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Public release date: 21-Dec-2012[ | E-mail |
Share ] Contact: Jillian Hurst
press_releases@the-jci.org
Journal of Clinical Investigation
The X-factor in liver metabolism
After you eat, your liver switches from producing glucose to storing it. At the same time, a cellular signaling pathway known as the unfolded protein response (UPR) is transiently activated, but it is not clear how this pathway contributes to the liver's metabolic switch. In this issue of the Journal of Clinical Investigation, researchers led by Phillip Scherer at the University of Texas Southwestern Medical Center report that activation of the UPR triggers the expression of Xbp1s, a protein that regulates genes needed for the metabolic switch. Scherer and colleagues found that they could induce changes in liver metabolism just by increasing expression of Xbps1. These results suggest that Xbps1 could play a role in metabolic disease.
TITLE:
The Xbp1s/GalE axis links ER stress to postprandial hepatic metabolism
AUTHOR CONTACT:
Philipp E. Scherer
The University of Texas Southwestern Medical Center, Dallas, TX, USA
Phone: (214) 648-8715; Fax: (214) 648-8720; E-mail: philipp.scherer@utsouthwestern.edu
View this article at: http://www.jci.org/articles/view/62819?key=17adb760d62c3d29b6fb
Low iron levels increase the risk of H. pylori-associated gastric cancer
H. pylori frequently causes gastric ulcers and is also one of the greatest risk factors for gastric cancer. H. pylori infection is also associated with another gastric cancer risk factor, iron deficiency. In this issue of the Journal of Clinical Investigation, researchers led by Richard Peek at Vanderbilt University investigated the influence of iron on H. pylori-induced gastric cancer. Peek and colleagues found that low iron accelerated the development of H. pylori-associated cancerous lesions in gerbils. Further, H. pylori strains isolated from a human population at high risk for gastric cancer were more virulent and produced greater inflammation if they came from patients with low iron levels. In an accompanying article, El-Omar Emad of Aberdeen University discusses how iron levels could be used to identify patients that are at a higher risk for gastric cancer after H. pylori infection.
TITLE:
Iron deficiency accelerates Helicobacter pylori-induced carcinogenesis in rodents and humans
AUTHOR CONTACT:
Richard M. Peek, Jr.
Vanderbilt University School of Medicine, Nashville, TN, USA
Phone: 615-322-5200; Fax: 615-343-6229; E-mail: richard.peek@vanderbilt.edu
View this article at: http://www.jci.org/articles/view/64373?key=95552f8a58ca300dd6bc
ACCOMPANYING ARTICLE
TITLE:
Iron deficiency and H. pylori-induced gastric cancer: too little, too bad
AUTHOR CONTACT:
Emad El-Omar
Aberdeen University, Foresterhill, Aberdeen, GBR
Phone: +44 (0)1224 437548; E-mail: e.el-omar@abdn.ac.uk
View this article at: http://www.jci.org/articles/view/67200?key=98b2d035a72beb6365c9
A critical genetic regulator of brown fat functionality
Obesity is a direct consequence of prolonged positive energy balance that occurs when energy intake (ie. calories) exceeds energy expenditure. In mammals, brown fat plays a critical role in energy metabolism due to its ability to burn energy by dissipating heat, a process known as thermogenesis. Therapeutics that target brown fat could possibly increase metabolism and correct the imbalance that leads to obesity. In this issue of the Journal of Clinical Investigation, researchers led by Matthias Tschp identified a protein in mice, p62, that is required for brown fat thermogenesis. Mice that did not express p62 in fat cells became obese and developed glucose intolerance, key features of metabolic syndrome in humans. These findings indicate that p62 is an important regulator of metabolism and energy balance and is could potentially serve as a therapeutic target for the treatment of metabolic syndrome.
TITLE:
p62 links beta-adrenergic input with mitochondrial function
AUTHOR CONTACT:
Matthias Tschoep
Helmholtz Zentrum Mnchen - German Research Center for Environmental Health, 85764 Neuherberg, UNK, DEU
Phone: + 49 89 3187 2103; E-mail: matthias.tschoep@helmholtz-muenchen.de
View this article at: http://www.jci.org/articles/view/64209?key=ffdc151cc8b44910eb6e
Dendritic cells play a protective role in atherosclerosis
Atherosclerosis is characterized by a chronic inflammatory immune response that increases the formation atherosclerotic plaques and lesions that could trigger atherothrombosis. Dendritic cells (DCs) are a type of immune cell that have been shown to play a complex role in atherosclerosis. In this issue of the Journal of Clinical Investigation, researchers led by Ira Tabas and Manikandan Subramanian at Columbia University used atherosclerosis-prone mice to elucidate the role of DCs in atherosclerosis. Tabas, Subramanian, and colleagues found that a protein known as MYD88 is required for the activation of DCs, which in turn activate another group of immune cells that protect against inflammation. These results demonstrate that MYD88-mediated DC activation is protective and could be a useful therapeutic target for the treatment of atherosclerosis.
TITLE:
Treg-mediated suppression of atherosclerosis requires MYD88 signaling in dendritic cells
AUTHOR CONTACT:
Ira Tabas
Rm PH 8-East 105F, New York, NY, USA
Phone: 212-305-9430; Fax: 212-305-4834; E-mail: iat1@columbia.edu
View this article at: http://www.jci.org/articles/view/64617?key=eca14ce8b148b3f41b08
Getting to the heart of thyroid hormone function
Thyroid hormone has profound effects on cardiovascular function and metabolism, regulating heart rate, blood pressure, food intake, and metabolic rate. Originally, thyroid hormone was thought to act directly on the target tissues; however, several recent studies have suggested that thyroid hormones effects are mediated by the central nervous system (CNS). In this issue of the Journal of Clinical Investigation, researchers led by Jens Mittag at the Karolinska Institute in Stockholm, Sweden identified a population of neurons in the hypothalamus that are required for thyroid hormone regulation of blood pressure and heart rate. Loss of these neurons in mice resulted in elevated blood pressure and heart rate. These findings demonstrate an important role for the hypothalamus in the regulation of cardiovascular function and indicate a connection between thyroid disease and cardiovascular disorders. In an accompanying commentary, Jrgen Wess of the National Institute of Diabetes and Digestive and Kidney Diseases discusses the link between developmental hypothyroidism and cardiovascular disease.
TITLE:
Thyroid hormone is required for hypothalamic neurons regulating cardiovascular functions
AUTHOR CONTACT:
Jens Mittag
Karolinska Institutet, Stockholm, SWE
Phone: 0046-8-52487367; E-mail: jens.mittag@ki.se
View this article at: http://www.jci.org/articles/view/65252?key=466251ab326b7eb25b00
ACCOMPANYING ARTICLE
TITLE:
A heartfelt response: new thyroid hormone-sensitive neurons in the hypothalamus
AUTHOR CONTACT:
Jrgen Wess
NIH-NIDDK, Bethesda, MD, USA
Phone: 301-402-3589; Fax: 301-480-3447; E-mail: jwess@helix.nih.gov
View this article at: http://www.jci.org/articles/view/67448?key=faf015181e57c5e9bfcb
Immune system-associated protein regulates metabolism
Hyperglycemia results from impaired insulin activity and is a hallmark of diabetes. In this issue of the Journal of Clinical Investigation, researchers led by Chih-Hao Li at Harvard University identified IL-13, a protein more commonly associated with the immune system, as a regulator of blood glucose levels. Mice lacking IL-13 had higher blood sugar and lipid levels compared with normal mice, and exhibited glucose intolerance and insulin resistance. Treatment with recombinant IL-13 reversed these effects. Li and colleagues found that IL-13 repressed glucose production in the liver, contributing to lower blood sugar levels. These findings suggest that IL-13 is an important regulator of metabolism and is a potential therapeutic target in the treatment of diabetes. In a companion commentary, Anna Mae Diehl and colleagues discuss how IL-13 connects inflammation and glucose homeostasis.
TITLE:
Direct control of hepatic glucose production by interleukin-13
AUTHOR CONTACT:
Chih-Hao Lee
Harvard University School of Public Health, Boston, MA, USA
Phone: 617 432-5778; E-mail: clee@hsph.harvard.edu
View this article at: http://www.jci.org/articles/view/64941?key=74c43c382975da2b5f58
ACCOMPANYING ARTICLE
TITLE:
The Benefits of Restraint: Pivotal Role for IL13 in Hepatic Glucose Homeostasis
AUTHOR CONTACT:
Anna Mae Diehl
Duke University Medical Center, Durham, NC, USA
Phone: 9196844173; Fax: 9196844183; E-mail: diehl004@mc.duke.edu
View this article at: http://www.jci.org/articles/view/67238?key=011b8166cae6828480b7
Cyclin D1b is a genetic reprogrammer that drives cancer progression
Cyclin D1b is a protein that is induced during cancer progression; however, it's exact function in cancer is poorly understood. In this issue of the Journal of Clinical Investigation, researchers led by Karen Knudsen at Thomas Jefferson University's Kimmel Cancer Center examined the role of cyclin D1b in prostate cancer. Using a mouse model of the disease, they found that cyclin D1b promoted the expression of genes that allow the cancer to grow and metastasize. Additionally, Knudsen and colleagues demonstrated that cyclin D1b's effects were dependent on androgen receptor signaling. These findings identify cyclin D1b as an important regulator of prostate cancer progression and suggest that this pathway is a potential therapeutic target in the treatment of prostate cancer.
TITLE:
Convergence of oncogenic and hormone receptor pathways promotes pro-metastatic phenotypes
AUTHOR CONTACT:
Karen Knudsen
Kimmel Cancer Center/Thomas Jefferson University, Philadelphia, PA, USA
Phone: 2155038574; E-mail: karen.knudsen@kimmelcancercenter.org
View this article at: http://www.jci.org/articles/view/64750?key=5aad919a3c76b31c3435
A new framework for ovarian cancer
Ovarian cancer is one of the most deadly cancers. It has a five year survival rate below 30% and a high rate of recurrence. It is a variable disease, with many different biological underpinnings that make it difficult to treat. In this issue of the Journal of Clinical Investigation, researchers led by Roel Verhaak at MD Anderson Cancer Center examined gene expression patterns in ovarian cancer tumor samples to identify gene expression signatures that correlated with patient prognosis. Using these data, they developed a model, Classification of Ovarian Cancer (CLOVAR), that could accurately classify ovarian cancer subtypes and predict patient outcomes. This new classification system may be useful in determining which treatments will be most effective for a given patient.
TITLE:
Prognostically relevant gene expression signatures of high grade serous ovarian carcinoma
AUTHOR CONTACT:
Roel Verhaak
MD Anderson Cancer Center, Houston, TX, USA
Phone: 7135632293; E-mail: RVerhaak@mdanderson.org
View this article at: http://www.jci.org/articles/view/65833?key=50b877c25971bfb0e0da
###
[ | E-mail | Share ] ?
AAAS and EurekAlert! are not responsible for the accuracy of news releases posted to EurekAlert! by contributing institutions or for the use of any information through the EurekAlert! system.
Public release date: 21-Dec-2012[ | E-mail |
Share ] Contact: Jillian Hurst
press_releases@the-jci.org
Journal of Clinical Investigation
The X-factor in liver metabolism
After you eat, your liver switches from producing glucose to storing it. At the same time, a cellular signaling pathway known as the unfolded protein response (UPR) is transiently activated, but it is not clear how this pathway contributes to the liver's metabolic switch. In this issue of the Journal of Clinical Investigation, researchers led by Phillip Scherer at the University of Texas Southwestern Medical Center report that activation of the UPR triggers the expression of Xbp1s, a protein that regulates genes needed for the metabolic switch. Scherer and colleagues found that they could induce changes in liver metabolism just by increasing expression of Xbps1. These results suggest that Xbps1 could play a role in metabolic disease.
TITLE:
The Xbp1s/GalE axis links ER stress to postprandial hepatic metabolism
AUTHOR CONTACT:
Philipp E. Scherer
The University of Texas Southwestern Medical Center, Dallas, TX, USA
Phone: (214) 648-8715; Fax: (214) 648-8720; E-mail: philipp.scherer@utsouthwestern.edu
View this article at: http://www.jci.org/articles/view/62819?key=17adb760d62c3d29b6fb
Low iron levels increase the risk of H. pylori-associated gastric cancer
H. pylori frequently causes gastric ulcers and is also one of the greatest risk factors for gastric cancer. H. pylori infection is also associated with another gastric cancer risk factor, iron deficiency. In this issue of the Journal of Clinical Investigation, researchers led by Richard Peek at Vanderbilt University investigated the influence of iron on H. pylori-induced gastric cancer. Peek and colleagues found that low iron accelerated the development of H. pylori-associated cancerous lesions in gerbils. Further, H. pylori strains isolated from a human population at high risk for gastric cancer were more virulent and produced greater inflammation if they came from patients with low iron levels. In an accompanying article, El-Omar Emad of Aberdeen University discusses how iron levels could be used to identify patients that are at a higher risk for gastric cancer after H. pylori infection.
TITLE:
Iron deficiency accelerates Helicobacter pylori-induced carcinogenesis in rodents and humans
AUTHOR CONTACT:
Richard M. Peek, Jr.
Vanderbilt University School of Medicine, Nashville, TN, USA
Phone: 615-322-5200; Fax: 615-343-6229; E-mail: richard.peek@vanderbilt.edu
View this article at: http://www.jci.org/articles/view/64373?key=95552f8a58ca300dd6bc
ACCOMPANYING ARTICLE
TITLE:
Iron deficiency and H. pylori-induced gastric cancer: too little, too bad
AUTHOR CONTACT:
Emad El-Omar
Aberdeen University, Foresterhill, Aberdeen, GBR
Phone: +44 (0)1224 437548; E-mail: e.el-omar@abdn.ac.uk
View this article at: http://www.jci.org/articles/view/67200?key=98b2d035a72beb6365c9
A critical genetic regulator of brown fat functionality
Obesity is a direct consequence of prolonged positive energy balance that occurs when energy intake (ie. calories) exceeds energy expenditure. In mammals, brown fat plays a critical role in energy metabolism due to its ability to burn energy by dissipating heat, a process known as thermogenesis. Therapeutics that target brown fat could possibly increase metabolism and correct the imbalance that leads to obesity. In this issue of the Journal of Clinical Investigation, researchers led by Matthias Tschp identified a protein in mice, p62, that is required for brown fat thermogenesis. Mice that did not express p62 in fat cells became obese and developed glucose intolerance, key features of metabolic syndrome in humans. These findings indicate that p62 is an important regulator of metabolism and energy balance and is could potentially serve as a therapeutic target for the treatment of metabolic syndrome.
TITLE:
p62 links beta-adrenergic input with mitochondrial function
AUTHOR CONTACT:
Matthias Tschoep
Helmholtz Zentrum Mnchen - German Research Center for Environmental Health, 85764 Neuherberg, UNK, DEU
Phone: + 49 89 3187 2103; E-mail: matthias.tschoep@helmholtz-muenchen.de
View this article at: http://www.jci.org/articles/view/64209?key=ffdc151cc8b44910eb6e
Dendritic cells play a protective role in atherosclerosis
Atherosclerosis is characterized by a chronic inflammatory immune response that increases the formation atherosclerotic plaques and lesions that could trigger atherothrombosis. Dendritic cells (DCs) are a type of immune cell that have been shown to play a complex role in atherosclerosis. In this issue of the Journal of Clinical Investigation, researchers led by Ira Tabas and Manikandan Subramanian at Columbia University used atherosclerosis-prone mice to elucidate the role of DCs in atherosclerosis. Tabas, Subramanian, and colleagues found that a protein known as MYD88 is required for the activation of DCs, which in turn activate another group of immune cells that protect against inflammation. These results demonstrate that MYD88-mediated DC activation is protective and could be a useful therapeutic target for the treatment of atherosclerosis.
TITLE:
Treg-mediated suppression of atherosclerosis requires MYD88 signaling in dendritic cells
AUTHOR CONTACT:
Ira Tabas
Rm PH 8-East 105F, New York, NY, USA
Phone: 212-305-9430; Fax: 212-305-4834; E-mail: iat1@columbia.edu
View this article at: http://www.jci.org/articles/view/64617?key=eca14ce8b148b3f41b08
Getting to the heart of thyroid hormone function
Thyroid hormone has profound effects on cardiovascular function and metabolism, regulating heart rate, blood pressure, food intake, and metabolic rate. Originally, thyroid hormone was thought to act directly on the target tissues; however, several recent studies have suggested that thyroid hormones effects are mediated by the central nervous system (CNS). In this issue of the Journal of Clinical Investigation, researchers led by Jens Mittag at the Karolinska Institute in Stockholm, Sweden identified a population of neurons in the hypothalamus that are required for thyroid hormone regulation of blood pressure and heart rate. Loss of these neurons in mice resulted in elevated blood pressure and heart rate. These findings demonstrate an important role for the hypothalamus in the regulation of cardiovascular function and indicate a connection between thyroid disease and cardiovascular disorders. In an accompanying commentary, Jrgen Wess of the National Institute of Diabetes and Digestive and Kidney Diseases discusses the link between developmental hypothyroidism and cardiovascular disease.
TITLE:
Thyroid hormone is required for hypothalamic neurons regulating cardiovascular functions
AUTHOR CONTACT:
Jens Mittag
Karolinska Institutet, Stockholm, SWE
Phone: 0046-8-52487367; E-mail: jens.mittag@ki.se
View this article at: http://www.jci.org/articles/view/65252?key=466251ab326b7eb25b00
ACCOMPANYING ARTICLE
TITLE:
A heartfelt response: new thyroid hormone-sensitive neurons in the hypothalamus
AUTHOR CONTACT:
Jrgen Wess
NIH-NIDDK, Bethesda, MD, USA
Phone: 301-402-3589; Fax: 301-480-3447; E-mail: jwess@helix.nih.gov
View this article at: http://www.jci.org/articles/view/67448?key=faf015181e57c5e9bfcb
Immune system-associated protein regulates metabolism
Hyperglycemia results from impaired insulin activity and is a hallmark of diabetes. In this issue of the Journal of Clinical Investigation, researchers led by Chih-Hao Li at Harvard University identified IL-13, a protein more commonly associated with the immune system, as a regulator of blood glucose levels. Mice lacking IL-13 had higher blood sugar and lipid levels compared with normal mice, and exhibited glucose intolerance and insulin resistance. Treatment with recombinant IL-13 reversed these effects. Li and colleagues found that IL-13 repressed glucose production in the liver, contributing to lower blood sugar levels. These findings suggest that IL-13 is an important regulator of metabolism and is a potential therapeutic target in the treatment of diabetes. In a companion commentary, Anna Mae Diehl and colleagues discuss how IL-13 connects inflammation and glucose homeostasis.
TITLE:
Direct control of hepatic glucose production by interleukin-13
AUTHOR CONTACT:
Chih-Hao Lee
Harvard University School of Public Health, Boston, MA, USA
Phone: 617 432-5778; E-mail: clee@hsph.harvard.edu
View this article at: http://www.jci.org/articles/view/64941?key=74c43c382975da2b5f58
ACCOMPANYING ARTICLE
TITLE:
The Benefits of Restraint: Pivotal Role for IL13 in Hepatic Glucose Homeostasis
AUTHOR CONTACT:
Anna Mae Diehl
Duke University Medical Center, Durham, NC, USA
Phone: 9196844173; Fax: 9196844183; E-mail: diehl004@mc.duke.edu
View this article at: http://www.jci.org/articles/view/67238?key=011b8166cae6828480b7
Cyclin D1b is a genetic reprogrammer that drives cancer progression
Cyclin D1b is a protein that is induced during cancer progression; however, it's exact function in cancer is poorly understood. In this issue of the Journal of Clinical Investigation, researchers led by Karen Knudsen at Thomas Jefferson University's Kimmel Cancer Center examined the role of cyclin D1b in prostate cancer. Using a mouse model of the disease, they found that cyclin D1b promoted the expression of genes that allow the cancer to grow and metastasize. Additionally, Knudsen and colleagues demonstrated that cyclin D1b's effects were dependent on androgen receptor signaling. These findings identify cyclin D1b as an important regulator of prostate cancer progression and suggest that this pathway is a potential therapeutic target in the treatment of prostate cancer.
TITLE:
Convergence of oncogenic and hormone receptor pathways promotes pro-metastatic phenotypes
AUTHOR CONTACT:
Karen Knudsen
Kimmel Cancer Center/Thomas Jefferson University, Philadelphia, PA, USA
Phone: 2155038574; E-mail: karen.knudsen@kimmelcancercenter.org
View this article at: http://www.jci.org/articles/view/64750?key=5aad919a3c76b31c3435
A new framework for ovarian cancer
Ovarian cancer is one of the most deadly cancers. It has a five year survival rate below 30% and a high rate of recurrence. It is a variable disease, with many different biological underpinnings that make it difficult to treat. In this issue of the Journal of Clinical Investigation, researchers led by Roel Verhaak at MD Anderson Cancer Center examined gene expression patterns in ovarian cancer tumor samples to identify gene expression signatures that correlated with patient prognosis. Using these data, they developed a model, Classification of Ovarian Cancer (CLOVAR), that could accurately classify ovarian cancer subtypes and predict patient outcomes. This new classification system may be useful in determining which treatments will be most effective for a given patient.
TITLE:
Prognostically relevant gene expression signatures of high grade serous ovarian carcinoma
AUTHOR CONTACT:
Roel Verhaak
MD Anderson Cancer Center, Houston, TX, USA
Phone: 7135632293; E-mail: RVerhaak@mdanderson.org
View this article at: http://www.jci.org/articles/view/65833?key=50b877c25971bfb0e0da
###
[ | E-mail | Share ] ?
AAAS and EurekAlert! are not responsible for the accuracy of news releases posted to EurekAlert! by contributing institutions or for the use of any information through the EurekAlert! system.
Source: http://www.eurekalert.org/pub_releases/2012-12/joci-jet121712.php
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