leptin primarily acts on joint tissues organ or tissue.
​on which organ or tissue does leptin primarily act?
joint tissues
this field of research had been almost unapproached until the leptin gene was discovered in 1994 by j. m. friedman's laboratory. these investigators postulated that leptin was a satiety factor. in the ob/ob mouse, mutations in the leptin gene resulted in the obese phenotype opening the possibility of leptin therapy for human obesity. however, soon thereafter j. f. caro's laboratory could not detect any mutations in the leptin gene in humans with obesity. on the contrary leptin expression was increased proposing the possibility of leptin-resistance in human obesity. since this discovery, many other hormonal mechanisms have been elucidated that participate in the regulation of appetite and food intake, storage patterns of adipose tissue, and development of insulin resistance. since leptin's discovery, ghrelin, insulin, orexin, pyy 3-36, cholecystokinin, adiponectin, as well as many other mediators have been studied. the adipokines are mediators produced by adipose tissue; their action is thought to modify many obesity-related diseases.
pathophysiology of obesity
another explanation of the relationship stems from the balance between two hormones, leptin and ghrelin, which act on the nuclei of the hypothalamus to monitor energy and food intake. leptin primarily inhibits appetite while ghrelin, which is the released by the stomach, works to stimulate appetite. sleep deprivation has been associated with increased levels of ghrelin and decreased levels of leptin in multiple studies. in addition to the hormonal variation, other research has also associated shortened sleep durations with a proportional increase in subjects' bmis.









































metabolism
sleep and weight