Lipid and Glucose Metabolism in Liver Diseases

A special issue of Biomolecules (ISSN 2218-273X). This special issue belongs to the section "Biomacromolecules: Lipids".

Deadline for manuscript submissions: closed (20 August 2023) | Viewed by 10931

Special Issue Editors

Department of Internal Medicine, University of Kansas Medical Center, 3901 Rainbow Blvd, Kansas City, KS 66160, USA
Interests: alcohol-associated liver disease; gut microbiota; lipid metabolism
Special Issues, Collections and Topics in MDPI journals
Department of Pathology and Laboratory Medicine, Tulane University, New Orleans, LA 70112, USA
Interests: hepatic progenitor cell activation; liver regeneration; alcoholic fibrosis; liver cancer
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

The liver is the major organ for lipometabolism and glycometabolism, through which lipids and carbohydrates can be converted to energy and substances for maintenance of homeostasis in the body. The synthesis, metabolism, storage, and redistribution of lipids and carbohydrates can be intertwined due to the complicated network of regulations by neuronal signals, hormones, enzymes, and transcriptional factors. Imbalance of the regulatory pathways may result in a broad spectrum of liver pathologies ranging from steatosis, steatohepatitis, and fibrosis to cirrhosis. The life-threatening conditions associated with metabolic syndromes include acute liver failure, alcoholic liver disease, non-alcoholic liver disease, and other chronic liver diseases. Failure of liver regeneration may eventually induce hepatic carcinogenesis. Therefore, there is a compelling need to determine the pathogenesis between dysregulations of hepatic lipid and glucose metabolism and the development and progression of liver damage. As the liver has close communications with extrahepatic tissues, including skeletal muscle, adipose tissue, gut, and the brain, the Special Issue also embraces liver–extrahepatic tissue crosstalk in the context of lipometabolism and glycometabolism.

Dr. Wei Zhong
Dr. Liya Pi
Guest Editors

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Keywords

  • lipometabolism
  • glycometabolism
  • liver diseases
  • organelle dysfunction

Published Papers (4 papers)

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Research

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18 pages, 3179 KiB  
Article
Ornithine Aspartate and Vitamin-E Combination Has Beneficial Effects on Cardiovascular Risk Factors in an Animal Model of Nonalcoholic Fatty Liver Disease in Rats
by Laura Bainy Rodrigues de Freitas, Larisse Longo, Eduardo Filippi-Chiela, Valessa Emanoele Gabriel de Souza, Luiza Behrens, Matheus Henrique Mariano Pereira, Luiza Cecília Leonhard, Giulianna Zanettini, Carlos Eduardo Pinzon, Eduardo Luchese, Guilherme Jorge Semmelmann Pereira Lima, Carlos Thadeu Cerski, Carolina Uribe-Cruz and Mário Reis Álvares-da-Silva
Biomolecules 2022, 12(12), 1773; https://doi.org/10.3390/biom12121773 - 28 Nov 2022
Cited by 2 | Viewed by 1520
Abstract
Cardiovascular (CV) disease is the main cause of death in nonalcoholic fatty liver disease (NAFLD), a clinical condition without any approved pharmacological therapy. Thus, we investigated the effects of ornithine aspartate (LOLA) and/or Vitamin E (VitE) on CV parameters in a steatohepatitis experimental [...] Read more.
Cardiovascular (CV) disease is the main cause of death in nonalcoholic fatty liver disease (NAFLD), a clinical condition without any approved pharmacological therapy. Thus, we investigated the effects of ornithine aspartate (LOLA) and/or Vitamin E (VitE) on CV parameters in a steatohepatitis experimental model. Adult Sprague Dawley rats were randomly assigned (10 animals each) and treated from 16 to 28 weeks with gavage as follows: controls (standard diet plus distilled water (DW)), NAFLD (high-fat choline-deficient diet (HFCD) plus DW), NAFLD+LOLA (HFCD plus LOLA (200 mg/kg/day)), NAFLD+VitE (HFCD plus VitE (150 mg twice a week)) or NAFLD+LOLA+VitE in the same doses. Atherogenic ratios were higher in NAFLD when compared with NAFLD+LOLA+VitE and controls (p < 0.05). Serum concentration of IL-1β, IL-6, TNF-α, MCP-1, e-selectin, ICAM-1, and PAI-1 were not different in intervention groups and controls (p > 0.05). NAFLD+LOLA decreased miR-122, miR-33a, and miR-186 (p < 0.05, for all) in relation to NAFLD. NAFLD+LOLA+VitE decreased miR-122, miR-33a and miR-186, and increased miR-126 (p < 0.05, for all) in comparison to NAFLD and NAFLD+VitE. NAFLD+LOLA and NAFLD+LOLA+VitE prevented liver collagen deposition (p = 0.006) in comparison to NAFLD. Normal cardiac fibers (size and shape) were lower in NAFLD in relation to the others; and the inverse was reported for the percentage of regular hypertrophic cardiomyocytes. NAFLD+LOLA+VitE promoted a significant improvement in atherogenic dyslipidemia, liver fibrosis, and paracrine signaling of lipid metabolism and endothelial dysfunction. This association should be further explored in the treatment of NAFLD-associated CV risk factors. Full article
(This article belongs to the Special Issue Lipid and Glucose Metabolism in Liver Diseases)
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Review

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11 pages, 711 KiB  
Review
Association between Impaired Ketogenesis and Metabolic-Associated Fatty Liver Disease
by Jaehyun Bae and Byung-Wan Lee
Biomolecules 2023, 13(10), 1506; https://doi.org/10.3390/biom13101506 - 11 Oct 2023
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Abstract
Metabolic (dysfunction) associated fatty liver disease (MAFLD) is generally developed with excessive accumulation of lipids in the liver. Ketogenesis is an efficient pathway for the disposal of fatty acids in the liver and its metabolic benefits have been reported. In this review, we [...] Read more.
Metabolic (dysfunction) associated fatty liver disease (MAFLD) is generally developed with excessive accumulation of lipids in the liver. Ketogenesis is an efficient pathway for the disposal of fatty acids in the liver and its metabolic benefits have been reported. In this review, we examined previous studies on the association between ketogenesis and MAFLD and reviewed the candidate mechanisms that can explain this association. Full article
(This article belongs to the Special Issue Lipid and Glucose Metabolism in Liver Diseases)
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14 pages, 1230 KiB  
Review
Role of TFEB in Autophagy and the Pathogenesis of Liver Diseases
by Shengmin Yan
Biomolecules 2022, 12(5), 672; https://doi.org/10.3390/biom12050672 - 06 May 2022
Cited by 15 | Viewed by 3453
Abstract
The transcription factor EB (TFEB) is a master regulator of lysosomal function and autophagy. Mechanistic target of rapamycin (mTOR)-mediated phosphorylation on TFEB is known to regulate TFEB subcellular localization and activity at the lysosomal surface. Recent studies have shown that TFEB also plays [...] Read more.
The transcription factor EB (TFEB) is a master regulator of lysosomal function and autophagy. Mechanistic target of rapamycin (mTOR)-mediated phosphorylation on TFEB is known to regulate TFEB subcellular localization and activity at the lysosomal surface. Recent studies have shown that TFEB also plays a critical role in physiological processes such as lipid metabolism, and dysfunction of TFEB has been observed in the pathogenesis of several diseases. Owing to its ability to improve disease status in murine models, TFEB has attracted attention as a therapeutic target for diseases. In this review, we will present the regulation of TFEB and its role in the pathogenesis of liver diseases, particularly non-alcoholic fatty liver disease (NAFLD). Full article
(This article belongs to the Special Issue Lipid and Glucose Metabolism in Liver Diseases)
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17 pages, 1305 KiB  
Review
Adipose Triglyceride Lipase in Hepatic Physiology and Pathophysiology
by Tianjiao Li, Wei Guo and Zhanxiang Zhou
Biomolecules 2022, 12(1), 57; https://doi.org/10.3390/biom12010057 - 31 Dec 2021
Cited by 17 | Viewed by 3744
Abstract
The liver is extremely active in oxidizing triglycerides (TG) for energy production. An imbalance between TG synthesis and hydrolysis leads to metabolic disorders in the liver, including excessive lipid accumulation, oxidative stress, and ultimately liver damage. Adipose triglyceride lipase (ATGL) is the rate-limiting [...] Read more.
The liver is extremely active in oxidizing triglycerides (TG) for energy production. An imbalance between TG synthesis and hydrolysis leads to metabolic disorders in the liver, including excessive lipid accumulation, oxidative stress, and ultimately liver damage. Adipose triglyceride lipase (ATGL) is the rate-limiting enzyme that catalyzes the first step of TG breakdown to glycerol and fatty acids. Although its role in controlling lipid homeostasis has been relatively well-studied in the adipose tissue, heart, and skeletal muscle, it remains largely unknown how and to what extent ATGL is regulated in the liver, responds to stimuli and regulators, and mediates disease progression. Therefore, in this review, we describe the current understanding of the structure–function relationship of ATGL, the molecular mechanisms of ATGL regulation at translational and post-translational levels, and—most importantly—its role in lipid and glucose homeostasis in health and disease with a focus on the liver. Advances in understanding the molecular mechanisms underlying hepatic lipid accumulation are crucial to the development of targeted therapies for treating hepatic metabolic disorders. Full article
(This article belongs to the Special Issue Lipid and Glucose Metabolism in Liver Diseases)
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