Plasma and cellular retinoid-binding proteins and transthyretin (prealbumin) are all localized in the islets of Langerhans in the rat.

Kato, Michimasa; Kato, K; Blaner, William S.; Chertow, Bruce S.; Goodman, DeWitt S.

doi:10.1073/pnas.82.8.2488

Cited by 49 publications

(30 citation statements)

References 24 publications

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“…CRABPs may have some role in development of islets because they are localized in adult islets (31), and transgenic mice overexpressing CRABP I die prematurely as a result of tumor originating from islet of Langerhans (32).…”

Section: Discussionmentioning

confidence: 99%

All-Trans Retinoic Acid Induces Differentiation of Ducts and Endocrine Cells by Mesenchymal/Epithelial Interactions in Embryonic Pancreas

et al. 2003

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Retinoids during the embryonic period act as a mesenchymal inducer in many organs, including kidney, lung, central nervous system, and gut. Retinoic acid (RA) demonstrates insulinotropic effects in adult pancreas, but only a limited study has elucidated its role in pancreatic organogenesis. In this study, we have analyzed the existence of RA-signaling machinery in embryonic pancreas and evaluated its role using

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Section: Discussionmentioning

confidence: 99%

All-Trans Retinoic Acid Induces Differentiation of Ducts and Endocrine Cells by Mesenchymal/Epithelial Interactions in Embryonic Pancreas

et al. 2003

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“…Islets were then thawed and homogenized in 1 ml of assay buffer containing 50 mM imidazole buffer pH 7.4,0.79% NaCl, 0.03% bovine serum albumin, 0.1I% thiomerosal, 0.0 1% leupeptin, and 1.0% Triton X-1I00. CRBP and CRABP levels were determined by recently developed sensitive and specific radioimmunoassays for each protein (7,20 Islet insulin and protein content. Islets were isolated from groups of normal, A-deficient, and retinoic acid-and retinyl palmitate-repleted rats.…”

Section: Methodsmentioning

confidence: 99%

“…Recent studies (7) have demonstrated the presence of relatively high levels ofCRBP, CRABP, TTR, and RBP in pancreatic rat islets. We have also shown that retinoids influence islet insulin secretion, ultrastructure and cell aggregation (8)(9)(10).…”

Section: Introductionmentioning

confidence: 99%

Effects of vitamin A deficiency and repletion on rat insulin secretion in vivo and in vitro from isolated islets.

Chertow¹,

Blaner²,

Baranetsky³

et al. 1987

J. Clin. Invest.

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“…We explored this issue in our experimental crosses. The rationale was that, since the FoxO1 transgene is expressed from the transthyretin promoter, it should affect proliferation not only of terminally differentiated β cells but also of duct cells, a site of transthyretin expression (28). We obtained 2 surrogate measures of β cell "neogenesis" by counting β cell singlets/doublets and β cells abutting the lumen of pancreatic ducts (4,21,22).…”

Section: Early-onset Diabetes In Double-mutant Mice Transgenic Mice mentioning

confidence: 99%

Role of the forkhead protein FoxO1 in cell compensation to insulin resistance

Okamoto

Hribal²,

Lin³

et al. 2006

Journal of Clinical Investigation

118

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Diabetes is associated with defective β cell function and altered β cell mass. The mechanisms regulating β cell mass and its adaptation to insulin resistance are unknown. It is unclear whether compensatory β cell hyperplasia is achieved via proliferation of existing β cells or neogenesis from progenitor cells embedded in duct epithelia. We have used transgenic mice expressing a mutant form of the forkhead-O1 transcription factor (FoxO1) in both pancreatic ductal and endocrine β cells to assess the contribution of these 2 compartments to islet expansion. We show that the mutant FoxO1 transgene prevents β cell replication in 2 models of β cell hyperplasia, 1 due to peripheral insulin resistance (Insulin receptor transgenic knockouts) and 1 due to ectopic local expression of IGF2 (Elastase-IGF2 transgenics), without affecting insulin secretion. In contrast, we failed to detect a specific effect of the FoxO1 transgene on the number of periductal β cells. We propose that β cell compensation to insulin resistance is a proliferative response of existing β cells to growth factor signaling and requires FoxO1 nuclear exclusion.

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Plasma and cellular retinoid-binding proteins and transthyretin (prealbumin) are all localized in the islets of Langerhans in the rat.

Abstract: The

Cited by 49 publications

References 24 publications

All-Trans Retinoic Acid Induces Differentiation of Ducts and Endocrine Cells by Mesenchymal/Epithelial Interactions in Embryonic Pancreas

All-Trans Retinoic Acid Induces Differentiation of Ducts and Endocrine Cells by Mesenchymal/Epithelial Interactions in Embryonic Pancreas

Effects of vitamin A deficiency and repletion on rat insulin secretion in vivo and in vitro from isolated islets.

Role of the forkhead protein FoxO1 in cell compensation to insulin resistance

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