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Dietary Fat and Metabolic Diseases

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

Deadline for manuscript submissions: 15 September 2025 | Viewed by 782

Special Issue Editor


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Guest Editor
Physiologie de la Nutrition & Toxicologie, UMR INSERM U1231, Center for Translational & Molecular Medicine (CTM), Université de Bourgogne, 21000 Dijon, France
Interests: fat taste; obesity; genetic polymorphism; epigenetics; fatty acids
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Special Issue Information

Dear Colleagues,

In the past, we have seen an unprecedent upsurge in metabolic diseases such as obesity, cardiovascular pathologies, and type II and gestational diabetes. Though a healthy lifestyle, balanced diet and regular sport activity are the best ways to reduce the risk of developing a metabolic disease, dietary lipids play a significant role in the progression of these pathologies. The target organs in these diseases are principally liver, heart, brain and adipose tissues. The fat receptors that are involved in the modulation of metabolic diseases are CD36, GPR120, GPR40 and other GPCRs that are localized not only in the oro-intestinal epithelium (from taste buds to intestinal cells), but also in cardiomyocytes and adipose tissues. Some fat receptors such as CD36, GPR120 and GPR40 act as sensors to detect dietary fatty acids in the tongue and may affect the pathophysiological aspects of metabolic diseases. Dietary fat also influences the oro-intestinal gut microbiota that produce short-chain fatty acids (SFCAs), which in turn may modulate not only fat-eating behavior, but also metabolic syndrome and other metabolism-dysregulated pathologies. Another important aspect of dietary fat is the inflammation that is triggered by fat-rich food. Inflammation (central or systemic) is the basis of a number of pathologies, including metabolic disorders. This Special Issue invites original or review articles from distinguished researchers to compile the exciting data on this burning area of research.

Prof. Dr. Naim Khan
Guest Editor

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Keywords

  • obesity
  • lipids
  • metabolic syndrome
  • adipose tissue
  • microbiota
  • inflammation
  • GPCR
  • NAFLD

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Published Papers (1 paper)

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Research

13 pages, 1309 KiB  
Article
Celastrol Improves Preference for a Fatty Acid, and Taste Bud and Systemic Inflammation in Diet-Induced Obese Mice
by Manal Benmouna, Chahid Benammar, Amira Sayed Khan, Fatima Zohra Djeziri, Aziz Hichami and Naim A. Khan
Nutrients 2025, 17(8), 1308; https://doi.org/10.3390/nu17081308 - 9 Apr 2025
Viewed by 496
Abstract
Background: Obesity is associated with the altered gustatory perception of dietary fatty acids. Celastrol, a triterpene, has been demonstrated to exert anti-obesity effects in rodents. We assessed the role of Celastrol in the modulation of the oro-sensory perception of lipids in control and [...] Read more.
Background: Obesity is associated with the altered gustatory perception of dietary fatty acids. Celastrol, a triterpene, has been demonstrated to exert anti-obesity effects in rodents. We assessed the role of Celastrol in the modulation of the oro-sensory perception of lipids in control and high-fat diet (HFD)-induced obese mice. Methods: Male mice of the C57B/6J strain were fed a HFD for 11 weeks and then were administered or not with Celastrol further for 4 weeks. The body weight was recorded weekly. Before the sacrifice, the animals were subjected to oro-sensory detection of a dietary long-chain fatty acid in a two-bottle choice paradigm. After the sacrifice, the fungiform taste buds were isolated and analyzed for mRNA expression, encoding fat sensors (CD36 and GPR120) and pro-inflammatory cytokines (IL-1β, IL-6 and TNF-α). Circulating concentrations of IL-6 and TNF-α were also determined, and liver was used to analyze the mRNA expression of lipogenic genes. Results: Celastrol administration in obese mice decreased body weight and also re-established the loss of oro-sensory perception for a dietary fatty acid, and this phenomenon was, in part, due to the upregulation of mRNA, encoding fat taste receptors (CD36 and GPR120) in tongue taste bud cells. Furthermore, Celastrol decreased inflammation both in taste buds and blood circulation. Conclusions: Our findings suggest that Celastrol decreases body weight gain, ameliorates the gustatory perception of lipids, and downregulates inflammation in obese mice. Full article
(This article belongs to the Special Issue Dietary Fat and Metabolic Diseases)
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