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Query: UMLS:C0017168 (
gastroesophageal reflux disease
)
11,783
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
Steatosis and steatohepatitis are associated with obesity. Despite florid histological changes, patients with non-alcoholic steatohepatitis generally remain asymptomatic, and it usually runs a relatively benign course. An elevated insulin level may be important in the pathogenesis. There is a marked regression of fatty changes after weight reduction. In obese subjects the risk of developing gallstones is increased due to an increased saturation of gallbladder bile with cholesterol and possible gallbladder stasis. During weight reduction with very low calorie diets the incidence in gallstones increases probably because of an increased saturation of bile during the loss of weight. Ursodeoxycholic acid appears to be a promising prophylactic agent.
Chenodeoxycholic acid
is not useful for these subjects. There is controversy over whether obesity contributes to
gastroesophageal reflux
and gastric emptying disturbances. There are changes in gastrointestinal peptide plasma levels in obesity but it is not clear if this contributes to its development. The risk for high-risk colorectal adenomas and carcinomas is reported to be increased in obese males. Vertical banded gastroplasty and gastric bypass procedures are nowadays the surgical options for the treatment of obesity. Nutritional deficiencies, particularly of vitamin B12, folate and iron are common after gastric bypass and must be sought and treated. Dumping is another potential complication of this operation. If stenosis and gastric outlet obstruction develop endoscopic dilatation is a good therapeutic option.
...
PMID:Gastrointestinal disturbances with obesity. 801 72
The role of weak acids with pH values in the range of 4-7 has been implicated in the symptoms of
gastroesophageal reflux disease
(
GERD
). Prostaglandin E
2
(PGE
2
) is associated with heartburn symptom in
GERD
patients; however, the precise productive mechanisms remain unclear. In this study, we revealed that exposure to weak acids increases PGE
2
production with a peak at pH 4-5, slightly in human normal oesophageal cells (Het-1A), and robustly in oesophageal squamous carcinoma cells (KYSE-270). Release of PGE
2
from the oesophageal mucosa was augmented by weak acid treatment in rat.
Chenodeoxycholic acid
(CDCA), a bile acid, upregulated cyclooxygenase-2 (COX-2) expression in Het-1A and KYSE-270 and induced PGE
2
production in KYSE-270 cells. Weak acid-induced PGE
2
production was significantly inhibited by cytosolic phospholipase A2 (cPLA2), ERK, and transient receptor potential cation channel subfamily V member 4 (TRPV4), a pH-sensing ion channel, inhibitors. Hangeshashinto, a potent inhibitor of COX-2, strongly decreased weak acid- and CDCA-induced PGE
2
levels in KYSE-270. These results indicated that weak acids induce PGE
2
production via TRPV4/ERK/cPLA2 in oesophageal epithelial cells, suggesting a role in
GERD
symptoms like heartburn. Interventions targeting pH values up to 5 may be necessary for the treatment of
GERD
.
...
PMID:Weak acids induce PGE
2
production in human oesophageal cells: novel mechanisms underlying GERD symptoms. 3324 92
