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  • 1
    Keywords: Medicine ; Toxicology ; Cell Physiology ; Endocrinology ; Metabolic Diseases ; Molecular Medicine ; Pharmacology/Toxicology ; Cell Physiology ; Endocrinology ; Metabolic Diseases ; Springer eBooks
    Description / Table of Contents: Part 1. Origin of Brown and Beige Adipocytes -- 1. Brown Adipose Tissue Development and Metabolism -- 2. Lessons from Cre-Mice and Indicator Mice -- 3. Aging of Brown and Beige/Brite Adipose Tissue -- 4. Adipogenesis in Primary Cell Culture -- 5. In Vitro Models for Study of Brown Adipocyte Biology -- 6. Brown-Like Adipocyte Progenitors Derived from Human iPS Cells: A New Tool for Anti-obesity Drug Discovery and Cell-Based Therapy? -- 7. Brown Adipose Tissue in Human Infants -- Part 2. Molecular Mechanisms of BAT Function and Signaling -- 8. Evolution of UCP1 -- 9. The Mechanism FA-Dependent H+ Transport by UCP1 -- 10. Role of cAMP and cGMP Signaling in Brown Fat -- 11. Fatty Acid Metabolites as Novel Regulators of Non-shivering Thermogenesis -- 12. Regulatory Small and Long Noncoding RNAs in Brite/Brown Adipose Tissue -- 13. Brown Adipokines -- Part 3 Detection of BAT in vivo -- 14. Infrared Thermography -- 15. In Vivo Detection of Human Brown Adipose Tissue During Cold and Exercise by PET/CT -- 16. Techniques and Applications of Magnetic Resonance Imaging for Studying Brown Adipose Tissue Morphometry and Function -- 17. Multispectral Optoacoustic Tomography of Brown Adipose Tissue -- 18. BAT Exosomes: Metabolic Crosstalk with Other Organs and Biomarkers for BAT Activity -- Part 4. Recruitment and Activation of human BAT -- 19. Activation of Human Brown Adipose Tissue (BAT): Focus on Nutrition and Eating -- 20. Translational Aspects of Brown Fat Activation by Food-Derived Stimulants -- 21. Translational Pharmacology and Physiology of Brown Adipose Tissue in Human Disease and Treatment
    Abstract: The main focus of this book is on brown adipose tissue and its metabolic function. The book provides a timely update on the latest research and shows where the field is heading. Brown adipose tissue (BAT) dissipates energy and has received considerable attention in the last few years, having been re-discovered in adult humans in 2007/9. Moreover, BAT might offer a target for novel therapies to address obesity, a health condition that has reached pandemic dimensions
    Pages: VIII, 424 p. 52 illus., 49 illus. in color. : online resource.
    ISBN: 9783030105136
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  • 2
    Unknown
    Cham : Springer International Publishing
    Keywords: Medicine ; Molecular Biology ; Pharmacology ; Metabolic Diseases ; Biomedicine ; Pharmacology/Toxicology ; Molecular Medicine ; Metabolic Diseases ; Springer eBooks
    Description / Table of Contents: 1 Central nervous system control of metabolism -- 2 Glucocorticoids and metabolic control -- 3 Anti-lipidemic drugs -- 4 Genomics and metabolism -- 5 cAMP signaling -- 6 cGMP and brown adipose tissue -- 7 Inflammatory signaling and metabolism -- 8 Insulin signaling -- 9 Nuclear receptor co-factors in metabolism -- 10 Novel treatment options in diabetes -- 11 Adipose tissue stem cells -- 12 Adipokines -- 13 Immune cells and metabolism -- 14 Brown adipose tissue in humans -- 15 Diabetes and Cancer -- 16 Cancer Cell Metabolism -- 17 Incretins
    Abstract: The HEP issue on Metabolic Control provides a state-of the art overview over both classical concepts and emerging areas in metabolism and associated disorders. In this context, metabolic control is highlighted at various levels of complexity ranging from transcriptional mechanisms in metabolic pathway control over metabolic communication routes in physiology and pathophysiology to current treatment modalities and options in metabolic disorders, including type 2 diabetes and obesity. Dedicated chapters by leading experts in their fields provide a concise overview over important areas in metabolic research at a molecular level, including the role of the central nervous system in metabolism, inflammation and metabolism, pancreatic hormone signaling, brown adipose tissue, and therapeutic concepts
    Pages: VIII, 469 p. 70 illus. in color. : online resource.
    Edition: 1st ed. 2016.
    ISBN: 9783319298061
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  • 3
    Keywords: ABNORMALITIES, ACCUMULATION, animal, animals, BIOLOGY, CELL, CELL BIOLOGY, DISRUPTION, ELEVATED PLAS
    Abstract: Aberrant accumulation of lipids in the liver ("fatty liver" or hepatic steatosis) represents a hallmark of the metabolic syndrome and is tightly associated with obesity, type II diabetes, starvation, or glucocorticoid (GC) therapy. While fatty liver has been connected with numerous abnormalities of liverfunction, the molecular mechanisms of fatty liver development remain largely enigmatic. Here we show that liver-specific disruption of glucocorticoid receptor (GR) action improves the steatotic phenotype in fatty liver mouse models and leads to the induction of transcriptional repressor hairy enhancer of split 1 (Hes1) gene expression. The GR directly interferes with Hes1 promoter activity, triggering the recruitment of histone deacetylase (HDAC) activities to the Hes1 gene. Genetic restoration of hepatic Hes1 levels in steatotic animals normalizes hepatic triglyceride (TG) levels. As glucocorticoid action is increased during starvation, myotonic dystrophy, and Cushing's syndrome, the inhibition of Hes1 through the GR might explain the fatty liver phenotype in these subjects
    Type of Publication: Journal article published
    PubMed ID: 18762022
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  • 4
    Keywords: ADIPOSE-TISSUE, bacterial, BINDING, BINDING PROTEIN, BLOOD, CREB-BINDING-PROTEIN, CYTOKINE, DEFICIEN
    Abstract: Inflammatory responses represent a hallmark of numerous pathologies including sepsis, bacterial infection, insulin resistance, and malign obesity. Here we describe an unexpected coactivator function for the nuclear receptor interacting protein 140 (RIP140) for nuclear factor kappa B (NF kappa B), a master transcriptional regulator of inflammation in multiple tissues. Previous work has shown that RIP140 suppresses the expression of metabolic gene networks, but we have found that genetic as well as acute deficiency of RIP140 leads to the inhibition of the proinflammatory program in macrophages. The ability of RIP140 to function as a coactivator for cytokine gene promoter activity relies on direct protein-protein interactions with the NF kappa B subunit RelA and histone acetylase cAMP-responsive element binding protein (CREB)-binding protein (CBP). RIP140-depenclent control of proinflammatory gene expression via RelA/CBP may, therefore, represent a molecular rational for the cellular integration of metabolic and inflammatory pathways
    Type of Publication: Journal article published
    PubMed ID: 18469200
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  • 5
    Keywords: BLOOD, CHYLOMICRON REMNANTS, CONTRAST, DIABETIC DYSLIPIDEMIA, ENERGY, EXPRESSION, Genetic, Germany,
    Abstract: OBJECTIVE-In mammals, proper storage and distribution of lipids in and between tissues is essential for the maintenance of energy homeostasis. In contrast, aberrantly high levels of triglycerides in the blood ("hypertriglyceridemia") represent a hallmark of the metabolic syndrome and type 2 diabetes. As hypertriglyceridemia has been identified as an important risk factor for cardiovascular complications, in this study we aimed to identify molecular mechanisms in aberrant triglyceride elevation under these conditions. RESEARCH DESIGN AND METHODS-To determine the importance of hepatic lipid handling for systemic dyslipidemia, we profiled the expression patterns of various hepatic lipid transporters and receptors under healthy and type 2 diabetic conditions. A differentially expressed lipoprotein receptor was functionally characterized by generating acute, liver-specific loss- and gain-of-function animal models. RESULTS-We show that the hepatic expression of lipid transporter lipolysis-stimulated lipoprotein receptor (LSR) is specifically impaired in mouse models of obesity and type 2 diabetes and can be restored by leptin replacement. Experimental imitation of this pathophysiological situation by liver-specific knockdown of LSR promotes hypertriglyceridemia and elevated apolipoprotein (Apo)B and E serum levels in lean wild-type and ApoE knockout mice. In contrast, genetic restoration of LSR expression in obese animals to wild-type levels improves serum triglyceride levels and serum profiles in these mice. CONCLUSIONS-The dysregulation of hepatic LSR under obese and diabetic conditions may provide a molecular rationale for systemic dyslipidemia in type 2 diabetes and the metabolic syndrome and represent a novel target for alternative treatment strategies in these patients. Diabetes 58:1040-1049, 2009
    Type of Publication: Journal article published
    PubMed ID: 19188430
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  • 6
    Keywords: EXPRESSION ; liver ; GENE ; GENE-EXPRESSION ; METABOLISM ; COMPLEX ; NECROSIS-FACTOR-ALPHA ; CARBOXYKINASE GTP GENE ; metabolic syndrome ; PROLIFERATOR-ACTIVATED-RECEPTOR ; CREB COACTIVATOR TORC2 ; DEPENDENT DIABETES-MELLITUS ; DIETARY-PROTEIN INTAKE ; FATTY-ACID OXIDATION ; LIVER X-RECEPTOR ; MITOCHONDRIAL 3-HYDROXY-3-METHYLGLUTARYL-COA SYNTHASE ; NUCLEAR HORMONE-RECEPTOR ; Transcriptional co-factors
    Abstract: After binding to their cognate DNA-binding partner, transcriptional co-factors exert their function through the recruitment of enzymatic, chromatin-modifying activities. In turn, the assembly of co-factor-associated multi-protein complexes efficiently impacts target gene expression. Recent advances have established transcriptional co-factor complexes as a critical regulatory level in energy homeostasis and aberrant co-factor activity has been linked to the pathogenesis of severe metabolic disorders including obesity, type 2 diabetes and other components of the Metabolic Syndrome. The liver represents the key peripheral organ for the maintenance of systemic energy homeostasis, and aberrations in hepatic glucose and lipid metabolism have been causally linked to the manifestation of disorders associated with the Metabolic Syndrome. Therefore, this review focuses on the role of distinct classes of transcriptional co-factors in hepatic glucose and lipid homeostasis, emphasizing pathway-specific functions of these co-factors under physiological and pathophysiological conditions.
    Type of Publication: Journal article published
    PubMed ID: 21112373
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  • 7
    Abstract: In mammals, glucocorticoids (GCs) and their intracellular receptor, the glucocorticoid receptor (GR), represent critical checkpoints in the endocrine control of energy homeostasis. Indeed, aberrant GC action is linked to severe metabolic stress conditions as seen in Cushing's syndrome, GC therapy and certain components of the Metabolic Syndrome, including obesity and insulin resistance. Here, we identify the hepatic induction of the mammalian conserved microRNA (miR)-379/410 genomic cluster as a key component of GC/GR-driven metabolic dysfunction. Particularly, miR-379 was up-regulated in mouse models of hyperglucocorticoidemia and obesity as well as human liver in a GC/GR-dependent manner. Hepatocyte-specific silencing of miR-379 substantially reduced circulating very-low-density lipoprotein (VLDL)-associated triglyceride (TG) levels in healthy mice and normalized aberrant lipid profiles in metabolically challenged animals, mediated through miR-379 effects on key receptors in hepatic TG re-uptake. As hepatic miR-379 levels were also correlated with GC and TG levels in human obese patients, the identification of a GC/GR-controlled miRNA cluster not only defines a novel layer of hormone-dependent metabolic control but also paves the way to alternative miRNA-based therapeutic approaches in metabolic dysfunction.
    Type of Publication: Journal article published
    PubMed ID: 25510864
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  • 8
    Keywords: animal, animals, BINDING PROTEIN-1C GENE, cachexia, CANCER, CHOLESTEROL EFFLUX, COACTIVATOR PGC-1, C
    Abstract: In mammals, triglycerides (TG) represent the most concentrated form of energy. Aberrant TG storage and availability are intimately linked to the negative energy balance under severe clinical conditions, such as starvation, sepsis, or cancer cachexia. Despite its crucial role for energy homeostasis, molecular key determinants of TG metabolism remain enigmatic. Here we show that the expression of nuclear receptor cofactor receptor interacting protein (RIP) 140 was induced in livers of starved, septic, and tumor-bearing mice. Liver-specific knockdown of RIP140 led to increased hepatic TG release and alleviated hepatic steatosis in tumor-bearing, cachectic animals. Indeed, hepatic RIP140 was found to control the expression of lipid-metabolizing genes in liver. Conclusion: By preventing the mobilization of hepatic TG stores, the induction of RIP140 in liver provides a molecular rationale for hepatic steatosis in starvation, sepsis, or cancer cachexia. Inhibition of hepatic RIP140 transcriptional activity might, thereby, provide an attractive adjunct scheme in the treatment of these conditions
    Type of Publication: Journal article published
    PubMed ID: 18712775
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  • 9
    Keywords: EXPRESSION ; IN-VITRO ; DISEASES ; GENE ; PROTEIN ; RAT ; hepatocytes ; BINDING ; ADENOASSOCIATED VIRUS VECTORS ; HIGHLY EFFICIENT TRANSDUCTION ; TRANSPORTERS
    Abstract: Systemic bile acid (BA) homeostasis is a critical determinant of dietary fat digestion, enterohepatic function, and postprandial thermogenesis. However, major checkpoints for the dynamics and the molecular regulation of BA homeostasis remain unknown. Here we show that hypothalamic-pituitary-adrenal (HPA) axis impairment in humans and liver-specific deficiency of the glucocorticoid receptor (GR) in mice disrupts the normal changes in systemic BA distribution during the fasted-to-fed transition. Fasted mice with hepatocyte-specific GA knockdown had smaller gallbladder BA content and were more susceptible to developing cholesterol gallstones when fed a cholesterol-rich diet. Hepatic GR deficiency impaired liver BA uptake/transport via lower expression of the major hepatocyte basolateral BA transporter, Na(+)-taurocholate transport protein (Ntcp/Slc10a1), which affected dietary fat absorption and brown adipose tissue activation. Our results demonstrate a role of the HPA axis in the endocrine regulation of BA homeostasis through the liver GR control of enterohepatic BA recycling
    Type of Publication: Journal article published
    PubMed ID: 21723510
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  • 10
    Keywords: EXPRESSION ; MICE ; ACTIVATION ; MACROPHAGES ; OBESITY ; RECRUITMENT ; inflammation ; INSULIN-RESISTANCE ; ADIPOCYTES ; THERMOGENESIS
    Abstract: Regulatory T (Treg) cells are critical determinants of both immune responses and metabolic control. Here we show that systemic ablation of Treg cells compromised the adaptation of whole-body energy expenditure to cold exposure, correlating with impairment in thermogenic marker gene expression and massive invasion of pro-inflammatory macrophages in brown adipose tissue (BAT). Indeed, BAT harbored a unique sub-set of Treg cells characterized by a unique gene signature. As these Treg cells respond to BAT activation upon cold exposure, this study defines a BAT-specific Treg sub-set with direct implications for the regulation of energy homeostasis in response to environmental stress.
    Type of Publication: Journal article published
    PubMed ID: 25714366
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