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Article ; Online: Reprogramming of Hepatic Metabolism and Microenvironment in Nonalcoholic Steatohepatitis.

Rui, Liangyou / Lin, Jiandie D

2022 Volume 42, Page(s) 91–113

Abstract: Nonalcoholic fatty liver disease (NAFLD), a spectrum of metabolic liver disease associated with obesity, ranges from relatively benign hepatic steatosis to nonalcoholic steatohepatitis (NASH). The latter is characterized by persistent liver injury, ... ...

Abstract	Nonalcoholic fatty liver disease (NAFLD), a spectrum of metabolic liver disease associated with obesity, ranges from relatively benign hepatic steatosis to nonalcoholic steatohepatitis (NASH). The latter is characterized by persistent liver injury, inflammation, and liver fibrosis, which collectively increase the risk for end-stage liver diseases such as cirrhosis and hepatocellular carcinoma. Recent work has shed new light on the pathophysiology of NAFLD/NASH, particularly the role of genetic, epigenetic, and dietary factors and metabolic dysfunctions in other tissues in driving excess hepatic fat accumulation and liver injury. In parallel, single-cell RNA sequencing studies have revealed unprecedented details of the molecular nature of liver cell heterogeneity, intrahepatic cross talk, and disease-associated reprogramming of the liver immune and stromal vascular microenvironment. This review covers the recent advances in these areas, the emerging concepts of NASH pathogenesis, and potential new therapeutic opportunities.
MeSH term(s)	Carcinoma, Hepatocellular/complications ; Carcinoma, Hepatocellular/pathology ; Humans ; Liver/metabolism ; Liver Cirrhosis/complications ; Liver Cirrhosis/pathology ; Liver Neoplasms/complications ; Liver Neoplasms/genetics ; Liver Neoplasms/pathology ; Non-alcoholic Fatty Liver Disease/metabolism ; Tumor Microenvironment
Language	English
Publishing date	2022-05-18
Publishing country	United States
Document type	Journal Article ; Review ; Research Support, Non-U.S. Gov't
ZDB-ID	406980-8
ISSN	1545-4312 ; 0199-9885
ISSN (online)	1545-4312
ISSN	0199-9885
DOI	10.1146/annurev-nutr-062220-105200
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: Neuregulin 4 mediates the metabolic benefits of mild cold exposure by promoting beige fat thermogenesis.

Chen, Zhimin / Zhang, Peng / Liu, Tongyu / Qiu, Xiaoxue / Li, Siming / Lin, Jiandie D

JCI insight

2024 Volume 9, Issue 1

Abstract: Interorgan crosstalk via secreted hormones and metabolites is a fundamental aspect of mammalian metabolic physiology. Beyond the highly specialized endocrine cells, peripheral tissues are emerging as an important source of metabolic hormones that ... ...

Abstract	Interorgan crosstalk via secreted hormones and metabolites is a fundamental aspect of mammalian metabolic physiology. Beyond the highly specialized endocrine cells, peripheral tissues are emerging as an important source of metabolic hormones that influence energy and nutrient metabolism and contribute to disease pathogenesis. Neuregulin 4 (Nrg4) is a fat-derived hormone that protects mice from nonalcoholic steatohepatitis (NASH) and NASH-associated liver cancer by shaping hepatic lipid metabolism and the liver immune microenvironment. Despite its enriched expression in brown fat, whether NRG4 plays a role in thermogenic response and mediates the metabolic benefits of cold exposure are areas that remain unexplored. Here we show that Nrg4 expression in inguinal white adipose tissue (iWAT) is highly responsive to chronic cold exposure. Nrg4 deficiency impairs beige fat induction and renders mice more susceptible to diet-induced metabolic disorders under mild cold conditions. Using mice with adipocyte and hepatocyte-specific Nrg4 deletion, we reveal that adipose tissue-derived NRG4, but not hepatic NRG4, is essential for beige fat induction following cold acclimation. Furthermore, treatment with recombinant NRG4-Fc fusion protein promotes beige fat induction in iWAT and improves metabolic health in mice with diet-induced obesity. These findings highlight a critical role of NRG4 in mediating beige fat induction and preserving metabolic health under mild cold conditions.
MeSH term(s)	Animals ; Mice ; Adipose Tissue, Beige/metabolism ; Adipose Tissue, Brown/metabolism ; Hormones ; Mammals ; Neuregulins/metabolism ; Non-alcoholic Fatty Liver Disease/metabolism ; Thermogenesis
Chemical Substances	Hormones ; Neuregulins ; neuregulin-4
Language	English
Publishing date	2024-01-09
Publishing country	United States
Document type	Journal Article
ISSN	2379-3708
ISSN (online)	2379-3708
DOI	10.1172/jci.insight.172957
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: Function and Mechanism of Long Noncoding RNAs in Adipocyte Biology.

Sun, Lei / Lin, Jiandie D

Diabetes

2019 Volume 68, Issue 5, Page(s) 887–896

Abstract: The last two decades have witnessed an explosion of interest in adipocyte biology, coinciding with the upsurge of obesity and metabolic syndrome. Now we have new perspectives on the distinct developmental origins of white, brown, and beige adipocytes and ...

Abstract	The last two decades have witnessed an explosion of interest in adipocyte biology, coinciding with the upsurge of obesity and metabolic syndrome. Now we have new perspectives on the distinct developmental origins of white, brown, and beige adipocytes and their role in metabolic physiology and disease. Beyond fuel metabolism, adipocytes communicate with the immune system and other tissues by releasing diverse paracrine and endocrine factors to orchestrate adipose tissue remodeling and maintain systemic homeostasis. Significant progress has been made in delineating the regulatory networks that govern different aspects of adipocyte biology. Here we provide an overview on the emerging role of long noncoding RNAs (lncRNAs) in the regulation of adipocyte development and metabolism and discuss the implications of the RNA-protein regulatory interface in metabolic control.
MeSH term(s)	Adipocytes/metabolism ; Adipose Tissue/metabolism ; Animals ; Humans ; RNA, Long Noncoding/genetics ; RNA, Long Noncoding/metabolism
Chemical Substances	RNA, Long Noncoding
Language	English
Publishing date	2019-04-21
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	80085-5
ISSN	1939-327X ; 0012-1797
ISSN (online)	1939-327X
ISSN	0012-1797
DOI	10.2337/dbi18-0009
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Article ; Online: GPNMB: expanding the code for liver-fat communication.

Kuang, Henry / Lin, Jiandie D

Nature metabolism

2019 Volume 1, Issue 5, Page(s) 507–508

Language	English
Publishing date	2019-10-14
Publishing country	Germany
Document type	Journal Article
ISSN	2522-5812
ISSN (online)	2522-5812
DOI	10.1038/s42255-019-0069-0
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Article ; Online: The hepatokine TSK maintains myofiber integrity and exercise endurance and contributes to muscle regeneration.

Wang, Qiuyu / Qiu, Xiaoxue / Liu, Tongyu / Ahn, Cheehoon / Horowitz, Jeffrey F / Lin, Jiandie D

JCI insight

2022 Volume 7, Issue 4

Abstract: Mammalian skeletal muscle contains heterogenous myofibers with different contractile and metabolic properties that sustain muscle mass and endurance capacity. The transcriptional regulators that govern these myofiber gene programs have been elucidated. ... ...

Abstract	Mammalian skeletal muscle contains heterogenous myofibers with different contractile and metabolic properties that sustain muscle mass and endurance capacity. The transcriptional regulators that govern these myofiber gene programs have been elucidated. However, the hormonal cues that direct the specification of myofiber types and muscle endurance remain largely unknown. Here, we uncover the secreted factor Tsukushi (TSK) as an extracellular signal that is required for maintaining muscle mass, strength, and endurance capacity and that contributes to muscle regeneration. Mice lacking TSK exhibited reduced grip strength and impaired exercise capacity. Muscle transcriptomic analysis revealed that TSK deficiency results in a remarkably selective impairment in the expression of myofibrillar genes, characteristic of slow-twitch muscle fibers, that is associated with abnormal neuromuscular junction formation. AAV-mediated overexpression of TSK failed to rescue these myofiber defects in adult mice, suggesting that the effects of TSK on myofibers are likely restricted to certain developmental stages. Finally, mice lacking TSK exhibited diminished muscle regeneration following cardiotoxin-induced muscle injury. These findings support a crucial role of TSK as a hormonal cue in the regulation of contractile gene expression, endurance capacity, and muscle regeneration.
MeSH term(s)	Animals ; Mice ; Mice, Transgenic ; Models, Animal ; Muscle Contraction/physiology ; Muscle Fibers, Slow-Twitch/metabolism ; Muscle, Skeletal/metabolism ; Muscle, Skeletal/physiopathology ; Proteoglycans/biosynthesis ; Proteoglycans/genetics ; Regeneration ; Transcription Factors
Chemical Substances	Proteoglycans ; Transcription Factors ; tsukushi protein, mouse
Language	English
Publishing date	2022-02-22
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ISSN	2379-3708
ISSN (online)	2379-3708
DOI	10.1172/jci.insight.154746
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Article ; Online: Myeloid-specific ablation of Basp1 ameliorates diet-induced NASH in mice by attenuating pro-inflammatory signaling.

Meng, Ziyi / Zhou, Linkang / Hong, Sungki / Qiu, Xiaoxue / Chen, Zhimin / Liu, Tongyu / Inoki, Ken / Lin, Jiandie D

Hepatology (Baltimore, Md.)

2023 Volume 79, Issue 2, Page(s) 409–424

Abstract: Background and aims: NASH represents a severe stage of fatty liver disease characterized by hepatocyte injury, inflammation, and liver fibrosis. Myeloid-derived innate immune cells, such as macrophages and dendritic cells, play an important role in host ...

Abstract	Background and aims: NASH represents a severe stage of fatty liver disease characterized by hepatocyte injury, inflammation, and liver fibrosis. Myeloid-derived innate immune cells, such as macrophages and dendritic cells, play an important role in host defense and disease pathogenesis. Despite this, the nature of transcriptomic reprogramming of myeloid cells in NASH liver and its contribution to disease progression remain incompletely defined. Approach and results: In this study, we performed bulk and single-cell RNA sequencing (sc-RNA seq) analysis to delineate the landscape of macrophage and dendritic cell transcriptomes in healthy and NASH livers. Our analysis uncovered cell type-specific patterns of transcriptomic reprogramming on diet-induced NASH. We identified brain-abundant membrane-attached signal protein 1 (Basp1) as a myeloid-enriched gene that is markedly induced in mouse and human NASH liver. Myeloid-specific inactivation of Basp1 attenuates the severity of diet-induced NASH pathologies, as shown by reduced hepatocyte injury and liver fibrosis in mice. Mechanistically, cultured macrophages lacking Basp1 exhibited a diminished response to pro-inflammatory stimuli, impaired NLRP3 inflammasome activation, and reduced cytokine secretion. Conclusions: Together, these findings uncover Basp1 as a critical regulator of myeloid inflammatory signaling that underlies NASH pathogenesis.
MeSH term(s)	Mice ; Humans ; Animals ; Non-alcoholic Fatty Liver Disease/pathology ; Liver/pathology ; Hepatocytes/metabolism ; Diet ; Liver Cirrhosis/pathology ; Mice, Inbred C57BL ; Disease Models, Animal
Language	English
Publishing date	2023-07-17
Publishing country	United States
Document type	Journal Article
ZDB-ID	604603-4
ISSN	1527-3350 ; 0270-9139
ISSN (online)	1527-3350
ISSN	0270-9139
DOI	10.1097/HEP.0000000000000537
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Zs.A 1660: Show issues

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Article: Functional overlap between the mammalian

Tang, Vi T / Xiang, Jie / Chen, Zhimin / McCormick, Joseph / Abbineni, Prabhodh S / Chen, Xiao-Wei / Hoenerhoff, Mark / Emmer, Brian T / Khoriaty, Rami / Lin, Jiandie D / Ginsburg, David

bioRxiv : the preprint server for biology

2024

Abstract: Proteins carrying a signal peptide and/or a transmembrane domain enter the intracellular secretory pathway at the endoplasmic reticulum (ER) and are transported to the Golgi apparatus via COPII vesicles or tubules. SAR1 initiates COPII coat assembly by ... ...

Abstract	Proteins carrying a signal peptide and/or a transmembrane domain enter the intracellular secretory pathway at the endoplasmic reticulum (ER) and are transported to the Golgi apparatus via COPII vesicles or tubules. SAR1 initiates COPII coat assembly by recruiting other coat proteins to the ER membrane. Mammalian genomes encode two
Language	English
Publishing date	2024-02-29
Publishing country	United States
Document type	Preprint
DOI	10.1101/2024.02.27.582310
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Article ; Online: A Single-Cell Perspective of the Mammalian Liver in Health and Disease.

Xiong, Xuelian / Kuang, Henry / Liu, Tongyu / Lin, Jiandie D

Hepatology (Baltimore, Md.)

2020 Volume 71, Issue 4, Page(s) 1467–1473

MeSH term(s)	Animals ; Cell Communication ; Cellular Reprogramming/genetics ; Humans ; Liver/cytology ; Liver/metabolism ; Liver Diseases/genetics ; Liver Diseases/metabolism ; Liver Diseases/pathology ; Mice ; RNA-Seq ; Single-Cell Analysis
Language	English
Publishing date	2020-01-29
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Review
ZDB-ID	604603-4
ISSN	1527-3350 ; 0270-9139
ISSN (online)	1527-3350
ISSN	0270-9139
DOI	10.1002/hep.31149
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Zs.A 1660: Show issues

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Article ; Online: Deletion of the Feeding-Induced Hepatokine TSK Ameliorates the Melanocortin Obesity Syndrome.

Wang, Qiuyu / Zhang, Peng / Cakir, Isin / Mi, Lin / Cone, Roger D / Lin, Jiandie D

Diabetes

2021 Volume 70, Issue 9, Page(s) 2081–2091

Abstract: Work in recent decades has established that metabolic hormones released by endocrine cells and diverse other cell types serve to regulate nutrient intake and energy homeostasis. Tsukushi (TSK) is a leucine-rich repeat-containing protein secreted ... ...

Abstract	Work in recent decades has established that metabolic hormones released by endocrine cells and diverse other cell types serve to regulate nutrient intake and energy homeostasis. Tsukushi (TSK) is a leucine-rich repeat-containing protein secreted primarily by the liver that exerts an inhibitory effect on brown fat sympathetic innervation and thermogenesis. Despite this, physiological regulation of TSK and the mechanisms underlying its effects on energy balance remain poorly understood. Here we show that hepatic expression and plasma concentrations of TSK are induced by feeding and regulated by melanocortin-4 receptor (MC4R) signaling. We generated TSK and MC4R-double-knockout mice to elucidate the nature of cross talk between TSK and the central regulatory circuit of energy balance. Remarkably, TSK inactivation restores energy balance, ameliorates hyperphagia, and improves metabolic health in MC4R-deficient mice. TSK ablation enhances thermogenic gene expression in brown fat, dampens obesity-association inflammation in the liver and adipose tissue, and protects MC4R-null mice from diet-induced nonalcoholic steatohepatitis. At the cellular level, TSK deficiency augments feeding-induced c-Fos expression in the paraventricular nucleus of the hypothalamus. These results illustrate physiological cross talk between TSK and the central regulatory circuit in maintaining energy balance and metabolic homeostasis.
MeSH term(s)	Adipose Tissue, Brown/drug effects ; Adipose Tissue, Brown/metabolism ; Adipose Tissue, White/drug effects ; Adipose Tissue, White/metabolism ; Animals ; Anti-Obesity Agents/pharmacology ; Energy Metabolism/physiology ; Hypothalamus/drug effects ; Hypothalamus/metabolism ; Liver/drug effects ; Liver/metabolism ; Mice ; Mice, Knockout ; Non-alcoholic Fatty Liver Disease/genetics ; Non-alcoholic Fatty Liver Disease/metabolism ; Obesity/genetics ; Obesity/metabolism ; Proteoglycans/genetics ; Proteoglycans/metabolism ; Receptor, Melanocortin, Type 4/genetics ; Receptor, Melanocortin, Type 4/metabolism ; Signal Transduction/physiology ; Thermogenesis/physiology ; alpha-MSH/analogs & derivatives ; alpha-MSH/pharmacology
Chemical Substances	Anti-Obesity Agents ; Proteoglycans ; Receptor, Melanocortin, Type 4 ; setmelanotide ; tsukushi protein, mouse ; alpha-MSH (581-05-5)
Language	English
Publishing date	2021-06-28
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	80085-5
ISSN	1939-327X ; 0012-1797
ISSN (online)	1939-327X
ISSN	0012-1797
DOI	10.2337/db21-0161
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Article: Long Noncoding RNAs: A New Regulatory Code in Metabolic Control.

Zhao, Xu-Yun / Lin, Jiandie D

Trends in biochemical sciences

2015 Volume 40, Issue 10, Page(s) 586–596

Abstract: Long noncoding RNAs (lncRNAs) are emerging as an integral part of the regulatory information encoded in the genome. lncRNAs possess the unique capability to interact with nucleic acids and proteins, and exert discrete effects on numerous biological ... ...

Abstract	Long noncoding RNAs (lncRNAs) are emerging as an integral part of the regulatory information encoded in the genome. lncRNAs possess the unique capability to interact with nucleic acids and proteins, and exert discrete effects on numerous biological processes. Recent studies have delineated multiple lncRNA pathways that control metabolic tissue development and function. The expansion of the regulatory code that links nutrient and hormonal signals to tissue metabolism gives new insights into the genetic and pathogenic mechanisms underlying metabolic disease. This review discusses lncRNA biology with a focus on their role in the development, signaling, and function of key metabolic tissues.
MeSH term(s)	Animals ; Energy Metabolism/genetics ; Energy Metabolism/physiology ; Humans ; RNA, Long Noncoding/genetics ; RNA, Long Noncoding/physiology
Chemical Substances	RNA, Long Noncoding
Language	English
Publishing date	2015-10
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	194216-5
ISSN	1362-4326 ; 0968-0004 ; 0376-5067
ISSN (online)	1362-4326
ISSN	0968-0004 ; 0376-5067
DOI	10.1016/j.tibs.2015.08.002
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Zs.A 1207: Show issues

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