1988
DOI: 10.1159/000242821
|View full text |Cite
|
Sign up to set email alerts
|

Influence of Hydrocortisone on the Development of Pancreas in Suckling Rats

Abstract: The effect of hydrocortisone on the growth and differentiation of the pancreas was examined in suckling rats. Three doses of hydrocortisone (40, 20, 5 mg/kg/day) were administered during the second week of life. Biochemical and ultrastructural morphometric studies were performed on the pancreas at the end of the treatment. Whatever the dose used, hydrocortisone induced pancreatic hypertrophy and significantly increased enzymatic activities by 70–200% for lipase and colipase, 140–340% for trypsinogen and chymot… Show more

Help me understand this report

Search citation statements

Order By: Relevance

Paper Sections

Select...
2
2
1

Citation Types

3
8
0

Year Published

1988
1988
2006
2006

Publication Types

Select...
9

Relationship

1
8

Authors

Journals

citations
Cited by 17 publications
(11 citation statements)
references
References 13 publications
3
8
0
Order By: Relevance
“…Indeed, the pancreas was the only digestive organ for which we found an absolute weight augmentation in hydrocorti sone-treated rats as compared with controls. Enzymatic activities also increased [24], This assured us of the treatment efficacy.…”
Section: Discussionmentioning
confidence: 85%
“…Indeed, the pancreas was the only digestive organ for which we found an absolute weight augmentation in hydrocorti sone-treated rats as compared with controls. Enzymatic activities also increased [24], This assured us of the treatment efficacy.…”
Section: Discussionmentioning
confidence: 85%
“…The parenteral exposure was not able to induce GI maturational effects as compared to the enteral exposure, although the plasma-corticosterone levels were equally elevated by both treatments. In addition, the pancreatic amylase activity did not increase due to the PHA treatments (enteral or parenteral), which has previously been demonstrated to be elevated by glucocorticoids in rats in vivo and in vitro [24][25][26] . Thus, the results implied that the maturation of GI tract and pancreatic function after PHA exposure was not primarily mediated via corticosterone, but rather by a corticosterone-independent pathway.…”
Section: Possible Pathways/mechanisms Of Phamentioning
confidence: 86%
“…A reduction in net fluid intake as well as nutritional supply secondary to aphagia is likely to play a direct role in the death of D1r Ϫ/Ϫ ;D2r ϩ/Ϫ (and probably also DKO) mice, because they will not develop GI ulcerations as long as they are fed hydrated food. Nutritional deficiency secondary to hypophagia during early postnatal development might partly contribute to the intestinal atrophy (55)(56)(57)(58).…”
Section: Discussionmentioning
confidence: 99%