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Lipid Metabolism in Obesity
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Lipid Metabolism in Obesity

A special issue of Current Issues in Molecular Biology (ISSN 1467-3045). This special issue belongs to the section "Biochemistry, Molecular and Cellular Biology".

Deadline for manuscript submissions: closed (30 April 2023) | Viewed by 11571

Special Issue Editors

Dr. Chuanhai Zhang

E-Mail Website
Guest Editor
The University of Texas Southwestern Medical Center, Dallas, TX 75390, USA
Interests: obesity and diabetes; lipid metabolism; brown adipose tissue; sympathetic innervation
Special Issues, Collections and Topics in MDPI journals
Dr. Qi Wang

E-Mail Website
Guest Editor
Institite of Infectious Diseases, Capital Medical University, Beijing, China
Interests: lipid metabolism and fatty liver; NASH; viral hepatitis
Dr. Quanwei Wei

E-Mail Website
Guest Editor
College of Animal Science and Technology, Nanjing Agricultural University, Nanjing 210095, China
Interests: lipid metabolism; reproductive system diseases

Special Issue Information

Dear Colleagues,

This Special Issue aims to further understand the role and molecular mechanism of lipid metabolism in obesity and related diseases, as well as its health impact. Lipid metabolism plays an essential role in the regulation of energy homeostasis. Dyslipidemia leads to adiposity and causes a series of metabolic diseases, such as fatty liver, insulin resistance, type 2 diabetes mellitus, cardiovascular disease, cancer, inflammation, and other related diseases. Lipid metabolism can be regulated by many molecular-level factors. The following research areas are within the scope for the Special Issue: molecular mechanisms underlying the effect of lipid metabolism and obesity-related disease; lipid metabolism and fatty liver, NASH, and liver cancer; lipid metabolism and obesity-related reproductive system diseases; lipid droplets function in tissue (such as adipose tissue, liver, and kidney); lipid droplets and other organelles contact; nutritional supplements in the management of obesity and dyslipidemia; the role of different types of lipids in obesity-related diseases; the role of gut microbiota-induced lipids in the management of obesity-related diseases; and food intake, lipid metabolism, the gut–brain axis, and the control of energy homeostasis. We welcome the submission of different article types to this collection, such as research articles (especially original), reviews, and mini reviews.

Dr. Chuanhai Zhang
Dr. Qi Wang
Dr. Quanwei Wei
Guest Editors

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. Current Issues in Molecular Biology 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 2200 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

  • lipid metabolism
  • lipid droplets
  • LD and organelles contact
  • obesity
  • fatty liver
  • cancer

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Published Papers (4 papers)

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Research

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11 pages, 7543 KiB  
Article
Network Meta-Analysis: Effect of Cold Stress on the Gene Expression of Swine Adipocytes ATGL, CIDEA, UCP2, and UCP3
by Zhenhua Guo, Lei Lv, Di Liu, Hong Ma, Liang Wang, Bo Fu and Fang Wang
Curr. Issues Mol. Biol. 2024, 46(5), 3866-3876; https://doi.org/10.3390/cimb46050240 - 25 Apr 2024
Cited by 1 | Viewed by 917
Abstract
Cold stress significantly affects gene expression in adipocytes; studying this phenomenon can help reveal the pathogeneses of conditions such as obesity and insulin resistance. Adipocyte triglyceride lipase (ATGL); cell death-inducing deoxyribonucleic acid (DNA) fragmentation factor subunit alpha (DFFA)-like effector (CIDEA [...] Read more.
Cold stress significantly affects gene expression in adipocytes; studying this phenomenon can help reveal the pathogeneses of conditions such as obesity and insulin resistance. Adipocyte triglyceride lipase (ATGL); cell death-inducing deoxyribonucleic acid (DNA) fragmentation factor subunit alpha (DFFA)-like effector (CIDEA); and uncoupling protein genes UCP1, UCP2, and UCP3 are the most studied genes in pig adipose tissues under cold stress. However, contradictory results have been observed in gene expression changes to UCP3 and UCP2 when adipose tissues under cold stress were examined. Therefore, we conducted a meta-analysis of 32 publications in total on the effect of cold stress on the expression of ATGL, CIDEA, UCP2, and UCP3. Our results showed that cold stress affected the expression of swine adipocyte genes; specifically, it was positively correlated with the expression of UCP3 in swine adipocytes. Conversely, expression of ATGL was negatively affected under cold stress conditions. In addition, the loss of functional UCP1 in pigs likely triggered a compensatory increase in UCP3 activity. We also simulated the docking results of UCP2 and UCP3. Our results showed that UCP2 could strongly bind to adenosine triphosphate (ATP), meaning that UCP3 played a more significant role in pig adipocytes. Full article
(This article belongs to the Special Issue Lipid Metabolism in Obesity)
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19 pages, 4390 KiB  
Article
SIRT1 Activator E1231 Alleviates Nonalcoholic Fatty Liver Disease by Regulating Lipid Metabolism
by Jiangxue Han, Shunwang Li, Weizhi Wang, Xinhai Jiang, Chao Liu, Lijuan Lei, Yining Li, Ren Sheng, Yuyan Zhang, Yexiang Wu, Jing Zhang, Yuhao Zhang, Yanni Xu and Shuyi Si
Curr. Issues Mol. Biol. 2023, 45(6), 5052-5070; https://doi.org/10.3390/cimb45060321 - 8 Jun 2023
Cited by 3 | Viewed by 2465
Abstract
Nonalcoholic fatty liver disease (NAFLD) is one of the most common liver diseases. Silencing information regulator 1 (SIRT1) was demonstrated to modulate cholesterol and lipid metabolism in NAFLD. Here, a novel SIRT1 activator, E1231, was studied for its potential improvement effects on NAFLD. [...] Read more.
Nonalcoholic fatty liver disease (NAFLD) is one of the most common liver diseases. Silencing information regulator 1 (SIRT1) was demonstrated to modulate cholesterol and lipid metabolism in NAFLD. Here, a novel SIRT1 activator, E1231, was studied for its potential improvement effects on NAFLD. C57BL/6J mice were fed a high-fat and high-cholesterol diet (HFHC) for 40 weeks to create a NAFLD mouse model, and E1231 was administered by oral gavage (50 mg/kg body weight, once/day) for 4 weeks. Liver-related plasma biochemistry parameter tests, Oil Red O staining, and hematoxylin-eosin staining results showed that E1231 treatment ameliorated plasma dyslipidemia, plasma marker levels of liver damage (alanine aminotransferase (ALT) and aspartate aminotransferase (AST)), liver total cholesterol (TC) and triglycerides (TG) contents, and obviously decreased hepatic steatosis score and NAFLD Activity Score (NAS) in the NAFLD mouse model. Western blot results showed that E1231 treatment significantly regulated lipid-metabolism-related protein expression. In particular, E1231 treatment increased SIRT1, PGC-1α, and p-AMPKα protein expression but decreased ACC and SCD-1 protein expression. Additionally, in vitro studies demonstrated that E1231 inhibited lipid accumulation and improved mitochondrial function in free-fatty-acid-challenged hepatocytes, and required SIRT1 activation. In conclusion, this study illustrated that the SIRT1 activator E1231 alleviated HFHC-induced NAFLD development and improved liver injury by regulating the SIRT1-AMPKα pathway, and might be a promising candidate compound for NAFLD treatment. Full article
(This article belongs to the Special Issue Lipid Metabolism in Obesity)
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Review

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13 pages, 668 KiB  
Review
The Role of GLP1-RAs in Direct Modulation of Lipid Metabolism in Hepatic Tissue as Determined Using In Vitro Models of NAFLD
by Ana Petrovic, Dunja Igrec, Karla Rozac, Kristina Bojanic, Lucija Kuna, Tea Omanovic Kolaric, Vjera Mihaljevic, Renata Sikora, Robert Smolic, Marija Glasnovic, George Y. Wu and Martina Smolic
Curr. Issues Mol. Biol. 2023, 45(6), 4544-4556; https://doi.org/10.3390/cimb45060288 - 24 May 2023
Cited by 12 | Viewed by 4759
Abstract
Glucagon-like peptide 1 receptor agonists (GLP-1RAs) have been shown to improve glucose and lipid homeostasis, promote weight loss, and reduce cardiovascular risk factors. They are a promising therapeutic option for non-alcoholic fatty liver disease (NAFLD), the most common liver disease, associated with T2DM, [...] Read more.
Glucagon-like peptide 1 receptor agonists (GLP-1RAs) have been shown to improve glucose and lipid homeostasis, promote weight loss, and reduce cardiovascular risk factors. They are a promising therapeutic option for non-alcoholic fatty liver disease (NAFLD), the most common liver disease, associated with T2DM, obesity, and metabolic syndrome. GLP-1RAs have been approved for the treatment of T2DM and obesity, but not for NAFLD. Most recent clinical trials have suggested the importance of early pharmacologic intervention with GLP-1RAs in alleviating and limiting NAFLD, as well as highlighting the relative scarcity of in vitro studies on semaglutide, indicating the need for further research. However, extra-hepatic factors contribute to the GLP-1RA results of in vivo studies. Cell culture models of NAFLD can be helpful in eliminating extrahepatic effects on the alleviation of hepatic steatosis, modulation of lipid metabolism pathways, reduction of inflammation, and prevention of the progression of NAFLD to severe hepatic conditions. In this review article, we discuss the role of GLP-1 and GLP-1RA in the treatment of NAFLD using human hepatocyte models. Full article
(This article belongs to the Special Issue Lipid Metabolism in Obesity)
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13 pages, 752 KiB  
Review
LSD1 for the Targeted Regulation of Adipose Tissue
by Li Chen, Xuan Sun, Daidi Chen and Qingjun Gui
Curr. Issues Mol. Biol. 2023, 45(1), 151-163; https://doi.org/10.3390/cimb45010012 - 27 Dec 2022
Cited by 1 | Viewed by 2851
Abstract
White and thermal (brown and beige) adipose tissue energy storage and oxidative regulation pathways play a central role in maintaining the energy balance throughout the body, and the dysregulation of these pathways is closely related to glucose and lipid metabolism disorders and adipose [...] Read more.
White and thermal (brown and beige) adipose tissue energy storage and oxidative regulation pathways play a central role in maintaining the energy balance throughout the body, and the dysregulation of these pathways is closely related to glucose and lipid metabolism disorders and adipose tissue dysfunction, including obesity, chronic inflammation, insulin resistance, mitochondrial dysfunction, and fibrosis. Recent epigenetic studies have identified the novel regulatory element LSD1, which controls the above parameters, and have provided new mechanistic possibilities for re-encoding the fate and function of adipocytes. In this review, we outline the current advances in adipocyte metabolism in physiology and disease and discuss possible strategies for LSD1 to alter the phenotype of adipose tissue and thus influence energy utilization to improve metabolic health. Full article
(This article belongs to the Special Issue Lipid Metabolism in Obesity)
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