The effect of dietary restriction on gastrin secretion in the obese Zucker rat.
It has been hypothesized that G-cell hyperplasia secondary to increased food consumption in the obese Zucker rat was responsible for the hypergastrinemia observed in vivo and from the isolated perfused stomach preparation. This possibility was investigated in pair-feeding experiments wherein the food intake of obese animals was restricted to match that of lean littermates from 5 to 8 weeks of age. Dietary restriction reduced the antral G-cell population of the obese rat to a similar level as that seen in lean animals, supporting the view that hyperphagia is the trigger for G-cell hyperplasia. However, basal gastrin levels measured in vivo and in vitro from the stomach preparation of the pair-fed obese animals were not significantly lower than those of obese animals fed ad libitum. Thus, abnormal feeding behavior in the obese phenotype cannot be directly related to gastrin hypersecretion and G-cell hyperplasia is not the primary cause of hypergastrinemia.
Campos
R V
RV
Department of Physiology, University of British Columbia, Vancouver, Canada.
Pederson
R A
RA
Buchan
A M
AM
Brown
J C
JC
D000818:Animals; D001835:Body Weight / Q000502:physiology; D004032:Diet; D004435:Eating / Q000502:physiology*; D005755:Gastrins / Q000097:blood / Q000378:metabolism*; D008954:Models, Biological; D009765:Obesity / Q000209:etiology / Q000503:physiopathology*; D011706:Pyloric Antrum / Q000378:metabolism*; D051381:Rats; D011924:Rats, Zucker
D005755:Gastrins