The Molecular and Pathophysiological Basis of Ectopic Fat Deposition in Non-Adipose Tissues

A special issue of Biomolecules (ISSN 2218-273X). This special issue belongs to the section "Molecular Medicine".

Deadline for manuscript submissions: 31 May 2025 | Viewed by 4184

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Center for Human Nutrition, University of Texas Southwestern Medical Center, 5323 Harry Hines Blvd., Dallas, TX 75390-9052, USA
Interests: metabolic basis of dyslipidemia; efficacy and safety of hypolipidemic drugs and nutrients; metabolic concomitants of obesity phenotypes
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Dear Colleagues,

We are inviting reviews and/or original research papers for the Special Issue “The Molecular and Pathophysiological Basis of Ectopic Fat Deposition in Non-adipose tissues” for the journal

Ectopic fat deposition is a growing concern in metabolic diseases that increases the risk of morbidity and mortality. There are several types of cells affected by the intracellular accumulation of triglycerides in tissues including the liver, skeletal muscles, the heart, the pancreas, the kidneys and macrophages. The intracellular nidation and accumulation of neutral lipids interfere with the normal functions of the affected tissues. Some of the molecules involved in this process have been identified, but more studies need to be conducted on the pathways affected by the excessive accumulation of triglycerides. In addition, it is important to differentiate between the relative contribution of fasting versus feeding to lipid droplet formation and the impact of diet composition and/or physical activity to the overall accumulation of intracellular triglycerides.

This Special Issue focuses on the current state-of-the-art molecules that have been identified in the ectopic fat accumulation in tissues, with the histological and metabolic transformations that render affected tissues dysfunctional. Molecules that are potential pharmacotherapy targets are also of interest.

The manuscripts should emphasize the molecular basis of steatosis. Deadline for submission is November 2024.

Prof. Dr. Gloria Lena Vega
Prof. Dr. Amalia Gastaldelli
Guest Editors

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Keywords

  • metabolic dysfunction-associated hepatosteatosis
  • myosteatosis
  • pancreatic steatosis
  • pancreatic adipocytes
  • visceral adipose tissue
  • cardiac steatosis
  • cardiac adipose tissue
  • kidney steatosis
  • macrophage steatosis
  • perirenal adipose tissue
  • lipophagy

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Published Papers (2 papers)

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Research

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19 pages, 2207 KiB  
Article
Effects of Obesity and Exercise on Hepatic and Pancreatic Lipid Content and Glucose Metabolism: PET Studies in Twins Discordant for BMI
by Martin S. Lietzén, Andrea Mari, Ronja Ojala, Jaakko Hentilä, Kalle Koskensalo, Riikka Lautamäki, Eliisa Löyttyniemi, Riitta Parkkola, Virva Saunavaara, Anna K. Kirjavainen, Johan Rajander, Tarja Malm, Leo Lahti, Juha O. Rinne, Kirsi H. Pietiläinen, Patricia Iozzo and Jarna C. Hannukainen
Biomolecules 2024, 14(9), 1070; https://doi.org/10.3390/biom14091070 - 27 Aug 2024
Cited by 1 | Viewed by 1401
Abstract
Obesity and sedentarism are associated with increased liver and pancreatic fat content (LFC and PFC, respectively) as well as impaired organ metabolism. Exercise training is known to decrease organ ectopic fat but its effects on organ metabolism are unclear. Genetic background affects susceptibility [...] Read more.
Obesity and sedentarism are associated with increased liver and pancreatic fat content (LFC and PFC, respectively) as well as impaired organ metabolism. Exercise training is known to decrease organ ectopic fat but its effects on organ metabolism are unclear. Genetic background affects susceptibility to obesity and the response to training. We studied the effects of regular exercise training on LFC, PFC, and metabolism in monozygotic twin pairs discordant for BMI. We recruited 12 BMI-discordant monozygotic twin pairs (age 40.4, SD 4.5 years; BMI 32.9, SD 7.6, 8 female pairs). Ten pairs completed six months of training intervention. We measured hepatic insulin-stimulated glucose uptake using [18F]FDG-PET and fat content using magnetic resonance spectroscopy before and after the intervention. At baseline LFC, PFC, gamma-glutamyl transferase (GT), and hepatic glucose uptake were significantly higher in the heavier twins compared to the leaner co-twins (p = 0.018, p = 0.02 and p = 0.01, respectively). Response to training in liver glucose uptake and GT differed between the twins (Time*group p = 0.04 and p = 0.004, respectively). Liver glucose uptake tended to decrease, and GT decreased only in the heavier twins (p = 0.032). In BMI-discordant twins, heavier twins showed higher LFC and PFC, which may underlie the observed increase in liver glucose uptake and GT. These alterations were mitigated by exercise. The small number of participants makes the results preliminary, and future research with a larger pool of participants is warranted. Full article
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Review

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16 pages, 745 KiB  
Review
Cardio-Lipotoxicity of Epicardial Adipose Tissue
by Monica L. Bodenstab, Ron T. Varghese and Gianluca Iacobellis
Biomolecules 2024, 14(11), 1465; https://doi.org/10.3390/biom14111465 - 18 Nov 2024
Cited by 2 | Viewed by 2192
Abstract
Epicardial adipose tissue is a unique visceral adipose tissue depot that plays a crucial role in myocardial metabolism. Epicardial adipose tissue is a major source of energy and free fatty acids for the adjacent myocardium. However, under pathological conditions, epicardial fat can affect [...] Read more.
Epicardial adipose tissue is a unique visceral adipose tissue depot that plays a crucial role in myocardial metabolism. Epicardial adipose tissue is a major source of energy and free fatty acids for the adjacent myocardium. However, under pathological conditions, epicardial fat can affect the heart through the excessive and abnormal influx of lipids. The cardio-lipotoxicity of the epicardial adipose tissue is complex and involves different pathways, such as increased inflammation, the infiltration of lipid intermediates such as diacylglycerol and ceramides, mitochondrial dysfunction, and oxidative stress, ultimately leading to cardiomyocyte dysfunction and coronary artery ischemia. These changes can contribute to the pathogenesis of various cardio-metabolic diseases including atrial fibrillation, coronary artery disease, heart failure, and obstructive sleep apnea. Hence, the role of the cardio-lipotoxicity of epicardial fat and its clinical implications are discussed in this review. Full article
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