著者
Satoshi SUZUKI Hiroyoshi TSUBOCHI Andrew DARNEL Takashi SUZUKI Hironobu SASANO Zigmunt S. KROZOWSKI Takashi KONDO
出版者
The Japan Endocrine Society
雑誌
Endocrine Journal (ISSN:09188959)
巻号頁・発行日
vol.50, no.4, pp.445-451, 2003 (Released:2003-09-11)
参考文献数
31
被引用文献数
7 13

11β-Hydroxysteroid dehydrogenase type 1 (11β-HSD1) behaves predominantly as an oxoreductase converting the receptor-inactive glucocorticoids to their active forms in vivo, while the type 2 isoform (11β-HSD2) possesses only dehydrogenase activity and inactivates cortisol in human or corticosterone in rat. We determined enzyme activity of 11β-HSD in rat lungs from fetus to adult, and examined whether 11β-HSD1 exists in alveolar type II cells, the most important site for the synthesis of pulmonary surfactant in mature lungs, by immunohistochemistry and reverse transcription-polymerase chain reaction (RT-PCR). Enzyme activity of 11β-HSD1 and 2 in lung tissue homogenate were determined as NADP+- and NAD+-dependent conversion of corticosterone to 11-dehydrocorticosterone, respectively. We found that 11β-HSD1 activity was increased progressively from 21 days gestation to 7 weeks after birth. 11 β-HSD2 activity was significantly lower than that of 11β-HSD1 throughout gestation and after birth. Immunoreactivity for 11β-HSD1 was detected in the cytoplasm of the cells in the alveolar region of adult rats. Some of these expressing 11β-HSD1 were considered to be alveolar type II cells, because of their cuboid shape and localization at the corner of the alveoli. RT-PCR demonstrated 11 β-HSD1 mRNA in isolated alveolar type II cells. Our results suggest that alveolar type II cells enhance intracellular glucocorticoid availability via 11β-HSD1. 11β-HSD1 in alveolar type II cells is thought of as an autocrine amplifier of glucocorticoid action in the lung.
著者
Tomomi GENDA Takashi KONDO Shingo HINO Shunsaku SUGIURA Naomichi NISHIMURA Tatsuya MORITA
出版者
Center for Academic Publications Japan
雑誌
Journal of Nutritional Science and Vitaminology (ISSN:03014800)
巻号頁・発行日
vol.64, no.5, pp.357-366, 2018-10-31 (Released:2018-10-31)
参考文献数
42
被引用文献数
14

The effects of fructo-oligosaccharides (FOS) on gut-barrier function are still controversial in human and animal studies. Diet conditions would be a major factor for the controversy in animal studies. We fed rats a semi-purified (SP) or a non-purified diet (NP) with or without FOS (60 g/kg diet) for 9 (experiment 1) or 10 d (experiment 2). We assessed microbial fermentation, gut permeability, and inflammatory responses in the cecum (experiment 1), and mucus layer in the cecum, intestinal transit time and microbiota composition (experiment 2). FOS supplementation induced a very acidic fermentation due to the accumulation of lactate and succinate in SP, while short-chain fatty acids were major products in NP. Gut permeability estimated by urinary chromium-EDTA excretion, bacterial translocation into mesenteric lymph nodes, myeloperoxidase activity, and expressions of the inflammatory cytokine genes in the cecal mucosa were greater in SP+FOS than in SP, but these alterations were not observed between NP and NP+FOS (experiment 1). FOS supplementation destroyed the mucus layer on the epithelial surface in SP, but not in NP. Intestinal transit time was 3-fold longer in SP+FOS than in SP, but this was not the case between NP and NP+FOS. Lower species richness of cecal microbiota was manifest solely in SP+FOS (experiment 2). These factors suggest that impact of FOS on gut permeability and inflammatory responses in the cecal mucosa quite differs between SP and NP. Increased gut permeability in SP+FOS could be evoked by the disruption of the mucus layer due to stasis of the very acidic luminal contents.