produced and external work. The internal heat produced is, in turn, mainly a sum of basal metabolic rate (BMR) and the thermic effect of food. External work may be estimated by measuring the physical activity level (PAL).

Imbalance
Further information: Nutrition disorder

The Set-Point Theory, 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 dieting, 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 weight loss and weight gain such as obesity. This review was conducted on short term studies, therefore such a mechanism cannot be excluded in the long term, as evidence is currently lacking on this timeframe.[11][12]

Positive balance

A positive balance is a result of energy intake being higher than what is consumed in external work and other bodily means of energy expenditure.

The main preventable causes are:

A positive balance results in energy being stored as fat and/or muscle, causing weight gain. In time, overweight and obesity may develop, with resultant complications.

Negative balance

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.

The main cause is undereating due to a medical condition such as decreased appetite, anorexia nervosa, digestive disease, or due to some circumstance such as fasting or lack of access to food. Hyperthyroidism can also be a cause.

Requirement

Normal energy requirement, and therefore normal energy intake, depends mainly on age, sex and physical activity level (PAL). The Food and Agriculture Organization (FAO) of the United Nations has compiled a detailed report on human energy requirements: Human energy requirements (Rome, 17–24 October 2001) An older but commonly used and fairly accurate method is the Harris-Benedict equation.

Yet, there are currently ongoing studies to show if calorie restriction to below normal values have beneficial effects, and even though they are showing positive indications in primates[13][14] it is still not certain if calorie restriction has a positive effect on longevity for primates and humans.[13][14] Calorie restriction may be viewed as attaining energy balance at 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.

Society and culture

There has been controversy over energy-balance messages that downplay energy intake being promoted by food industry groups.[15]

See also

References
  1. Frayn KN (2013). "Chapter 11: Energy Balance and Body Weight Regulation". Metabolic Regulation: A Human Perspective (3rd ed.). John Wiley & Sons. pp. 329–349. ISBN 9781118685334. Retrieved 9 January 2017.
  2. Malenka RC, Nestler EJ, Hyman SE (2009). Sydor A, Brown RY (ed.). Molecular Neuropharmacology: A Foundation for Clinical Neuroscience (2nd ed.). New York: McGraw-Hill Medical. pp. 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. Morton GJ, Meek TH, Schwartz MW (2014). "Neurobiology of food intake in health and disease". Nat. Rev. Neurosci. 15 (6): 367–378. doi:10.1038/nrn3745. PMC 4076116. PMID 24840801. 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 (2016). "Central nervous system regulation of eating: Insights from human brain imaging". Metab. Clin. Exp. 65 (5): 699–713. doi:10.1016/j.metabol.2016.02.002. PMC 4834455. PMID 27085777.
  5. Kevin G. Murphy & Stephen R. Bloom (December 14, 2006). "Gut hormones and the regulation of energy homeostasis". Nature. 444 (7121): 854–859. Bibcode:2006Natur.444..854M. doi:10.1038/nature05484. PMID 17167473. S2CID 1120344.
  6. David Halliday, Robert Resnick, Jearl Walker, Fundamentals of physics, 9th edition,John Wiley & Sons, Inc., 2011, p. 485
  7. Field JB (1989). "Exercise and deficient carbohydrate storage and intake as causes of hypoglycemia". Endocrinol. Metab. Clin. North Am. 18 (1): 155–161. doi:10.1016/S0889-8529(18)30394-3. PMID 2645124.
  8. Ziauddeen H, Alonso-Alonso M, Hill JO, Kelley M, Khan NA (2015). "Obesity and the neurocognitive basis of food reward and the control of intake". Adv Nutr. 6 (4): 474–86. doi:10.3945/an.115.008268. PMC 4496739. PMID 26178031.
  9. Weingarten HP (1985). "Stimulus control of eating: implications for a two-factor theory of hunger". Appetite. 6 (4): 387–401. doi:10.1016/S0195-6663(85)80006-4. PMID 3911890. S2CID 21137202.
  10. Klok MD, Jakobsdottir S, Drent ML (January 2007). "The role of leptin and ghrelin in the regulation of food intake and body weight in humans: a review". Obes Rev. 8 (1): 21–34. doi:10.1111/j.1467-789X.2006.00270.x. PMID 17212793.
  11. 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". Appetite. 133: 337–343. doi:10.1016/j.appet.2018.11.017. PMID 30476522. S2CID 53712116.
  12. Harris, RB (December 1990). "Role of set-point theory in regulation of body weight". FASEB Journal. 4 (15): 3310–8. doi:10.1096/fasebj.4.15.2253845. PMID 2253845.
  13. Anderson RM, Shanmuganayagam D, Weindruch R (2009). "Caloric restriction and aging: studies in mice and monkeys". Toxicol Pathol. 37 (1): 47–51. doi:10.1177/0192623308329476. PMC 3734859. PMID 19075044.
  14. Rezzi S, Martin FP, Shanmuganayagam D, Colman RJ, Nicholson JK, Weindruch R (May 2009). "Metabolic shifts due to long-term caloric restriction revealed in nonhuman primates". Exp. Gerontol. 44 (5): 356–62. doi:10.1016/j.exger.2009.02.008. PMC 2822382. PMID 19264119.
  15. O’Connor, Anahad (2015-08-09). "Coca-Cola Funds Scientists Who Shift Blame for Obesity Away From Bad Diets". Well. Retrieved 2018-03-24.
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