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Biomedicines
Special Issues
Interaction between Liver and Adipose Tissues
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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: 30 April 2025 | Viewed by 3151

Special Issue Editor

Dr. Yongke Lu

E-Mail Website
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

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Biomedicines is an international peer-reviewed open access monthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2600 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

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

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Further information on MDPI's Special Issue policies can be found here.

Published Papers (2 papers)

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Research

13 pages, 1488 KiB  
Article
Olanzapine Modulate Lipid Metabolism and Adipose Tissue Accumulation via Hepatic Muscarinic M3 Receptor-Mediated Alk-Related Signaling
by Yueqing Su, Chenyun Cao, Shiyan Chen, Jiamei Lian, Mei Han, Xuemei Liu and Chao Deng
Biomedicines 2024, 12(7), 1403; https://doi.org/10.3390/biomedicines12071403 - 25 Jun 2024
Viewed by 1357
Abstract
Olanzapine is an atypical antipsychotic drug and a potent muscarinic M3 receptor (M3R) antagonist. Olanzapine has been reported to cause metabolic disorders, including dyslipidemia. Anaplastic lymphoma kinase (Alk), a tyrosine kinase receptor well known in the pathogenesis of cancer, has been [...] Read more.
Olanzapine is an atypical antipsychotic drug and a potent muscarinic M3 receptor (M3R) antagonist. Olanzapine has been reported to cause metabolic disorders, including dyslipidemia. Anaplastic lymphoma kinase (Alk), a tyrosine kinase receptor well known in the pathogenesis of cancer, has been recently identified as a key gene in the regulation of thinness via the regulation of adipose tissue lipolysis. This project aimed to investigate whether Olanzapine could modulate the hepatic Alk pathway and lipid metabolism via M3R. Female rats were treated with Olanzapine and/or Cevimeline (an M3R agonist) for 9 weeks. Lipid metabolism and hepatic Alk signaling were analyzed. Nine weeks’ treatment of Olanzapine caused metabolic disturbance including increased body mass index (BMI), fat mass accumulation, and abnormal lipid metabolism. Olanzapine treatment also led to an upregulation of Chrm3, Alk, and its regulator Ptprz1, and a downregulation of Lmo4, a transcriptional repressor of Alk in the liver. Moreover, there were positive correlations between Alk and Chrm3, Alk and Ptprz1, and a negative correlation between Alk and Lmo4. However, cotreatment with Cevimeline significantly reversed the lipid metabolic disturbance and adipose tissue accumulation, as well as the upregulation of the hepatic Alk signaling caused by Olanzapine. This study demonstrates evidence that Olanzapine may cause metabolic disturbance by modulating hepatic Alk signaling via M3R, which provides novel insight for modulating the hepatic Alk signaling and potential interventions for targeting metabolic disorders. Full article
(This article belongs to the Special Issue Interaction between Liver and Adipose Tissues)
►▼ Show Figures

Figure 1

Figure 1
<p>Profiles of metabolic changes in rats after treatment with Olanzapine. (<b>A</b>) BMI (body weight (g) divided by squared body length (cm)); (<b>B</b>) white adipose tissue index (adipose tissue weight/body weight × 100); (<b>C</b>) liver: body mass ratio (liver weight/body weight × 100); (<b>D</b>) lipid parameters in the plasma. Olanzapine: 6 mg/kg/day, 9 weeks. Data presented as mean ± SD (Olanzapine: n = 11, control: n = 12). * <span class="html-italic">p</span> ≤ 0.05, ** <span class="html-italic">p</span> &lt; 0.01 vs. control. Abbreviations: BMI, body mass index; TG, triglyceride; TC, total cholesterol; HDL-c high-density lipoprotein cholesterol; LDL-c low-density lipoprotein cholesterol.</p> Full article ">Figure 2
<p>Effect of Olanzapine on gene expression of <span class="html-italic">Alk</span> and related pathways in the liver. (<b>A</b>) <span class="html-italic">Chrm3</span>, (<b>B</b>) <span class="html-italic">Alk</span>, (<b>C</b>) <span class="html-italic">Ptprz1</span>, (<b>D</b>) <span class="html-italic">Lmo4</span>, (<b>E</b>) <span class="html-italic">Ptn</span>. Data are presented as mean ± SD. The sample size is 6 per group. * <span class="html-italic">p</span> &lt; 0.05, ** <span class="html-italic">p</span> &lt; 0.01 vs. control.</p> Full article ">Figure 3
<p>Profiles of metabolic changes after treatment with Olanzapine and/or Cevimeline. (<b>A</b>) BMI (body weight (g) divided by squared body length (cm)); (<b>B</b>) white adipose tissue index (adipose tissue weight/body weight × 100); (<b>C</b>) liver: body mass ratio (liver weight/body weight × 100); (<b>D</b>) lipid parameters in the plasma. Data presented as mean ± SD. The sample size is 12 per group. * <span class="html-italic">p</span> &lt; 0.05, ** <span class="html-italic">p</span> &lt; 0.01, *** <span class="html-italic">p</span> &lt; 0.01 vs. control; @@ <span class="html-italic">p</span> &lt; 0.01, @@@ <span class="html-italic">p</span> &lt; 0.001 vs. Olanzapine. Abbreviations; BMI, body mass index; TG, triglyceride; TC, total cholesterol; HDL-c, high-density lipoprotein cholesterol; LDL-c, low-density lipoprotein cholesterol.</p> Full article ">Figure 4
<p>Effect of Olanzapine and/or Cevimeline on mRNA expression of <span class="html-italic">Alk</span> and related pathways in the liver. (<b>A</b>) <span class="html-italic">Chrm3</span>, (<b>B</b>) <span class="html-italic">Alk</span>, (<b>C</b>) <span class="html-italic">Ptprz1</span>, (<b>D</b>) <span class="html-italic">Lmo4</span>, (<b>E</b>) Ptn. Data are presented as mean ± SD. The sample size is 6 per group. * <span class="html-italic">p</span> &lt; 0.05, ** <span class="html-italic">p</span> &lt; 0.01 vs. control; @@ <span class="html-italic">p</span> &lt; 0.01 vs. Olanzapine.</p> Full article ">
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 1332
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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Figure 1

Figure 1
<p>HFD-induced body weight gain in the <span class="html-italic">Pex16<sup>fl/fl</sup></span> mice and <span class="html-italic">Pex16<sup>AdipoQ-Cre</sup></span> mice but not in the <span class="html-italic">Pex16<sup>Alb-Cre</sup></span> mice. (<b>A</b>) Body weight gain in the HFD-fed mice (n = 5); (<b>B</b>) Repeated Measures ANOVA analysis; (<b>C</b>) Liver index (n = 5); (<b>D</b>) Fat index (n = 5); (<b>E</b>) H&amp;E staining showing adipose inflammation as indicated by “Crown”. The images are representatives of the 5 mice. (<b>F</b>) H&amp;E staining showing lipid droplets (Arrows) in liver sections. The images are representatives of the 5 mice. WT, <span class="html-italic">Pex16<sup>fl/fl</sup></span> mice; AKO, adipose-specific PEX16 knockout (<span class="html-italic">Pex16<sup>AdipoQ-Cre</sup></span>) mice; LKO, liver-specific PEX16 knockout (<span class="html-italic">Pex16<sup>Alb-Cre</sup></span>) mice.</p> Full article ">Figure 2
<p>HFD-induced glucose intolerance in the <span class="html-italic">Pex16<sup>fl/fl</sup></span> mice but not in the <span class="html-italic">Pex16<sup>Alb-Cre</sup></span> mice. (<b>A</b>) HFD-induced gonadal adipose tissue expansion as indicated by fat index (n = 5); (<b>B</b>) HFD-induced hyperglycemia (n = 5); (<b>C</b>) Glucose tolerance test (n = 3).</p> Full article ">Figure 3
<p>HFD-induced steatosis in the <span class="html-italic">Pex16<sup>fl/fl</sup></span> mice but not in the <span class="html-italic">Pex16<sup>Alb-Cre</sup></span> mice. (<b>A</b>) Liver index (n = 5); (<b>B</b>) Liver TG contents (n = 5); (<b>C</b>) H&amp;E staining showing lipid droplets (Arrows) in liver sections; (<b>D</b>) Steatosis quantification (n = 5); (<b>E</b>) Hepatocyte nuclear number (n = 5).</p> Full article ">Figure 4
<p>The absence of liver PEX16 leads to hepatocyte proliferation. (<b>A</b>) PCNA positive staining was observed in the <span class="html-italic">Pex16<sup>Alb-Cre</sup></span> mice, but not in the <span class="html-italic">Pex16<sup>fl/fl</sup></span> mice. Arrows show representative positive staining. The images are representative of the 5 mice. (<b>B</b>) PCNA staining quantification (n = 5). (<b>C</b>) Ki67 staining was observed in the <span class="html-italic">Pex16<sup>Alb-Cre</sup></span> mice, but not in the <span class="html-italic">Pex16<sup>fl/fl</sup></span> mice. Arrows show representative positive staining. The images are representative of the 5 mice. (<b>D</b>) Ki67 staining quantification (n = 5). Arrows show representative positive staining.</p> Full article ">Figure 5
<p>The absence of liver PEX16 lowered serum-free fatty acids, ketone bodies and TG. (<b>A</b>) Expression of liver peroxisomal fatty acid β-oxidation enzymes; (<b>B</b>) Serum fatty acids (n = 5); (<b>C</b>) Serum β-hydroxybutyrate (n = 5); (<b>D</b>) Expression of fat metabolism enzymes; (<b>E</b>) Serum TG (n = 5).</p> Full article ">Figure 6
<p>The absence of liver PEX16 altered cholesterol and bile acid metabolism. (<b>A</b>) Expression of liver cholesterol and bile acid synthetic enzymes; (<b>B</b>) Serum cholesterol (n = 5); (<b>C</b>) Serum bile acids (n = 5).</p> Full article ">Figure 7
<p>H&amp;E staining in the liver sections from patients with chronic liver diseases. Yellow arrows, green arrows, and red arrows indicate lipid droplets, inflammation foci, and fibrosis, respectively. Black arrows show ballooning degeneration. The images are representatives of the 37 patients with chronic liver diseases.</p> Full article ">Figure 8
<p>IHC staining in liver sections from patients with chronic liver diseases. The images are representatives of the 37 patients with chronic liver diseases.</p> Full article ">Figure 9
<p>Pathways of peroxisomal β-oxidation. The small font size of ACOX3 means that ACOX3 plays a minor role in the β-oxidation compared with ACOX2. BFP, bifunctional protein; BAAT, bile acyl-CoA: amino acid acyltransferase. Enzymes in red color were measured in this study. Acetyl-CoA and Propionyl-CoA are distinguished in green and blue fonts, respectively. The rounds of β-oxidation are indicated in purple fonts.</p> Full article ">
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