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Dietary Patterns, Lipid Metabolism and Fatty Liver Disease

A special issue of Nutrients (ISSN 2072-6643). This special issue belongs to the section "Lipids".

Deadline for manuscript submissions: 25 September 2025 | Viewed by 461

Special Issue Editors


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Guest Editor
Department of Pharmacology, University of Barcelona, Barcelona, Spain
Interests: diabetes; liver; metabolism; pharmacology; pathology; clinical nutrition
Department of Pharmacology, University of Barcelona, Barcelona, Spain
Interests: insulin resistance; lipid metabolism; glucose metabolism; pharmacology; molecular biology; diabetes; MASLD; metabolic diseases; nutrition; adeno-associated viral vectors

Special Issue Information

Dear Colleagues,

For years, the impact of diet on metabolic health has been recognized as a growing global concern. Dietary patterns such as high-fat, ketogenic, and restricted diets, or the addition of specific nutrients like vitamins, fructose, probiotics, and omega-3s, influence lipid metabolism in different ways. While some dietary approaches may support metabolic health, others can disrupt lipid balance, promoting insulin resistance, obesity, cardiovascular diseases and MASLD—conditions that are rising at an alarming rate worldwide. Regarding this, MASLD is currently the most common liver disorder worldwide. The significant risk of progression of MASLD to cirrhosis and hepatocellular carcinoma, coupled with the fact that treatment options remain limited, underscores the urgent need for novel strategies to prevent this disorder.

In addition, dietary patterns also play a key role in shaping the composition and functions of the gut microbiota. Microbiota dysbiosis has been linked to weight gain, adiposity and the development of several metabolic disorders, resulting in a complex process that requires in-depth investigation.

Therefore, this Special Issue aims to present original research exploring the mechanisms through which dietary patterns exert their beneficial or harmful effects while highlighting novel therapeutic interventions for the treatment of metabolic diseases.

Dr. Emma Barroso
Dr. Laia Vilà
Guest Editors

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Keywords

  • dietary patterns
  • MASLD
  • lipid metabolism
  • insulin resistance
  • gut microbiota
  • obesity
  • therapy

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Published Papers (1 paper)

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Research

19 pages, 2368 KiB  
Article
Hepatic OLFR734 Deficiency Worsens Hepatic Glucose Metabolism and Induces MASLD in Mice
by Eva Prida, Diego Muñoz-Moreno, Eva Novoa, Tamara Parracho, Laura Diaz-Garzón Dopico, Raquel Perez-Lois, Miguel Bascoy-Otero, Ana Senra, Sergio Romero-Rodriguez, Beatriz Brea-García, Jaime Dobarro, Adrián Fernández Marcos, Javier Baltar, Fernando Santos, Amaia Rodríguez, Gema Frühbeck, Ruben Nogueiras, Luisa María Seoane, Mar Quiñones and Omar Al-Massadi
Nutrients 2025, 17(15), 2426; https://doi.org/10.3390/nu17152426 - 25 Jul 2025
Viewed by 307
Abstract
Background/Objectives: Asprosin is the endogenous ligand of the olfactory Olfr734 receptor linked to MASLD and glucose metabolism. Despite the involvement of asprosin in these processes, little has been published on the specific role of Olfr734 in liver function. The aim of this work [...] Read more.
Background/Objectives: Asprosin is the endogenous ligand of the olfactory Olfr734 receptor linked to MASLD and glucose metabolism. Despite the involvement of asprosin in these processes, little has been published on the specific role of Olfr734 in liver function. The aim of this work is therefore to study the specific role of the olfactory Olfr734 receptor in MASLD and glucose metabolism. Methods: To achieve this objective, we performed a genetic inhibition specifically to inhibit Olfr734 in the livers of male mice. We then studied the progression of MASLD in DIO mice. In addition, we studied the glucose metabolism in hypoglycemia states and postprandial glucose production in standard diet-fed mice. Finally, analyses of liver biopsies from patients with obesity and with or without T2DM were conducted. Results: We found that hepatic Olfr734 levels vary according to changes in nutritional status and its knockdown effect in the liver is to increase the hepatic lipid content in DIO mice. Our results also showed that OLFR734 expression is involved in the adaptive response in terms of glucose production to nutrient availability. Finally, the hepatic human Olfr734 ortholog named OR4M1 has been observed to be at significantly higher levels in male patients with T2DM. Conclusions: This study increases understanding of the mechanisms by which the modulation of Olfr734 expression affects liver function. Full article
(This article belongs to the Special Issue Dietary Patterns, Lipid Metabolism and Fatty Liver Disease)
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