Energy homeostasis

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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[edit]

In the US, biological energy is expressed using the energy unit Calorie with a capital C (i.e. 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:

Energy intake (food) = Energy expended (heat + work) + Energy stored.[1]

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 eaten enters a body, ultimately 100% of that calorie will be converted to heat, resulting in three particular short-term effects: a portion of that calorie is either stored as fat, transferred to the body's cells as chemical energy, by Adenosine triphosphate (ATP), a coenzyme and used for mechanical work or chemical synthesis, or immediately dissipated through heat.[5]

Energy[edit]

Intake[edit]

Energy intake is calories consumed as food, which is determined by hunger (hypothalamus) and choice (cerebral cortex). Hunger is determined by the impact of the hormones leptin and ghrelin on the hypothalamus.[7]

Expenditure[edit]

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).[citation needed]

Imbalance[edit]

Further information: Nutrition disorder

Positive balance[edit]

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.[citation needed]

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[edit]

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[edit]

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[8][9] it is still not certain if calorie restriction has a positive effect on longevity for primates and humans.[8][9] 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.

See also[edit]

References[edit]

  1. ^ a b Keith N. Frayn (2013). Metabolic Regulation: A Human Perspective. John Wiley & Sons. ISBN 1118685334. 
  2. ^ a b 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. ^ a b 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 4076116Freely accessible. 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. PMID 27085777. 
  5. ^ a b Kevin G. Murphy & Stephen R. Bloom (December 14, 2006). "Gut hormones and the regulation of energy homeostasis". 444 (7121). Nature: 854–859. doi:10.1038/nature05484. PMID 17167473. 
  6. ^ David Halliday, Robert Resnick, Jearl Walker, Fundamentals of physics, 9th edition,John Wiley & Sons, Inc., 2011, p. 485
  7. ^ M. D. Klok, S. Jakobsdottir and M. L. Drent. The role of leptin and ghrelin in the regulation of food intake and body weight in humans: a review. http://onlinelibrary.wiley.com/doi/10.1111/j.1467-789X.2006.00270.x/full
  8. ^ a b 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. PMID 19075044. 
  9. ^ a b 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 2822382Freely accessible. PMID 19264119. 

External links[edit]