PubMed Health⌕ Search

PubMed · 1766136

[Development of pancreatic exocrine function including intestinal negative feedback regulation using oral trypsin inhibitor in rats].

Abstract

To investigate the development of pancreatic exocrine function and intestinal negative feedback regulation with aging in rats, we measured pancreas weight, content of amylase and trypsinogen in the rat pancreas and plasma CCK concentrations, activity of amylase and trypsin in the small intestine at an hour after oral administration of trypsin inhibitor (TI), and also examined amylase secretory response to CCK-8 in the rat pancreatic acini at various ages in vitro. As a result, amylase content per pancreas weight increased with the age and amylase activity in the small intestine at al ages showed a significant increase in TI group compared to controls. Plasma CCK concentrations were elevated after administration of TI at all ages. Amylase release from pancreatic acini stimulated by CCK-8 responded poorly on days 7, then gradually increased with age, showing a biphasic dose response curve with maximal response of 10(-10) M of CCK-8 from 14-day-old to 66-day-old. The results indicated that the mechanism of pancreatic secretory response to TI already might exist at the stage of sucking rat and secretory response to CCK-8 in vitro showed a low response, and developed with age.

Explore related subjects

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

S Ozawa, Y Hatta. 1991. [Development of pancreatic exocrine function including intestinal negative feedback regulation using oral trypsin inhibitor in rats].. https://pubmed.ncbi.nlm.nih.gov/1766136/

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related citations

Alginate microparticles as novel carrier for oral insulin delivery.

Alginate microparticles produced by emulsification/internal gelation were investigated as a promising carrier for insulin delivery. The procedure involves the dispersion of alginate solution containing insulin protein, into a water immiscible phase. Gelation is triggered in situ by instantaneous release of ionic calcium from carbonate complex via gentle pH adjustment. Particle size is controlled through the emulsification parameters, yielding insulin-loaded microparticles. Particle recovery was compared using several washing protocols. Recovery strategies are proposed and the influence on particle mean size, morphology, recovery yield (RY), encapsulation efficiency, insulin release profile, and structural integrity of released insulin were evaluated. Spherical micron-sized particles loaded with insulin were produced. The recovery process was optimized, improving yield, and ensuring removal of residual oil from the particle surface. The optimum recovery strategy consisted in successive washing with a mixture of acetone/hexane/isopropanol coupled with centrifugation. This strategy led to small spherical particles with an encapsulation efficiency of 80% and a RY around 70%. In vitro release studies showed that alginate itself was not able to suppress insulin release in acidic media; however, this strategy preserves the secondary structure of insulin. Particles had a mean size lower than the critical diameter necessary to be orally absorbed through the intestinal mucosa followed by their passage to systemic circulation and thus can be considered as a promising technology for insulin delivery.

Administration, Oral↗

Treatment of recurrent pulmonary vein stenoses with endovascular stenting and adjuvant oral sirolimus.

The increasing use of radiofrequency catheter ablation for the cure of atrial fibrillation has led to iatrogenic pulmonary vein stenosis as a new clinical entity. The optimal diagnostic modality and treatment for pulmonary vein stenosis and restenosis remain unclear. We report the successful treatment of pulmonary vein restenosis following percutaneous balloon angioplasty, and for the first time, following surgical bovine pericardial patch angioplasty, with endovascular stenting and adjuvant oral sirolimus. Both patients remain asymptomatic at 1 year follow-up without evidence of restenosis.

Administration, Oral↗

Induction of salivary polypeptides associated with parotid hypertrophy by gallotannins administered topically into the mouse mouth.

Isoproterenol-induced salivary polypeptides (IISP), a group of proline-rich proteins synthesized by mouse parotids, have been considered as markers for isoproterenol-induced parotid hypertrophy. Rodents fed diets containing high-tannin cereals (sorghum), also develop parotid hypertrophy. To test whether tannins are directly involved in provoking sialotrophic growth, we studied the effect of intraperitoneal and topical oral administrations of tannic acid (TA) on the induction of IISP polypeptides in endogamic mice (A/Snell). TA was characterized by HPLC chromatography and spectral analysis and shown to be composed solely of gallotannins, a complex family of glucose and gallic acid esters. IISP polypeptides were monitored in saliva by SDS-polyacrylamide gel electrophoresis during 36 h after ending TA stimulation. Single daily intraperitoneal administrations of TA for 3 consecutive days (0.033 mg/g bw/day), at variance of parallel administrations of isoproterenol (0.042 mg/g bw/day) failed to induce IISP polypeptides. However, repeated topical applications of TA into the mouse mouths (1.21 mg/g bw divided into three equal doses given at 4-h intervals within a single day) resulted in unequivocal induction of IISP polypeptides. That response was clearly intensified by increasing the stimulation frequency to eight equivalent doses given at 1.5-h intervals within a single day (corresponding to 3.23 mg/g bw) and even further by repeating this protocol for 3 days. Under these productive schemes of stimulations by TA, electrophoretic fractionation of parotid homogenates showed new polypeptide bands migrating in parallel to salivary IISP. These results suggest that topically administered gallotannins are effective inducers of trophic growth in mouse parotids.

Administration, Oral↗