Morbid Obesity Clinical Trial
Official title:
Hunger/Satiety's Physiopathologic Study in Morbidly Obese Patients: Relation Between Hunger/Satiety, Gastric Emptying, Gallbladder Motility and Peripheral Neurohormonal Signs
The mechanisms that regulate appetite in the morbidly obese are multifactorial and not
well-known. Different peripheral signals (such as ghrelin or cholecystokinin) play an
important role in the central regulation of appetite and hunger. Postprandial ghrelin and
cholecystokinin (CCK) response has also an effect on gastric emptying that, in turn, has an
effect on satiety sensation.
On the other hand, bariatric surgery is supposed to affect hunger and satiety in and also
promotes changes in gastric emptying which are not clearly defined.
Aim: To better understand the physiologic mechanisms involved in the regulation of hunger
and satiety in morbidly obese individuals, especially those related with gallbladder and
gastric emptying, as well as those related with the response of the gastrointestinal
hormones ghrelin, CCK and glucagon-like peptide-1 (GLP-1), before and after bariatric
surgery (sleeve gastrectomy). Methodology: Three groups of individuals will be studied and
compared: group A) non obese healthy subjects, group B) morbidly obese subjects and group C)
morbidly obese subjects who had had a previous sleeve gastrectomy. In all subjects a
standard meal test after a fasting night will be administered and appetite, satiety and
hormonal response (ghrelin, CCK, GLP-1 and insulin) during 4 hours post-ingestion assessed,
as well as postprandial gallbladder and gastric emptying by means of ultrasonography and the
paracetamol absorption technique.
n/a
Observational Model: Case Control, Time Perspective: Prospective
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