Caloric restriction causes secretagogue specific changes of gastric acid secretion in rats

Shunichi Higashide; Kyo U. Chu; Guillermo Gomez; George H. Greeley; James C. Thompson; Courtney M. Townsend

doi:10.1016/S0167-0115(96)02124-6

Caloric restriction causes secretagogue specific changes of gastric acid secretion in rats

Shunichi Higashide, Kyo U. Chu, Guillermo Gomez, George H. Greeley, James C. Thompson, Courtney M. Townsend

Surgery

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Abstract

The purpose of this study was to examine the effects of short-term caloric restriction (CR) for 4, 8 and 16 weeks on gastric acid secretion in rats. CR rats were fed 60% of normal food intake for 4, 8 or 16 weeks and then prepared with gastric fistulas. Histamine- and carbachol-stimulated gastric acid secretion were significantly (P < 0.05) decreased after more than 4 weeks and 8 weeks of caloric restriction, respectively. In contrast, gastrin-stimulated acid secretion was unaffected by CR. The 1-h-integrated acid output to a submaximal dose of gastrin (40 μg · kg^-1) was significantly higher than that of histamine (5 mg · kg^-1) after 8 weeks of CR (63 ± 13 and 27 ± 4 μEq · h^-1, respectively). Gastrin treatment (5 μg · kg^-1 · h^-1) of CR rats restored the gastric acid responses to both histamine and carbachol. These results suggest that CR can selectively decrease the gastric acid responses to both histamine and carbachol by depletion of the endogenous tissue stores of gastrin. More importantly, these results indicate that under an in vivo gastrin-diminished condition, histamine is not the final secretagogue for gastric acid secretion.

Original language	English (US)
Pages (from-to)	205-210
Number of pages	6
Journal	Regulatory Peptides
Volume	68
Issue number	3
DOIs	https://doi.org/10.1016/S0167-0115(96)02124-6
State	Published - Feb 26 1997

Keywords

Carbachol
Gastrin
Histamine

ASJC Scopus subject areas

Physiology
Biochemistry
Endocrinology
Clinical Biochemistry
Cellular and Molecular Neuroscience

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10.1016/S0167-0115(96)02124-6

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title = "Caloric restriction causes secretagogue specific changes of gastric acid secretion in rats",

abstract = "The purpose of this study was to examine the effects of short-term caloric restriction (CR) for 4, 8 and 16 weeks on gastric acid secretion in rats. CR rats were fed 60% of normal food intake for 4, 8 or 16 weeks and then prepared with gastric fistulas. Histamine- and carbachol-stimulated gastric acid secretion were significantly (P < 0.05) decreased after more than 4 weeks and 8 weeks of caloric restriction, respectively. In contrast, gastrin-stimulated acid secretion was unaffected by CR. The 1-h-integrated acid output to a submaximal dose of gastrin (40 μg · kg-1) was significantly higher than that of histamine (5 mg · kg-1) after 8 weeks of CR (63 ± 13 and 27 ± 4 μEq · h-1, respectively). Gastrin treatment (5 μg · kg-1 · h-1) of CR rats restored the gastric acid responses to both histamine and carbachol. These results suggest that CR can selectively decrease the gastric acid responses to both histamine and carbachol by depletion of the endogenous tissue stores of gastrin. More importantly, these results indicate that under an in vivo gastrin-diminished condition, histamine is not the final secretagogue for gastric acid secretion.",

keywords = "Carbachol, Gastrin, Histamine",

author = "Shunichi Higashide and Chu, {Kyo U.} and Guillermo Gomez and Greeley, {George H.} and Thompson, {James C.} and Townsend, {Courtney M.}",

note = "Funding Information: We would like to thank Eileen Figueroa, Larry Janecka, Karen Martin, Steve Schuenke and Bob Todd for their assistance in preparation of this manuscript. This work was supported by grants from the National Institutes of Health (DK 15241, DK 35608).",

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AU - Higashide, Shunichi

AU - Chu, Kyo U.

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AU - Thompson, James C.

AU - Townsend, Courtney M.

N1 - Funding Information: We would like to thank Eileen Figueroa, Larry Janecka, Karen Martin, Steve Schuenke and Bob Todd for their assistance in preparation of this manuscript. This work was supported by grants from the National Institutes of Health (DK 15241, DK 35608).

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N2 - The purpose of this study was to examine the effects of short-term caloric restriction (CR) for 4, 8 and 16 weeks on gastric acid secretion in rats. CR rats were fed 60% of normal food intake for 4, 8 or 16 weeks and then prepared with gastric fistulas. Histamine- and carbachol-stimulated gastric acid secretion were significantly (P < 0.05) decreased after more than 4 weeks and 8 weeks of caloric restriction, respectively. In contrast, gastrin-stimulated acid secretion was unaffected by CR. The 1-h-integrated acid output to a submaximal dose of gastrin (40 μg · kg-1) was significantly higher than that of histamine (5 mg · kg-1) after 8 weeks of CR (63 ± 13 and 27 ± 4 μEq · h-1, respectively). Gastrin treatment (5 μg · kg-1 · h-1) of CR rats restored the gastric acid responses to both histamine and carbachol. These results suggest that CR can selectively decrease the gastric acid responses to both histamine and carbachol by depletion of the endogenous tissue stores of gastrin. More importantly, these results indicate that under an in vivo gastrin-diminished condition, histamine is not the final secretagogue for gastric acid secretion.

AB - The purpose of this study was to examine the effects of short-term caloric restriction (CR) for 4, 8 and 16 weeks on gastric acid secretion in rats. CR rats were fed 60% of normal food intake for 4, 8 or 16 weeks and then prepared with gastric fistulas. Histamine- and carbachol-stimulated gastric acid secretion were significantly (P < 0.05) decreased after more than 4 weeks and 8 weeks of caloric restriction, respectively. In contrast, gastrin-stimulated acid secretion was unaffected by CR. The 1-h-integrated acid output to a submaximal dose of gastrin (40 μg · kg-1) was significantly higher than that of histamine (5 mg · kg-1) after 8 weeks of CR (63 ± 13 and 27 ± 4 μEq · h-1, respectively). Gastrin treatment (5 μg · kg-1 · h-1) of CR rats restored the gastric acid responses to both histamine and carbachol. These results suggest that CR can selectively decrease the gastric acid responses to both histamine and carbachol by depletion of the endogenous tissue stores of gastrin. More importantly, these results indicate that under an in vivo gastrin-diminished condition, histamine is not the final secretagogue for gastric acid secretion.

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Caloric restriction causes secretagogue specific changes of gastric acid secretion in rats

Abstract

Keywords

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