Background: @entity1949 ( @entity1949 ) is highly prevalent and may constitute an important contributing factor to excessive @entity1017 . Increased endoplasmic reticulum (ER) stress and activation of the unfolded protein response (UPR) leading to the attenuation of @entity18070 signaling in the hypothalamus leads to @entity28 and @entity209 . Methods: @entity19 were exposed to @entity1949 and sleep control (SC) for varying periods of time during which ingestive behaviors were monitored. UPR pathways and @entity18070 signaling were assessed in hypothalami. To further examine the mechanistic role of ER stress, changes in @entity18070 ( @entity18070 ) signaling were also examined in wild-type @entity19 treated with the ER chaperone tauroursodeoxycholic acid (TUDCA), as well as in @entity13841 -/+ @entity19 . Results: Fragmented sleep in male @entity19 induced @entity101 starting day 3 and thereafter, which was preceded by increases in ER stress and activation of all three UPR pathways in the hypothalamus. Although @entity18070 expression was unchanged, @entity10433 ( @entity10433 ) phosphorylation was decreased, suggesting reduced @entity18070 signaling. Unchanged @entity26102 ( @entity26102 ) expression and increases in @entity63682 ( @entity63682 ) expression and activity emerged with @entity1949 , along with reduced p- @entity10433 responses to exogenous @entity3237 . @entity1949 -induced effects were reversed following TUDCA treatment and were absent in @entity13841 -/+ @entity19 . Conclusions: @entity1949 induces hyperphagic behaviors and reduced @entity3237 signaling in hypothalamus that are mediated by activation of ER stress, and ultimately lead to increased @entity63682 activity. ER stress pathways are therefore potentially implicated in @entity1949 -induced @entity1017 and @entity209 , and may represent a viable therapeutic target.

Chronic Sleep Fragmentation During the Sleep Period Induces Hypothalamic Endoplasmic Reticulum Stress and @entity63682 -Mediated XXXX Resistance in Male @entity19 .

@entity18070 :: ('16847(Tax:10090)', 'Gene') :: ['ObR', 'leptin receptor'] @entity1949 :: ('MESH:D012892', 'Disease') :: ['SF', 'Sleep fragmentation'] @entity101 :: ('MESH:D006973', 'Disease') :: ['increased food intake'] @entity28 :: ('MESH:D009765', 'Disease') :: ['obesity'] @entity13841 :: ('13198(Tax:10090)', 'Gene') :: ['CHOP'] @entity19 :: ('10090', 'Species') :: ['mice', 'Mice', 'transgenic mice'] @entity10433 :: ('20848(Tax:10090)', 'Gene') :: ['STAT3', 'signal transducer and activator of transcription 3'] @entity3237 :: ('16846(Tax:10090)', 'Gene') :: ['leptin'] @entity26102 :: ('12702(Tax:10090)', 'Gene') :: ['SOCS3', 'suppressor of cytokine signaling-3'] @entity63682 :: ('19246(Tax:10090)', 'Gene') :: ['PTP1B', 'protein-tyrosine phosphatase 1B'] @entity1017 :: ('MESH:D015430', 'Disease') :: ['weight gain', 'weight gain and the metabolic syndrome'] @entity209 :: ('MESH:D008659', 'Disease') :: ['metabolic dysfunction']
@entity3237 :: (16846(Tax:10090),Gene) :: ['Leptin']
