1 40 5 Text A resource consisting primarily of words for reading. Examples include books, letters, dissertations, poems, newspapers, articles, archives of mailing lists. Note that facsimiles or images of texts are still of the genre Text. URL Address <a href="http://doi.org/10.1177/153537020222700207" target="_blank" rel="noreferrer noopener">http://doi.org/10.1177/153537020222700207</a> Pages 125–132 Issue 2 Volume 227 Dublin Core The Dublin Core metadata element set is common to all Omeka records, including items, files, and collections. For more information see, http://dublincore.org/documents/dces/. Title A name given to the resource Effect of massive sympathetic nervous system activation on coronary blood flow and myocardial energy pool. Publisher An entity responsible for making the resource available Experimental biology and medicine (Maywood, N.J.) Date A point or period of time associated with an event in the lifecycle of the resource 2002 2002-02 Subject The topic of the resource Animals; Coronary Circulation/*physiology; Energy Metabolism; Female; Heart/innervation/*physiology; Male; Rabbits; Sympathetic Nervous System/drug effects/*physiology; Veratrine/pharmacology Creator An entity primarily responsible for making the resource Smith Jennifer M; Pilati Charles F Description An account of the resource Our previous work indicates that myocardial ischemia could be the mechanism responsible for the left ventricular (LV) dysfunction that frequently develops after massive sympathetic nervous system (SNS) activation. In this study, coronary blood flow (CBF) and myocardial ATP, creatine phosphate, and lactate concentrations were measured after massively activating the SNS of anesthetized rabbits with an intracisternal injection of veratrine. CBF was measured at time 0 (baseline), and at 2, 10, and 20 min after SNS activation in one group, and at 0, 45, 90, and 150 min in a second group. Myocardial ATP, creatine phosphate, and lactate were measured at 0, 2, 10, 20, 90, and 150 min in separate groups of rabbits. SNS activation caused LV dysfunction in approximately 60% of the rabbits. SNS-related increases in CBF kept pace with the increases in myocardial energy demand as determined from the systolic pressure-heart rate product. The subendocardial-to-subepicardial blood flow ratio did not change significantly. Myocardial creatine phosphate concentration was depressed 2 min after SNS activation and remained depressed for at least 20 min. ATP fell continuously and was significantly lower than baseline by 20 min. Tissue lactate concentration was elevated at this time. By 90 min, the concentrations of all three metabolites had recovered. These results indicate that myocardial high-energy phosphate compounds fall after massive SNS activation, but ischemia does not appear to be the underlying mechanism. Identifier An unambiguous reference to the resource within a given context <a href="http://doi.org/10.1177/153537020222700207" target="_blank" rel="noreferrer noopener">10.1177/153537020222700207</a> Rights Information about rights held in and over the resource Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s). 2002 Animals Coronary Circulation/*physiology Energy Metabolism Experimental biology and medicine (Maywood, N.J.) Female Heart/innervation/*physiology Male Pilati Charles F Rabbits Smith Jennifer M Sympathetic Nervous System/drug effects/*physiology Veratrine/pharmacology Text A resource consisting primarily of words for reading. Examples include books, letters, dissertations, poems, newspapers, articles, archives of mailing lists. Note that facsimiles or images of texts are still of the genre Text. URL Address <a href="http://doi.org/10.1097/MOG.0000000000000156" target="_blank" rel="noreferrer noopener">http://doi.org/10.1097/MOG.0000000000000156</a> Pages 159–165 Issue 2 Volume 31 Dublin Core The Dublin Core metadata element set is common to all Omeka records, including items, files, and collections. For more information see, http://dublincore.org/documents/dces/. Title A name given to the resource Bile acids as metabolic regulators. Publisher An entity responsible for making the resource available Current Opinion in Gastroenterology Date A point or period of time associated with an event in the lifecycle of the resource 2015 2015-03 Subject The topic of the resource Bile Acids and Salts/*metabolism; Biological Transport; Cholesterol 7-alpha-Hydroxylase/metabolism; Cytoplasmic and Nuclear/metabolism; Diabetes Mellitus; Energy Metabolism; Homeostasis; Humans; Inflammation/*metabolism; Intestine; Liver/*metabolism/pathology; Obesity/*metabolism; Receptors; Signal Transduction; Small/*metabolism/pathology; Type 2/*metabolism Creator An entity primarily responsible for making the resource Li Tiangang; Chiang John Y L Description An account of the resource PURPOSE OF REVIEW: This review focuses on the latest understanding of the molecular mechanisms underlying the complex interactions between intestine and liver bile acid signaling, gut microbiota, and their impact on whole-body lipid, glucose and energy metabolism. RECENT FINDINGS: Hepatic bile acid synthesis is tightly regulated by the bile acid negative feedback mechanisms. Modulating the enterohepatic bile acid signaling greatly impacts the whole-body metabolic homeostasis. Recently, a positive feedback mechanism through intestine farnesoid X receptor (FXR) antagonism has been proposed to link gut microbiota to the regulation of bile acid composition and pool size. Two studies identified intestine Diet1 and hepatic SHP-2 as novel regulators of CYP7A1 and bile acid synthesis through the gut-liver FXR-fibroblast growth factor 15/19-FGF receptor four signaling axis. New evidence suggests that enhancing bile acid signaling in the distal ileum and colon contributes to the metabolic benefits of bile acid sequestrants and bariatric surgery. SUMMARY: Small-molecule ligands that target TGR5 and FXR have shown promise in treating various metabolic and inflammation-related human diseases. New insights into the mechanisms underlying the bariatric surgery and bile acid sequestrant treatment suggest that targeting the enterohepatic circulation to modulate gut-liver bile acid signaling, incretin production and microbiota represents a new strategy to treat obesity and type 2 diabetes. Identifier An unambiguous reference to the resource within a given context <a href="http://doi.org/10.1097/MOG.0000000000000156" target="_blank" rel="noreferrer noopener">10.1097/MOG.0000000000000156</a> Rights Information about rights held in and over the resource Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s). 2015 Bile Acids and Salts/*metabolism Biological Transport Chiang John Y L Cholesterol 7-alpha-Hydroxylase/metabolism Current opinion in gastroenterology Cytoplasmic and Nuclear/metabolism Department of Integrative Medical Sciences Diabetes Mellitus Energy Metabolism Homeostasis Humans Inflammation/*metabolism Intestine Li Tiangang Liver/*metabolism/pathology NEOMED College of Medicine Obesity/*metabolism Receptors Signal Transduction Small/*metabolism/pathology Type 2/*metabolism Text A resource consisting primarily of words for reading. Examples include books, letters, dissertations, poems, newspapers, articles, archives of mailing lists. Note that facsimiles or images of texts are still of the genre Text. URL Address <a href="http://doi.org/10.1074/mcp.RA118.000961" target="_blank" rel="noreferrer noopener">http://doi.org/10.1074/mcp.RA118.000961</a> Pages 2371–2386 Issue 12 Volume 17 Dublin Core The Dublin Core metadata element set is common to all Omeka records, including items, files, and collections. For more information see, http://dublincore.org/documents/dces/. Title A name given to the resource Hepatic Mitochondrial Defects in a Nonalcoholic Fatty Liver Disease Mouse Model Are Associated with Increased Degradation of Oxidative Phosphorylation Subunits. Publisher An entity responsible for making the resource available Molecular & cellular proteomics : MCP Date A point or period of time associated with an event in the lifecycle of the resource 2018 2018-12 Subject The topic of the resource Energy metabolism; heavy water; Mass Spectrometry; metabolic labeling; Mitochondria function or biology; oxidative phosphorylation; Oxidative stress; Protein Degradation; Protein Turnover Creator An entity primarily responsible for making the resource Lee Kwangwon; Haddad Andrew; Osme Abdullah; Kim Chunki; Borzou Ahmad; Ilchenko Sergei; Allende Daniela; Dasarathy Srinivasan; McCullough Arthur; Sadygov Rovshan G; Kasumov Takhar Description An account of the resource Nonalcoholic fatty liver disease (NAFLD) is associated with hepatic mitochondrial dysfunction characterized by reduced ATP synthesis. We applied the (2)H2O-metabolic labeling approach to test the hypothesis that the reduced stability of oxidative phosphorylation proteins contributes to mitochondrial dysfunction in a diet-induced mouse model of NAFLD. A high fat diet containing cholesterol (a so-called Western diet (WD)) led to hepatic oxidative stress, steatosis, inflammation and mild fibrosis, all markers of NAFLD, in low density cholesterol (LDL) receptor deficient (LDLR(-/-)) mice. In addition, compared with controls (LDLR(-/-) mice on normal diet), livers from NAFLD mice had reduced citrate synthase activity and ATP content, suggesting mitochondrial impairment. Proteome dynamics study revealed that mitochondrial defects are associated with reduced average half-lives of mitochondrial proteins in NAFLD mice (5.41 +/- 0.46 versus 5.15 +/- 0.49 day, p \textless 0.05). In particular, the WD reduced stability of oxidative phosphorylation subunits, including cytochrome b-c1 complex subunit 1 (5.9 +/- 0.1 versus 3.4 +/- 0.8 day), ATP synthase subunit alpha (6.3 +/- 0.4 versus 5.5 +/- 0.4 day) and ATP synthase F(0) complex subunit B1 of complex V (8.5 +/- 0.6 versus 6.5 +/- 0.2 day) (p \textless 0.05). These changes were associated with impaired complex III and F0F1-ATP synthase activities. Markers of mitophagy were increased, but proteasomal degradation activity were reduced in NAFLD mice liver, suggesting that ATP deficiency because of reduced stability of oxidative phosphorylation complex subunits contributed to inhibition of ubiquitin-proteasome and activation of mitophagy. In conclusion, the (2)H2O-metabolic labeling approach shows that increased degradation of hepatic oxidative phosphorylation subunits contributed to mitochondrial impairment in NAFLD mice. Identifier An unambiguous reference to the resource within a given context <a href="http://doi.org/10.1074/mcp.RA118.000961" target="_blank" rel="noreferrer noopener">10.1074/mcp.RA118.000961</a> Rights Information about rights held in and over the resource Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s). 2018 Allende Daniela Borzou Ahmad Dasarathy Srinivasan Department of Pharmaceutical Sciences Energy Metabolism Haddad Andrew Heavy water Ilchenko Sergei Kasumov Takhar Kim Chunki Lee Kwangwon Mass spectrometry McCullough Arthur metabolic labeling Mitochondria function or biology Molecular & cellular proteomics : MCP NEOMED College of Pharmacy Osme Abdullah oxidative phosphorylation Oxidative Stress Protein Degradation Protein Turnover Sadygov Rovshan G Text A resource consisting primarily of words for reading. Examples include books, letters, dissertations, poems, newspapers, articles, archives of mailing lists. Note that facsimiles or images of texts are still of the genre Text. URL Address <a href="http://doi.org/10.1016/j.drudis.2014.05.001" target="_blank" rel="noreferrer noopener">http://doi.org/10.1016/j.drudis.2014.05.001</a> Pages 1601–1606 Issue 10 Volume 19 Dublin Core The Dublin Core metadata element set is common to all Omeka records, including items, files, and collections. For more information see, http://dublincore.org/documents/dces/. Title A name given to the resource mitoNEET as a novel drug target for mitochondrial dysfunction. Publisher An entity responsible for making the resource available Drug Discovery Today Date A point or period of time associated with an event in the lifecycle of the resource 2014 2014-10 Subject The topic of the resource Animals; Drug Delivery Systems; Energy Metabolism; Humans; Mitochondria/*metabolism; Mitochondrial Proteins/chemistry/*metabolism; Protein Conformation; Thiazolidinediones/pharmacology Creator An entity primarily responsible for making the resource Geldenhuys Werner J; Leeper Thomas C; Carroll Richard T Description An account of the resource Mitochondrial dysfunction plays an important part in the pathology of several diseases, including Alzheimer's disease and Parkinson's disease. Targeting mitochondrial proteins shows promise in treating and attenuating the neurodegeneration seen in these diseases, especially considering their complex and pleiotropic origins. Recently, the mitochondrial protein mitoNEET [also referred to as CDGSH iron sulfur domain 1 (CISD1)] has emerged as the mitochondrial target of thiazolidinedione drugs such as the antidiabetic pioglitazone. In this review, we evaluate the current understanding regarding how mitoNEET regulates cellular bioenergetics as well as the structural requirements for drug compound association with mitoNEET. With a clear understanding of mitoNEET function, it might be possible to develop therapeutic agents useful in several different diseases including neurodegeneration, breast cancer, diabetes and inflammation. Identifier An unambiguous reference to the resource within a given context <a href="http://doi.org/10.1016/j.drudis.2014.05.001" target="_blank" rel="noreferrer noopener">10.1016/j.drudis.2014.05.001</a> Rights Information about rights held in and over the resource Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s). 2014 Animals Carroll Richard T Drug Delivery Systems Drug Discovery Today Energy Metabolism Geldenhuys Werner J Humans Leeper Thomas C Mitochondria/*metabolism Mitochondrial Proteins/chemistry/*metabolism Protein Conformation Thiazolidinediones/pharmacology Text A resource consisting primarily of words for reading. Examples include books, letters, dissertations, poems, newspapers, articles, archives of mailing lists. Note that facsimiles or images of texts are still of the genre Text. URL Address <a href="http://doi.org/10.1002/hep.28472" target="_blank" rel="noreferrer noopener">http://doi.org/10.1002/hep.28472</a> Pages 1860–1874 Issue 6 Volume 63 Dublin Core The Dublin Core metadata element set is common to all Omeka records, including items, files, and collections. For more information see, http://dublincore.org/documents/dces/. Title A name given to the resource Carboxylesterase 2 prevents liver steatosis by modulating lipolysis, endoplasmic reticulum stress, and lipogenesis and is regulated by hepatocyte nuclear factor 4 alpha in mice. Publisher An entity responsible for making the resource available Hepatology (Baltimore, Md.) Date A point or period of time associated with an event in the lifecycle of the resource 2016 2016-06 Subject The topic of the resource *Lipid Metabolism; Adiposity; Animals; Carboxylesterase/*metabolism; Carboxylic Ester Hydrolases/genetics/*metabolism; Diabetes Mellitus; Diet; Endoplasmic Reticulum Stress; Energy Metabolism; Experimental/enzymology; Gene Knockdown Techniques; Glucose Tolerance Test; Glucose/metabolism; Hepatocyte Nuclear Factor 4/*metabolism; High-Fat/adverse effects; Homeostasis; Humans; Inbred C57BL; Lipogenesis; Lipolysis; Liver/enzymology; Male; Mice; Non-alcoholic Fatty Liver Disease/*etiology/metabolism; Obesity/enzymology/etiology; Sterol Regulatory Element Binding Protein 1/metabolism Creator An entity primarily responsible for making the resource Li Yuanyuan; Zalzala Munaf; Jadhav Kavita; Xu Yang; Kasumov Takhar; Yin Liya; Zhang Yanqiao Description An account of the resource UNLABELLED: Nonalcoholic fatty liver disease (NAFLD) is a common liver disease that ranges from simple steatosis to nonalcoholic steatohepatitis (NASH). So far, the underlying mechanism remains poorly understood. Here, we show that hepatic carboxylesterase 2 (CES2) is markedly reduced in NASH patients, diabetic db/db mice, and high-fat diet (HFD)-fed mice. Restoration of hepatic CES2 expression in db/db or HFD-fed mice markedly ameliorates liver steatosis and insulin resistance. In contrast, knockdown of hepatic CES2 causes liver steatosis and damage in chow- or Western diet-fed C57BL/6 mice. Mechanistically, we demonstrate that CES2 has triglyceride hydrolase activity. As a result, gain of hepatic CES2 function increases fatty acid oxidation and inhibits lipogenesis, whereas loss of hepatic CES2 stimulates lipogenesis by inducing endoplasmic reticulum stress. We further show that loss of hepatic CES2 stimulates lipogenesis in a sterol regulatory element-binding protein 1 (SREBP-1)-dependent manner. Finally, we show that hepatocyte nuclear factor 4 alpha (HNF-4alpha) plays a key role in controlling hepatic CES2 expression in diabetes, obesity, or NASH. CONCLUSION: CES2 plays a protective role in development of NAFLD. Targeting the Identifier An unambiguous reference to the resource within a given context <a href="http://doi.org/10.1002/hep.28472" target="_blank" rel="noreferrer noopener">10.1002/hep.28472</a> Rights Information about rights held in and over the resource Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s). *Lipid Metabolism 2016 Adiposity Animals Carboxylesterase/*metabolism Carboxylic Ester Hydrolases/genetics/*metabolism Department of Integrative Medical Sciences Department of Pharmaceutical Sciences Diabetes Mellitus Diet Endoplasmic Reticulum Stress Energy Metabolism Experimental/enzymology Gene Knockdown Techniques Glucose Tolerance Test Glucose/metabolism Hepatocyte Nuclear Factor 4/*metabolism Hepatology (Baltimore, Md.) High-Fat/adverse effects Homeostasis Humans Inbred C57BL Jadhav Kavita Kasumov Takhar Li Yuanyuan Lipogenesis Lipolysis Liver/enzymology Male Mice NEOMED College of Medicine NEOMED College of Pharmacy Non-alcoholic Fatty Liver Disease/*etiology/metabolism Obesity/enzymology/etiology Sterol Regulatory Element Binding Protein 1/metabolism Xu Yang Yin Liya Zalzala Munaf Zhang Yanqiao