Interaction between Liver and Adipose Tissues

A special issue of Biomedicines (ISSN 2227-9059). This special issue belongs to the section "Cell Biology and Pathology".

Deadline for manuscript submissions: 31 October 2024 | Viewed by 784

Special Issue Editor


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Guest Editor
Department of Biomedical Sciences, Joan C. Edwards School of Medicine, Marshall University, Huntington, WV 25755, USA
Interests: alcohol-related liver disease; non-alcoholic fatty liver disease; PPARα; peroxisomes; PEX16; catalase; ACOX (Acyl-CoA Oxidase); CYP2E1; CYP2A5; ethanol; nicotine; FGF21; prostaglandins; bile acid; phytanic acid; phytol

Special Issue Information

Dear Colleagues,

In the body, the liver and adipose tissues are two important organs that interact to regulate energy balance and metabolic processes. It is well known that obesity causes steatohepatitis. In contrast, the liver may also affect the development of obesity. In this Special Issue, we accept new research articles or review articles focusing on the interaction between the liver and adipose tissues under normal or pathophysiological conditions. The topics may include, but are not limited to, the following aspects:

  • Fat mobilization to the liver: effects of adipolipolysis on liver fat accumulation and steatohepatitis; on fat trafficking proteins, including CD36, MTTP, apoB, and VLDL synthesis and secretion; and on liver phospholipid and cholesterol synthesis for membranous organelles and the cytoplasm membrane during liver regeneration.
  • Hormone and extracellular vesicles (exosomes): Adipokines like adiponectin on the liver; hepatokines like FGF21 on adipose tissues; other hormones, like growth hormones, thyroid hormones, or glucocorticoids, on the interaction between the liver and adipose tissues; and exosome connections between adipose tissues and the liver.  
  • Ethanol metabolism: Effects of ethanol on adipose lipolysis, liver fatty acid oxidation, and liver lipogenesis; effects of adipogenesis on ethanol metabolism and alcoholic steatohepatitis.
  • Bile acid signaling: Effects of adipose tissues on liver bile acid synthesis; bile acid receptors including FXR and TGR5 on obesity.
  • Glucose homeostasis: Effects of adipose tissues on glycogen storage in the liver; effects of liver gluconeogenesis on the development of obesity; interactions between the liver and adipose tissues during diabetes.

Dr. Yongke Lu
Guest Editor

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Keywords

  • ethanol
  • bile acid
  • gluconeogenesis
  • steatosis
  • obesity
  • fatty acid oxidation
  • extracellular vesicles

Published Papers (1 paper)

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Research

15 pages, 9538 KiB  
Article
Hepatocyte-Specific PEX16 Abrogation in Mice Leads to Hepatocyte Proliferation, Alteration of Hepatic Lipid Metabolism, and Resistance to High-Fat Diet (HFD)-Induced Hepatic Steatosis and Obesity
by Xue Chen, Long Wang, Krista L. Denning, Anna Mazur, Yujuan Xu, Kesheng Wang, Logan M. Lawrence, Xiaodong Wang and Yongke Lu
Biomedicines 2024, 12(5), 988; https://doi.org/10.3390/biomedicines12050988 - 30 Apr 2024
Viewed by 567
Abstract
Obesity results in hepatic fat accumulation, i.e., steatosis. In addition to fat overload, impaired fatty acid β-oxidation also promotes steatosis. Fatty acid β-oxidation takes place in the mitochondria and peroxisomes. Usually, very long-chain and branched-chain fatty acids are the first to be oxidized [...] Read more.
Obesity results in hepatic fat accumulation, i.e., steatosis. In addition to fat overload, impaired fatty acid β-oxidation also promotes steatosis. Fatty acid β-oxidation takes place in the mitochondria and peroxisomes. Usually, very long-chain and branched-chain fatty acids are the first to be oxidized in peroxisomes, and the resultant short chain fatty acids are further oxidized in the mitochondria. Peroxisome biogenesis is regulated by peroxin 16 (PEX16). In liver-specific PEX16 knockout (Pex16Alb-Cre) mice, hepatocyte peroxisomes were absent, but hepatocytes proliferated, and liver mass was enlarged. These results suggest that normal liver peroxisomes restrain hepatocyte proliferation and liver sizes. After high-fat diet (HFD) feeding, body weights were increased in PEX16 floxed (Pex16fl/fl) mice and adipose-specific PEX16 knockout (Pex16AdipoQ-Cre) mice, but not in the Pex16Alb-Cre mice, suggesting that the development of obesity is regulated by liver PEX16 but not by adipose PEX16. HFD increased liver mass in the Pex16fl/fl mice but somehow reduced the already enlarged liver mass in the Pex16Alb-Cre mice. The basal levels of serum triglyceride, free fatty acids, and cholesterol were decreased, whereas serum bile acids were increased in the Pex16Alb-Cre mice, and HFD-induced steatosis was not observed in the Pex16Alb-Cre mice. These results suggest that normal liver peroxisomes contribute to the development of liver steatosis and obesity. Full article
(This article belongs to the Special Issue Interaction between Liver and Adipose Tissues)
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