It is almost impossible to separate regulation of adipose tissue from digestive processes and functions of the central nervous system. These interconected hormonal and neural signals emanating from the adipose tissue, alimentary tract, and central nervous system form the brain–gut–adipose axis that regulates appetite, hunger, satiety, and energy homeostasis (Fig 9. 4).
The amount of an individual’s adipose tissue is determined by two physiologic systems: One associated with short-term weight regulation, the other with long-term weight regulation.
The amount of adipose tissue in an individual is regulated by two physiologic systems. The first system, which is associated with short-term weight regulation, controls appetite and metabolism on a daily basis. Recently, two small peptide hormones produced in the gastrointestinal tract— ghrelin, an appetite stimulant, and peptide YY (PYY), an appetite suppressant—have been linked to this system. The second system, which is associated with long-term weight regulation, controls appetite and metabolism on a continual basis (over months and years). Two major hormones influence this system, leptin and insulin, along with other hormones, including thyroid hormone, glucocorticoids, and hormones of the pituitary gland (see Fig. 9.4).
Ghrelin and peptide YY control appetite as part of the short-term weight control system.
The recently discovered potent appetite stimulant ghrelin is a small, 28-amino-acid polypeptide produced by gastric epithelial cells. In addition to its appetite stimulatory role, it acts on the anterior lobe of the pituitary gland to release growth hormone. In humans, ghrelin functions through receptors located in the hypothalamus, increasing the sense of hunger. As such it is considered a “meal initiator” factor. A genetic mutation in chromosome 15 causes Prader-Willi syndrome, in which an overproduction of ghrelin leads to morbid obesity. In individuals with this syndrome,  compulsive eating and an obsession with food usually arise at an early age. The urge to eat
FIGURE 9.2 • White adipose tissue. a. Photomicrograph of white adipose tissue, showing its characteristic meshwork in an H&E–stained paraffin preparation. Each space represents a single large drop of lipid before its dissolution from the cell during tissue preparation. The surrounding eosin-stained material represents the cytoplasm of the adjoining cells and some intervening connective tissue. 320. b. High-power photomicrograph of a glutaraldehyde-preserved, plastic-embedded specimen of white adipose tissue. The cytoplasm of the individual adipose cells is recognizable in some areas, and part of the nucleus of one of the cells is included in the plane of section. A second nucleus (arrow), which appears intimately related to one of the adipose cells, may actually belong to a fibroblast; it is difficult to tell with assurance. Because of the large size of adipose cells, the nucleus is infrequently observed in a given cell. A capillary and a small venule are also evident in the photomicrograph. 950.
in these individuals is physiologic, overwhelming, and very difficult to control. If not treated, these individuals often die before age 30 of complications attributable to obesity.
The small, 36-amino-acid long gastrointestinal hormone peptide YY is produced by the small intestine and plays an important role in promoting and maintaining weight loss by inducing a greater sense of fullness soon after a meal. It also acts through receptors in the hypothalamus that suppress appetite. It decreases food intake in individuals by inducing satiety or a sense of fullness and the desire to stop eating. In experimental clinical studies, the infusion of PYY into humans has been shown to reduce food intake by 33% over a period of 24 hours.