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Nutritional Approaches for Managing Obesity-Associated Metabolic Diseases

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

Deadline for manuscript submissions: 15 September 2025 | Viewed by 115

Special Issue Editor


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Guest Editor
Department of Kinesiology and Nutrition Sciences, School of Integrated Health Sciences, University of Nevada, Las Vegas, NV 89154, USA
Interests: dietary patterns; functional foods; obesity; aging; health outcomes; functional performance

Special Issue Information

Dear Colleagues,

Obesity is a leading global health issue that contributes to the development of metabolic disorders such as type-2 diabetes, cardiovascular disease, and non-alcoholic fatty liver disease (NAFLD). These metabolic disorders share the underlying conditions and mechanisms that contribute to their development and progression, including insulin resistance, chronic inflammation, oxidative stress, hypertension, endothelial dysfunction, and dyslipidemia. For this Special Issue, we invite papers that focus on specific metabolic disorders associated with obesity, particularly Type-2 diabetes and insulin resistance, cardiovascular diseases, NAFLD, dyslipidemia, and metabolic syndrome. We encourage research that explores nutritional interventions that target these disorders, with an emphasis on personalized, sustainable dietary strategies. Diets rich in whole foods, fruits, vegetables, lean proteins, and whole grains play a vital role in managing obesity-related metabolic risk factors. Studies on the Mediterranean diet (and other healthful dietary patterns), functional foods, and nutraceuticals are welcomed, as these approaches show promise in mitigating obesity-related metabolic risks. We seek contributions that investigate the biological mechanisms connecting obesity with these metabolic disorders, as well as how dietary modifications can influence key metabolic pathways and improve associated health outcomes.

Dr. Neda Akhavan
Guest Editor

Manuscript Submission Information

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Keywords

  • cardiometabolic disorders
  • inflammation
  • adiposity
  • dietary patterns
  • functional foods

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Published Papers (1 paper)

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Research

17 pages, 5043 KiB  
Article
Cannabigerol Alleviates Liver Damage in Metabolic Dysfunction-Associated Steatohepatitis Female Mice via Inhibition of Transforming Growth Factor Beta 1
by Raznin Joly, Fariha Tasnim, Kelsey Krutsinger, Zhuorui Li, Nicholas A. Pullen and Yuyan Han
Nutrients 2025, 17(9), 1524; https://doi.org/10.3390/nu17091524 - 30 Apr 2025
Abstract
Background and Aims: Metabolic dysfunction-associated steatohepatitis (MASH), a progressive form of metabolic dysfunction-associated steatotic liver disease (MASLD), involves inflammation, fibrosis, steatosis, and oxidative stress. Previous research from our lab shows that cannabigerol (CBG) reduces inflammation and fibrosis in male MASH mice, but its [...] Read more.
Background and Aims: Metabolic dysfunction-associated steatohepatitis (MASH), a progressive form of metabolic dysfunction-associated steatotic liver disease (MASLD), involves inflammation, fibrosis, steatosis, and oxidative stress. Previous research from our lab shows that cannabigerol (CBG) reduces inflammation and fibrosis in male MASH mice, but its effects in females remain unknown. Given immune cell population changes in MASLD patients, this study examines CBG’s impact on methionine-choline deficient (MCD) diet-induced MASH in female mice. Methods: MCD-fed female mice are supplemented with two different doses for three weeks. Liver fibrosis, steatosis, oxidative stress, ductular reaction, and inflammation are assessed via Sirius Red, Oil Red O, immunohistochemistry, and immunofluorescence staining. Immune cell changes in non-parenchymal cells (NPCs) are analyzed via flow cytometry. Results: CBG treatment improves liver health by reducing leukocyte infiltration. Both CBG doses significantly decrease fibrosis, oxidative stress, ductular proliferation, and inflammation in MCD-fed mice, including monocyte and T lymphocyte reductions. Additionally, CBG downregulates mast cell activation, inhibiting transforming growth factor (TGF)-β1 release, thereby suppressing hepatic stellate cell activation. This reduces collagen deposition, fibrosis, and ductular proliferation. Conclusions: Our findings provide insights for pre-clinical and clinical research, highlighting CBG’s potential therapeutic role and dosage considerations in mitigating liver fibrosis and inflammation in female patients. Full article
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