Energy Homoeostasis Summary - pediagenosis
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Saturday, May 8, 2021

Energy Homoeostasis Summary

Energy Homoeostasis Summary
Clinical background
In recent years, adipose tissue has become recognized as a highly metabolically active organ. In 1994, the hormone leptin was identified, a peptide almost exclusively secreted by adipose cells and with receptors both in the hypothalamus and peripheral tissues. Leptin has a number of actions both in relation to signalling satiety and altering energy metabolism. The identification of a rare family with leptin deficiency, extreme obesity and insulin resistance was followed by treatment of two children with recombinant leptin and successful loss of weight. However, in the majority of non-leptin-deficient obese individuals, circulating leptin levels are high and correlated with body fat mass, suggesting that leptin resistance may play a role in human obesity. Further work is needed to establish the exact role of this hormone in energy homeostasis.

Energy Homoeostasis: I Summary

Endocrine hormones and energy metabolism
The neuroendocrine system plays a critical role in energy metabolism and homeostasis and is implicated in the control of feeding behaviour. Energy metabolism centres on the maintenance of an adequate supply of glucose for metabolism and on the balance between energy storage and utilization (Fig. 44a). The rapid spread of obesity, with attendant diabetes and heart disease, in western affluent societies has promoted research that has identified previously unknown endocrine hormones that regulate, and indeed dictate, feeding behaviour in other species (see below and Chapter 45).

Energy stores
Fats are the main energy stores in the body. Fats provide the most efficient means of storing energy in terms of kJ/g, and the body can store seemingly unlimited amounts of fat, a fact evident from the phenomenon of extreme obesity. Carbohydrate constitutes <1% of energy stores, and tissues such as the brain are absolutely dependent on a constant supply of glucose, which must be supplied in the diet or by gluconeogenesis. Proteins contain about 20% of the body’s energy stores, but since proteins have a structural and functional role, their integrity is defended, except in fasting, and these stores are therefore not readily available.
Circulating glucose can be considered as a glucose pool (Fig. 44b), which is in a dynamic state of equilibrium, balancing the inflow and outflow of glucose. The sources of inflow are the diet (carbohydrates) and hepatic glycogenolysis. The outflows are to the tissues, for glycogen synthesis, for energy use, or, if plasma concentrations reach a sufficient level, into the urine. This  level  is  not  usually  reached  in  normal,  healthy people.
Regulation of the glucose flows is through the action of endocrine hormones, these being epinephrine, growth hormone, insulin, glucagon, glucocorticoids and thyroxine. Insulin is the only hormone with a hypoglycaemic action, whereas all the others are hyperglycaemic, since they stimulate glycogenolysis. Thus, falling blood glucose stimulates their release, while raised glucose stimulates insulin release, an example of dual negative-feedback control.
Integration of fat, carbohydrate and protein metabolism is essential for the effective control of the glucose pool. Two other pools are drawn upon for this, these being the free fatty acid (FFA) pool and the amino acid (AA) pool (Fig. 44b). The FFA pool comprises the balance between dietary FFA absorbed from the GIT, FFA released from adipose tissue after lipolysis, and FFA entering the metabolic process. Insulin drives FFA into storage as lipids, while glucagon, growth hormone and epinephrine stimulate lipolysis. The AA pool in the bloodstream comprises the balance between protein synthesis and the entry of amino acids into the gluconeogenic pathways. A summary of metabolism is shown in Fig. 44c.

Endocrine control of food intake
The discovery of the hormone leptin, which is secreted from adipose tissue and which inhibits feeding behaviour in rodents, has stimulated an interest in the role of the neuroendocrine system in feeding behaviour and the occurrence of obesity. There is now evidence for a feedback system in the hypothalamus (see Chapter 45). In humans, food intake is determined by a number of factors, including the peripheral balance between usage and storage of energy, and by the brain, which through its appetite and satiety centres can trigger and terminate feeding behaviour (Fig. 44a). Leptin is secreted by human adipocytes but it may be more important (in the human) in the long-term maintenance of adequate energy stores during periods of energy deficit, rather than as a short-term satiety hormone.
Feeding behaviour in humans can be initiated and sustained not only through hunger, but also through an awareness of the availability of especially palatable foods and by emotional states; the central mechanisms underlying this behaviour are poorly understood. Conversely, feeding behaviour can be deliberately suppressed, as in anorexia nervosa, when the patient fasts regardless of the knowledge of the consequence of this behaviour. There is, however, a growing body of evidence that in some families there may be genetic contributions, for example mutations of the gene that expresses the melanocortin-4 receptor (MCR-4) gene has been described in rare families with obesity in which satiety is not recognized. The relative contributions of cultural, genetic and non-transmissible factors in the development of obesity are shown in Fig. 44d.

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