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1,278 results on '"Spiegelman, Bruce M."'

2. Architecture of the outbred brown fat proteome defines regulators of metabolic physiology

Author

Xiao, Haopeng, Bozi, Luiz HM, Sun, Yizhi, Riley, Christopher L, Philip, Vivek M, Chen, Mandy, Li, Jiaming, Zhang, Tian, Mills, Evanna L, Emont, Margo P, Sun, Wenfei, Reddy, Anita, Garrity, Ryan, Long, Jiani, Becher, Tobias, Vitas, Laura Potano, Laznik-Bogoslavski, Dina, Ordonez, Martha, Liu, Xinyue, Chen, Xiong, Wang, Yun, Liu, Weihai, Tran, Nhien, Liu, Yitong, Zhang, Yang, Cypess, Aaron M, White, Andrew P, He, Yuchen, Deng, Rebecca, Schöder, Heiko, Paulo, Joao A, Jedrychowski, Mark P, Banks, Alexander S, Tseng, Yu-Hua, Cohen, Paul, Tsai, Linus T, Rosen, Evan D, Klein, Samuel, Chondronikola, Maria, McAllister, Fiona E, Van Bruggen, Nick, Huttlin, Edward L, Spiegelman, Bruce M, Churchill, Gary A, Gygi, Steven P, and Chouchani, Edward T

Subjects
Biochemistry and Cell Biology, Biological Sciences, Genetics, Nutrition, Obesity, 2.1 Biological and endogenous factors, 1.1 Normal biological development and functioning, Underpinning research, Aetiology, Humans, Mice, Animals, Adipose Tissue, Brown, Proteome, Thermogenesis, Adiposity, Mice, Inbred C57BL, Proto-Oncogene Proteins, Medical and Health Sciences, Developmental Biology, Biological sciences, Biomedical and clinical sciences
Abstract

Brown adipose tissue (BAT) regulates metabolic physiology. However, nearly all mechanistic studies of BAT protein function occur in a single inbred mouse strain, which has limited the understanding of generalizable mechanisms of BAT regulation over physiology. Here, we perform deep quantitative proteomics of BAT across a cohort of 163 genetically defined diversity outbred mice, a model that parallels the genetic and phenotypic variation found in humans. We leverage this diversity to define the functional architecture of the outbred BAT proteome, comprising 10,479 proteins. We assign co-operative functions to 2,578 proteins, enabling systematic discovery of regulators of BAT. We also identify 638 proteins that correlate with protection from, or sensitivity to, at least one parameter of metabolic disease. We use these findings to uncover SFXN5, LETMD1, and ATP1A2 as modulators of BAT thermogenesis or adiposity, and provide OPABAT as a resource for understanding the conserved mechanisms of BAT regulation over metabolic physiology.

Published
2022

3. Single-nucleus transcriptomics identifies separate classes of UCP1 and futile cycle adipocytes

Author

Wang, Tongtong, Sharma, Anand Kumar, Wu, Chunyan, Maushart, Claudia Irene, Ghosh, Adhideb, Yang, Wu, Stefanicka, Patrik, Kovanicova, Zuzana, Ukropec, Jozef, Zhang, Jing, Arnold, Myrtha, Klug, Manuel, De Bock, Katrien, Schneider, Ulrich, Popescu, Cristina, Zheng, Bo, Ding, Lianggong, Long, Fen, Dewal, Revati Sumukh, Moser, Caroline, Sun, Wenfei, Dong, Hua, Takes, Martin, Suelberg, Dominique, Mameghani, Alexander, Nocito, Antonio, Zech, Christoph Johannes, Chirindel, Alin, Wild, Damian, Burger, Irene A., Schön, Michael R., Dietrich, Arne, Gao, Min, Heine, Markus, Sun, Yizhi, Vargas-Castillo, Ariana, Søberg, Susanna, Scheele, Camilla, Balaz, Miroslav, Blüher, Matthias, Betz, Matthias Johannes, Spiegelman, Bruce M., and Wolfrum, Christian

Published
2024
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4. Mustn1 is a smooth muscle cell-secreted microprotein that modulates skeletal muscle extracellular matrix composition

Author

Ducommun, Serge, Jannig, Paulo R., Cervenka, Igor, Murgia, Marta, Mittenbühler, Melanie J., Chernogubova, Ekaterina, Dias, José M., Jude, Baptiste, Correia, Jorge C., Van Vranken, Jonathan G., Ocana-Santero, Gabriel, Porsmyr-Palmertz, Margareta, McCann Haworth, Sarah, Martínez-Redondo, Vicente, Liu, Zhengye, Carlström, Mattias, Mann, Matthias, Lanner, Johanna T., Teixeira, Ana I., Maegdefessel, Lars, Spiegelman, Bruce M., and Ruas, Jorge L.

Published
2024
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5. Isthmin-1 is an adipokine that promotes glucose uptake and improves glucose tolerance and hepatic steatosis

Author

Jiang, Zewen, Zhao, Meng, Voilquin, Laetitia, Jung, Yunshin, Aikio, Mari A, Sahai, Tanushi, Dou, Florence Y, Roche, Alexander M, Carcamo-Orive, Ivan, Knowles, Joshua W, Wabitsch, Martin, Appel, Eric A, Maikawa, Caitlin L, Camporez, Joao Paulo, Shulman, Gerald I, Tsai, Linus, Rosen, Evan D, Gardner, Christopher D, Spiegelman, Bruce M, and Svensson, Katrin J

Subjects
Biochemistry and Cell Biology, Biological Sciences, Digestive Diseases, Obesity, Chronic Liver Disease and Cirrhosis, Nutrition, Diabetes, Liver Disease, 2.1 Biological and endogenous factors, 1.1 Normal biological development and functioning, Metabolic and endocrine, Adipokines, Animals, Diabetes Mellitus, Type 2, Diet, High-Fat, Fatty Liver, Glucose, Insulin Resistance, Intercellular Signaling Peptides and Proteins, Lipid Metabolism, Lipogenesis, Liver, Mice, Mice, Inbred C57BL, Phosphatidylinositol 3-Kinases, adipokine, cellular signaling, diabetes, glucose uptake, hepatic steatosis, lipogenesis, Medical Biochemistry and Metabolomics, Endocrinology & Metabolism, Biochemistry and cell biology, Medical biochemistry and metabolomics
Abstract

With the increasing prevalence of type 2 diabetes and fatty liver disease, there is still an unmet need to better treat hyperglycemia and hyperlipidemia. Here, we identify isthmin-1 (Ism1) as an adipokine and one that has a dual role in increasing adipose glucose uptake while suppressing hepatic lipid synthesis. Ism1 ablation results in impaired glucose tolerance, reduced adipose glucose uptake, and reduced insulin sensitivity, demonstrating an endogenous function for Ism1 in glucose regulation. Mechanistically, Ism1 activates a PI3K-AKT signaling pathway independently of the insulin and insulin-like growth factor receptors. Notably, while the glucoregulatory function is shared with insulin, Ism1 counteracts lipid accumulation in the liver by switching hepatocytes from a lipogenic to a protein synthesis state. Furthermore, therapeutic dosing of recombinant Ism1 improves diabetes in diet-induced obese mice and ameliorates hepatic steatosis in a diet-induced fatty liver mouse model. These findings uncover an unexpected, bioactive protein hormone that might have simultaneous therapeutic potential for diabetes and fatty liver disease.

Published
2021

6. Amelioration of pathologic α-synuclein-induced Parkinson’s disease by irisin

Author

Kam, Tae-In, Park, Hyejin, Chou, Shih-Ching, Van Vranken, Jonathan G., Mittenb€uhler, Melanie J., Kim, Hyeonwoo, A, Mu, Choi, Yu Ree, Biswas, Devanik, Wang, Justin, Shin, Yu, Loder, Alexis, Karuppagounder, Senthilkumar S., Wrann, Christiane D., Dawson, Valina L., Spiegelman, Bruce M., and Dawson, Ted M.

Published
2022

8. Creatine kinase B controls futile creatine cycling in thermogenic fat

Author

Rahbani, Janane F, Roesler, Anna, Hussain, Mohammed F, Samborska, Bozena, Dykstra, Christien B, Tsai, Linus, Jedrychowski, Mark P, Vergnes, Laurent, Reue, Karen, Spiegelman, Bruce M, and Kazak, Lawrence

Subjects
Biochemistry and Cell Biology, Biomedical and Clinical Sciences, Biological Sciences, Diabetes, Nutrition, Obesity, Metabolic and endocrine, Adipocytes, Adipose Tissue, Animals, Creatine, Creatine Kinase, BB Form, Cyclic AMP, Energy Metabolism, Female, Glucose, Homeostasis, Humans, Male, Mice, Mitochondria, Signal Transduction, Thermogenesis, General Science & Technology
Abstract

Obesity increases the risk of mortality because of metabolic sequelae such as type 2 diabetes and cardiovascular disease1. Thermogenesis by adipocytes can counteract obesity and metabolic diseases2,3. In thermogenic fat, creatine liberates a molar excess of mitochondrial ADP-purportedly via a phosphorylation cycle4-to drive thermogenic respiration. However, the proteins that control this futile creatine cycle are unknown. Here we show that creatine kinase B (CKB) is indispensable for thermogenesis resulting from the futile creatine cycle, during which it traffics to mitochondria using an internal mitochondrial targeting sequence. CKB is powerfully induced by thermogenic stimuli in both mouse and human adipocytes. Adipocyte-selective inactivation of Ckb in mice diminishes thermogenic capacity, increases predisposition to obesity, and disrupts glucose homeostasis. CKB is therefore a key effector of the futile creatine cycle.

Published
2021

10. CD81 Controls Beige Fat Progenitor Cell Growth and Energy Balance via FAK Signaling

Author

Oguri, Yasuo, Shinoda, Kosaku, Kim, Hyeonwoo, Alba, Diana L, Bolus, W Reid, Wang, Qiang, Brown, Zachary, Pradhan, Rachana N, Tajima, Kazuki, Yoneshiro, Takeshi, Ikeda, Kenji, Chen, Yong, Cheang, Rachel T, Tsujino, Kazuyuki, Kim, Caroline R, Greiner, Vanille Juliette, Datta, Ritwik, Yang, Christopher D, Atabai, Kamran, McManus, Michael T, Koliwad, Suneil K, Spiegelman, Bruce M, and Kajimura, Shingo

Subjects
Biochemistry and Cell Biology, Biological Sciences, Obesity, Stem Cell Research - Nonembryonic - Non-Human, Nutrition, Diabetes, Stem Cell Research, 2.1 Biological and endogenous factors, 1.1 Normal biological development and functioning, Cancer, Metabolic and endocrine, Adipocytes, Adipogenesis, Adipose Tissue, Beige, Adipose Tissue, White, Adult, Animals, Ataxin-1, Energy Metabolism, Female, Fibronectins, Focal Adhesion Kinase 1, Humans, Inflammation, Insulin Resistance, Integrins, Male, Mice, Mice, Inbred C57BL, Mice, Knockout, Middle Aged, RNA-Seq, Receptor, Platelet-Derived Growth Factor alpha, Signal Transduction, Single-Cell Analysis, Stem Cells, Tetraspanin 28, adipocyte progenitors, adipogenesis, beige fat, brown fat, diabetes, metabolic adaptation, metabolic disease, metabolism, obesity, tissue remodeling, Medical and Health Sciences, Developmental Biology, Biological sciences, Biomedical and clinical sciences
Abstract

Adipose tissues dynamically remodel their cellular composition in response to external cues by stimulating beige adipocyte biogenesis; however, the developmental origin and pathways regulating this process remain insufficiently understood owing to adipose tissue heterogeneity. Here, we employed single-cell RNA-seq and identified a unique subset of adipocyte progenitor cells (APCs) that possessed the cell-intrinsic plasticity to give rise to beige fat. This beige APC population is proliferative and marked by cell-surface proteins, including PDGFRα, Sca1, and CD81. Notably, CD81 is not only a beige APC marker but also required for de novo beige fat biogenesis following cold exposure. CD81 forms a complex with αV/β1 and αV/β5 integrins and mediates the activation of integrin-FAK signaling in response to irisin. Importantly, CD81 loss causes diet-induced obesity, insulin resistance, and adipose tissue inflammation. These results suggest that CD81 functions as a key sensor of external inputs and controls beige APC proliferation and whole-body energy homeostasis.

Published
2020

11. Irisin acts through its integrin receptor in a two-step process involving extracellular Hsp90α

Author

A, Mu, Wales, Thomas E., Zhou, Haixia, Draga-Coletă, Sorin-Valeriu, Gorgulla, Christoph, Blackmore, Katherine A., Mittenbühler, Melanie J., Kim, Caroline R., Bogoslavski, Dina, Zhang, Qiuyang, Wang, Zi-Fu, Jedrychowski, Mark P., Seo, Hyuk-Soo, Song, Kijun, Xu, Andrew Z., Sebastian, Luke, Gygi, Steven P., Arthanari, Haribabu, Dhe-Paganon, Sirano, Griffin, Patrick R., Engen, John R., and Spiegelman, Bruce M.

Published
2023
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13. H+ transport is an integral function of the mitochondrial ADP/ATP carrier.

Author

Bertholet, Ambre M, Chouchani, Edward T, Kazak, Lawrence, Angelin, Alessia, Fedorenko, Andriy, Long, Jonathan Z, Vidoni, Sara, Garrity, Ryan, Cho, Joonseok, Terada, Naohiro, Wallace, Douglas C, Spiegelman, Bruce M, and Kirichok, Yuriy

Subjects
Mitochondria, Animals, Mice, Protons, Coenzymes, Fatty Acids, Mitochondrial ADP, ATP Translocases, Adenosine Diphosphate, Adenosine Triphosphate, Ion Transport, Oxygen Consumption, Male, Mitochondrial ADP, ATP Translocases, General Science & Technology
Abstract

The mitochondrial ADP/ATP carrier (AAC) is a major transport protein of the inner mitochondrial membrane. It exchanges mitochondrial ATP for cytosolic ADP and controls cellular production of ATP. In addition, it has been proposed that AAC mediates mitochondrial uncoupling, but it has proven difficult to demonstrate this function or to elucidate its mechanisms. Here we record AAC currents directly from inner mitochondrial membranes from various mouse tissues and identify two distinct transport modes: ADP/ATP exchange and H+ transport. The AAC-mediated H+ current requires free fatty acids and resembles the H+ leak via the thermogenic uncoupling protein 1 found in brown fat. The ADP/ATP exchange via AAC negatively regulates the H+ leak, but does not completely inhibit it. This suggests that the H+ leak and mitochondrial uncoupling could be dynamically controlled by cellular ATP demand and the rate of ADP/ATP exchange. By mediating two distinct transport modes, ADP/ATP exchange and H+ leak, AAC connects coupled (ATP production) and uncoupled (thermogenesis) energy conversion in mitochondria.

Published
2019

17. Exercise hormone irisin is a critical regulator of cognitive function

Author

Islam, Mohammad R., Valaris, Sophia, Young, Michael F., Haley, Erin B., Luo, Renhao, Bond, Sabrina F., Mazuera, Sofia, Kitchen, Robert R., Caldarone, Barbara J., Bettio, Luis E. B., Christie, Brian R., Schmider, Angela B., Soberman, Roy J., Besnard, Antoine, Jedrychowski, Mark P., Kim, Hyeonwoo, Tu, Hua, Kim, Eunhee, Choi, Se Hoon, Tanzi, Rudolph E., Spiegelman, Bruce M., and Wrann, Christiane D.

Published
2021
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18. p38α kinase governs muscle strength through PGC1α in mice.

Author

Herrera‐Melle, Leticia, Cicuéndez, Beatriz, López, Juan Antonio, Dumesic, Phillip A., Wilensky, Sarah E., Rodríguez, Elena, Leiva‐Vega, Luis, Caballero, Ainoa, León, Marta, Vázquez, Jesús, Spiegelman, Bruce M., Folgueira, Cintia, Mora, Alfonso, and Sabio, Guadalupe

Subjects
MITOCHONDRIAL dynamics, MUSCLE weakness, MUSCLE strength, SKELETAL muscle, HUMAN body
Abstract

Aims: Skeletal muscle, with its remarkable plasticity and dynamic adaptation, serves as a cornerstone of locomotion and metabolic homeostasis in the human body. Muscle tissue, with its extraordinary capacity for force generation and energy expenditure, plays a fundamental role in the movement, metabolism, and overall health. In this context, we sought to determine the role of p38α in mitochondrial metabolism since mitochondrial dynamics play a crucial role in the development of muscle‐related diseases that result in muscle weakness. Methods: We conducted our study using male mice (MCK‐cre, p38αMCK‐KO and PGC1α MCK‐KO) and mouse primary myoblasts. We analyzed mitochondrial metabolic, physiological parameters as well as proteomics, western blot, RNA‐seq analysis from muscle samples. Results: Our findings highlight the critical involvement of muscle p38α in the regulation of mitochondrial function, a key determinant of muscle strength. The absence of p38α triggers changes in mitochondrial dynamics through the activation of PGC1α, a central regulator of mitochondrial biogenesis. These results have substantial implications for understanding the complex interplay between p38α kinase, PGC1α activation, and mitochondrial content, thereby enhancing our knowledge in the control of muscle biology. Conclusions: This knowledge holds relevance for conditions associated with muscle weakness, where disruptions in these molecular pathways are frequently implicated in diminishing physical strength. Our research underscores the potential importance of targeting the p38α and PGC1α pathways within muscle, offering promising avenues for the advancement of innovative treatments. Such interventions hold the potential to improve the quality of life for individuals affected by muscle‐related diseases. [ABSTRACT FROM AUTHOR]

Published
2024
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22. Ergothioneine boosts mitochondrial respiration and exercise performance via direct activation of MPST

Author

Sprenger, Hans-Georg, primary, Mittenbühler, Melanie J., additional, Sun, Yizhi, additional, Van Vranken, Jonathan G., additional, Schindler, Sebastian, additional, Jayaraj, Abhilash, additional, Khetarpal, Sumeet A., additional, Vargas-Castillo, Ariana, additional, Puszynska, Anna M., additional, Spinelli, Jessica B., additional, Armani, Andrea, additional, Kunchok, Tenzin, additional, Ryback, Birgitta, additional, Seo, Hyuk-Soo, additional, Song, Kijun, additional, Sebastian, Luke, additional, O’Young, Coby, additional, Braithwaite, Chelsea, additional, Dhe-Paganon, Sirano, additional, Burger, Nils, additional, Mills, Evanna L., additional, Gygi, Steven P., additional, Arthanari, Haribabu, additional, Chouchani, Edward T., additional, Sabatini, David M., additional, and Spiegelman, Bruce M., additional

Published
2024
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24. The Secreted Enzyme PM20D1 Regulates Lipidated Amino Acid Uncouplers of Mitochondria

Author

Long, Jonathan Z, Svensson, Katrin J, Bateman, Leslie A, Lin, Hua, Kamenecka, Theodore, Lokurkar, Isha A, Lou, Jesse, Rao, Rajesh R, Chang, Mi Ra, Jedrychowski, Mark P, Paulo, Joao A, Gygi, Steven P, Griffin, Patrick R, Nomura, Daniel K, and Spiegelman, Bruce M

Subjects
Biochemistry and Cell Biology, Biomedical and Clinical Sciences, Biological Sciences, Nutrition, Biotechnology, Obesity, Diabetes, 1.1 Normal biological development and functioning, Underpinning research, Adipocytes, Amidohydrolases, Amino Acids, Animals, Cell Respiration, Energy Metabolism, Fatty Acids, Glucose, Homeostasis, Male, Metabolic Networks and Pathways, Mice, Mice, Inbred C57BL, Mitochondria, Mitochondrial Proteins, Thermogenesis, Medical and Health Sciences, Developmental Biology, Biological sciences, Biomedical and clinical sciences
Abstract

Brown and beige adipocytes are specialized cells that express uncoupling protein 1 (UCP1) and dissipate chemical energy as heat. These cells likely possess alternative UCP1-independent thermogenic mechanisms. Here, we identify a secreted enzyme, peptidase M20 domain containing 1 (PM20D1), that is enriched in UCP1(+) versus UCP1(-) adipocytes. We demonstrate that PM20D1 is a bidirectional enzyme in vitro, catalyzing both the condensation of fatty acids and amino acids to generate N-acyl amino acids and also the reverse hydrolytic reaction. N-acyl amino acids directly bind mitochondria and function as endogenous uncouplers of UCP1-independent respiration. Mice with increased circulating PM20D1 have augmented respiration and increased N-acyl amino acids in blood. Lastly, administration of N-acyl amino acids to mice improves glucose homeostasis and increases energy expenditure. These data identify an enzymatic node and a family of metabolites that regulate energy homeostasis. This pathway might be useful for treating obesity and associated disorders.

Published
2016

26. Cardiomyocyte PGC-1α enables physiological adaptations to endurance exercise through suppression of GDF15 and cardiac atrophy

Author

Khetarpal, Sumeet A., primary, Li, Haobo, additional, Vitale, Tevis, additional, Rhee, James, additional, Grauvogel, Louisa, additional, Castro, Claire, additional, Mittenbühler, Melanie J., additional, Houstis, Nicholas E., additional, Vargas-Castillo, Ariana, additional, Smythers, Amanda L., additional, Liu, Jing, additional, Curtin, Casie, additional, Sprenger, Hans-Georg, additional, Blackmore, Katherine A., additional, Kuznetsov, Alexandra, additional, Freeman, Rebecca, additional, Bogoslavski, Dina, additional, Ellinor, Patrick T., additional, Asnani, Aarti, additional, Dumesic, Phillip A., additional, Puigserver, Pere, additional, Roh, Jason D., additional, Spiegelman, Bruce M., additional, and Rosenzweig, Anthony, additional

Published
2024
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29. Ablation of PM20D1 reveals N -acyl amino acid control of metabolism and nociception

Author

Long, Jonathan Z., Roche, Alexander M., Berdan, Charles A., Louie, Sharon M., Roberts, Amanda J., Svensson, Katrin J., Dou, Florence Y., Bateman, Leslie A., Mina, Amir I., Deng, Zhaoming, Jedrychowski, Mark P., Lin, Hua, Kamenecka, Theodore M., Asara, John M., Griffin, Patrick R., Banks, Alexander S., Nomura, Daniel K., and Spiegelman, Bruce M.

Published
2018

31. Irisin Mediates Effects on Bone and Fat via αV Integrin Receptors

Author

Kim, Hyeonwoo, Wrann, Christiane D., Jedrychowski, Mark, Vidoni, Sara, Kitase, Yukiko, Nagano, Kenichi, Zhou, Chenhe, Chou, Joshua, Parkman, Virginia-Jeni A., Novick, Scott J., Strutzenberg, Timothy S., Pascal, Bruce D., Le, Phuong T., Brooks, Daniel J., Roche, Alexander M., Gerber, Kaitlyn K., Mattheis, Laura, Chen, Wenjing, Tu, Hua, Bouxsein, Mary L., Griffin, Patrick R., Baron, Roland, Rosen, Clifford J., Bonewald, Lynda F., and Spiegelman, Bruce M.

Published
2018
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35. Adipsin preserves beta cells in diabetic mice and associates with protection from type 2 diabetes in humans

Author

Gómez-Banoy, Nicolás, Guseh, J. Sawalla, Li, Ge, Rubio-Navarro, Alfonso, Chen, Tong, Poirier, BreAnne, Putzel, Gregory, Rosselot, Carolina, Pabón, Maria A., Camporez, João Paulo, Bhambhani, Vijeta, Hwang, Shih-Jen, Yao, Chen, Perry, Rachel J., Mukherjee, Sushmita, Larson, Martin G., Levy, Daniel, Dow, Lukas E., Shulman, Gerald I., Dephoure, Noah, Garcia-Ocana, Adolfo, Hao, Mingming, Spiegelman, Bruce M., Ho, Jennifer E., and Lo, James C.

Published
2019
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37. Development of a functional beige fat cell line uncovers independent subclasses of cells expressing UCP1 and the futile creatine cycle

Author

Vargas-Castillo, Ariana, Sun, Yizhi, Smythers, Amanda L., Grauvogel, Louisa, Dumesic, Phillip A., Emont, Margo P., Tsai, Linus T., Rosen, Evan D., Zammit, Nathan W., Shaffer, Sydney M., Ordonez, Martha, Chouchani, Edward T., Gygi, Steven P., Wang, Tongtong, Sharma, Anand K., Balaz, Miroslav, Wolfrum, Christian, and Spiegelman, Bruce M.

Published
2024
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44. Apolipoprotein CIII Promotes Ca2+-Dependent β Cell Death in Type 1 Diabetes

Author

Juntti-Berggren, Lisa, Refai, Essam, Appelskog, Ioulia, Andersson, Mats, Imreh, Gabriela, Dekki, Nancy, Uhles, Sabine, Yu, Lina, Griffiths, William J., Zaitsev, Sergei, Leibiger, Ingo, Yang, Shao-Nian, Olivecronal, Gunilla, Jörnvall, Hans, Berggren, Per-Olof, and Spiegelman, Bruce M.

Published
2004

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