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CNS changes after chronic sleep deprivation: roles in both food intake and metabolism
Author(s) -
Hoffman Gloria
Publication year - 2009
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.23.1_supplement.417.1
Subject(s) - endocrinology , medicine , proopiomelanocortin , histidine decarboxylase , sleep deprivation , neuropeptide y receptor , wakefulness , histamine , leptin , hypothalamus , glucose homeostasis , sleep (system call) , biology , diabetes mellitus , insulin resistance , neuropeptide , circadian rhythm , obesity , neuroscience , enzyme , biochemistry , receptor , electroencephalography , histidine , computer science , operating system
In humans and animal models, chronic sleep loss stimulates feeding and leads to metabolic interactions associated with signs of the metabolic syndrome and progression to diabetes II. Understanding how sleep deprivation might produce these effects is more complicated and involves dissection of central nervous system pathways that normally regulate food intake and those which control peripheral metabolism. For the former, hypothalamic neuropeptide Y (NPY) and proopiomelanocortin (POMC) are key systems governing feeding. Sleep deprivation up‐regulates NPY and down‐regulates POMC in the hypothalamus that accounts for the hyperphagia. For the changes in metabolism, usually hyperphagia is accompanied by a slowing of metabolic rate but the opposite is seen in chronic sleep deprivation. The CNS's role in regulating metabolic rate is less well understood, although histamine may be involved. Central histamine neurons not only affect the maintenance of wakefulness, but are also regulators of peripheral metabolism via actions at the preganglionic sympathetic neurons. The rate‐limiting enzyme for histamine synthesis, histidine decarboxylase, is up‐regulated during sleep deprivation, and these changes predict the attenuation of body weight (prompted by hypermetabolism). The relationship of changes in histamine synthesis to those of glucose suggests that the amine might also be responsible for changes which lead to metabolic syndrome. Elevations in glucose:insulin ratios in sleep deprived rats were positively correlated with the extent of increased histidine decarboxylase gene expression. Together, these data raise the possibility that a dysregulation of histamine function when sleep is impaired might serve to trigger increased sympathetic tone and metabolic changes leading to diabetes. Supported by a Pilot and Feasibility grant from the Clinical Nutrition Research Unit of Maryland, P30DK072488.