Thioredoxin interacting protein is a potential regulator of glucose and energy homeostasis in endogenous Cushing's syndrome.

Recent studies have described bone as an endocrine organ regulating glucose metabolism, with insulin signaling regulating osteocalcin secretion and osteocalcin regulating β cell function. We have previously demonstrated increased bone expression of TXNIP in patients with endogenous Cushing's sy...

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Autores principales:	Tove Lekva, Jens Bollerslev, Afaf Sahraoui, Hanne Scholz, Hege Bøyum, Johan Arild Evang, Kristin Godang, Pål Aukrust, Thor Ueland
Formato:	article
Lenguaje:	EN
Publicado:	Public Library of Science (PLoS) 2013
Materias:	Medicine R Science Q
Acceso en línea:	https://doaj.org/article/f9358be4873b416f82d3d86b721f18b6
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spelling	oai:doaj.org-article:f9358be4873b416f82d3d86b721f18b62021-11-18T07:45:16ZThioredoxin interacting protein is a potential regulator of glucose and energy homeostasis in endogenous Cushing's syndrome.1932-620310.1371/journal.pone.0064247https://doaj.org/article/f9358be4873b416f82d3d86b721f18b62013-01-01T00:00:00Zhttps://www.ncbi.nlm.nih.gov/pmc/articles/pmid/23691179/?tool=EBIhttps://doaj.org/toc/1932-6203Recent studies have described bone as an endocrine organ regulating glucose metabolism, with insulin signaling regulating osteocalcin secretion and osteocalcin regulating β cell function. We have previously demonstrated increased bone expression of TXNIP in patients with endogenous Cushing's syndrome (CS), and we hypothesized that TXNIP could contribute to the dysregulated glucose metabolism in CS. We studied 33 CS patients and 29 matched controls, with bone biopsies from nine patients, before and after surgical treatment. In vitro, the effect of silencing TXNIP (siTXNIP) in osteoblasts, including its effect on human islet cells, was examined. Our major findings were: (i) The high mRNA levels of TXNIP in bone from CS patients were significantly associated with high levels of glucose and insulin, increased insulin resistance, and decreased insulin sensitivity in these patients. (ii) Silencing TXNIP in osteoblasts enhanced their OC response to insulin and glucose and down-regulated interleukin (IL)-8 levels in these cells. (iii) Conditional media from siTXNIP-treated osteoblasts promoted insulin content and anti-inflammatory responses in human islet cells. We recently demonstrated that the thioredoxin/TXNIP axis may mediate some detrimental effects of glucocorticoid excess on bone tissue in CS. Here we show that alterations in this axis also may affect glucose metabolism in these patients.Tove LekvaJens BollerslevAfaf SahraouiHanne ScholzHege BøyumJohan Arild EvangKristin GodangPål AukrustThor UelandPublic Library of Science (PLoS)articleMedicineRScienceQENPLoS ONE, Vol 8, Iss 5, p e64247 (2013)
institution	DOAJ
collection	DOAJ
language	EN
topic	Medicine R Science Q
spellingShingle	Medicine R Science Q Tove Lekva Jens Bollerslev Afaf Sahraoui Hanne Scholz Hege Bøyum Johan Arild Evang Kristin Godang Pål Aukrust Thor Ueland Thioredoxin interacting protein is a potential regulator of glucose and energy homeostasis in endogenous Cushing's syndrome.
description	Recent studies have described bone as an endocrine organ regulating glucose metabolism, with insulin signaling regulating osteocalcin secretion and osteocalcin regulating β cell function. We have previously demonstrated increased bone expression of TXNIP in patients with endogenous Cushing's syndrome (CS), and we hypothesized that TXNIP could contribute to the dysregulated glucose metabolism in CS. We studied 33 CS patients and 29 matched controls, with bone biopsies from nine patients, before and after surgical treatment. In vitro, the effect of silencing TXNIP (siTXNIP) in osteoblasts, including its effect on human islet cells, was examined. Our major findings were: (i) The high mRNA levels of TXNIP in bone from CS patients were significantly associated with high levels of glucose and insulin, increased insulin resistance, and decreased insulin sensitivity in these patients. (ii) Silencing TXNIP in osteoblasts enhanced their OC response to insulin and glucose and down-regulated interleukin (IL)-8 levels in these cells. (iii) Conditional media from siTXNIP-treated osteoblasts promoted insulin content and anti-inflammatory responses in human islet cells. We recently demonstrated that the thioredoxin/TXNIP axis may mediate some detrimental effects of glucocorticoid excess on bone tissue in CS. Here we show that alterations in this axis also may affect glucose metabolism in these patients.
format	article
author	Tove Lekva Jens Bollerslev Afaf Sahraoui Hanne Scholz Hege Bøyum Johan Arild Evang Kristin Godang Pål Aukrust Thor Ueland
author_facet	Tove Lekva Jens Bollerslev Afaf Sahraoui Hanne Scholz Hege Bøyum Johan Arild Evang Kristin Godang Pål Aukrust Thor Ueland
author_sort	Tove Lekva
title	Thioredoxin interacting protein is a potential regulator of glucose and energy homeostasis in endogenous Cushing's syndrome.
title_short	Thioredoxin interacting protein is a potential regulator of glucose and energy homeostasis in endogenous Cushing's syndrome.
title_full	Thioredoxin interacting protein is a potential regulator of glucose and energy homeostasis in endogenous Cushing's syndrome.
title_fullStr	Thioredoxin interacting protein is a potential regulator of glucose and energy homeostasis in endogenous Cushing's syndrome.
title_full_unstemmed	Thioredoxin interacting protein is a potential regulator of glucose and energy homeostasis in endogenous Cushing's syndrome.
title_sort	thioredoxin interacting protein is a potential regulator of glucose and energy homeostasis in endogenous cushing's syndrome.
publisher	Public Library of Science (PLoS)
publishDate	2013
url	https://doaj.org/article/f9358be4873b416f82d3d86b721f18b6
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Thioredoxin interacting protein is a potential regulator of glucose and energy homeostasis in endogenous Cushing's syndrome.

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