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Mechanisms and Pathophysiology of Obesity
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Mechanisms and Pathophysiology of Obesity

A special issue of Current Issues in Molecular Biology (ISSN 1467-3045). This special issue belongs to the section "Molecular Medicine".

Deadline for manuscript submissions: 31 August 2025 | Viewed by 893

Special Issue Editor

Dr. Padmamalini Baskaran

E-Mail Website
Guest Editor
College of Pharmacy, Howard University, Washington, DC 20059, USA
Interests: TRPV1; capsaicin; obesity; insulin resistance; metabolic dysfunction-associated steatotic liver disease

Special Issue Information

Dear Colleagues,

Obesity is a chronic, relapsing condition characterized by excess body fat. It occurs when the balance is lost between energy intake vs. expenditure. Obesity is caused by many factors, including genetics, viruses, environment, physical activity and diet, insulin resistance, inflammation, gut microbiome, medications, circadian rhythms, psychological distress and stress, pollution, parental body mass index, maternal smoking, etc. Hormones, growth factors, and organs and tissues regulate the progression of obesity. The molecular mechanisms and pathophysiology of obesity involve a complex interplay of various factors.

There are serious health consequences due to obesity. Excessive fat accumulation not only disrupts the normal function of adipose tissue but also places a burden on organs such as the heart and liver, elevating the risk of multiple chronic diseases. Therefore, research is important to understand the unexplored mechanisms and develop effective interventions to improve health outcomes and digital tools to monitor and provide real-time feedback to help patients.

Dr. Padmamalini Baskaran
Guest Editor

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Current Issues in Molecular Biology is an international peer-reviewed open access monthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2200 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • understanding genetic factors for obesity at the molecular level
  • understanding environmental factors for obesity at the molecular level
  • contribution of insulin resistance to obesity and ways to combat
  • circadian misalignment–molecular level understanding of its contribution to obesity and ways to mitigate it
  • effective and individualized obesity treatment strategies for stress
  • molecular understanding of the influence of parental obesity on childhood overweight
  • molecular mechanisms of maternal smoking on childhood obesity
  • therapeutic interventions for obesity through recombinant hormones
  • role of gut hormones in the treatment of obesity
  • development of new digital tools for weight management interventions

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Published Papers (1 paper)

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Research

18 pages, 2745 KiB  
Article
Obesity-Induced MASLD Is Reversed by Capsaicin via Hepatic TRPV1 Activation
by Padmamalini Baskaran, Ryan Christensen, Kimberley D. Bruce and Robert H. Eckel
Curr. Issues Mol. Biol. 2025, 47(8), 618; https://doi.org/10.3390/cimb47080618 - 4 Aug 2025
Viewed by 510
Abstract
Background and Objectives: Metabolic dysfunction-associated steatotic liver disease (MASLD) is a progressive liver disorder associated with metabolic risk factors such as obesity, type 2 diabetes, and cardiovascular disease. If left untreated, the accumulation of excess hepatic fat can lead to inflammation, fibrosis, cirrhosis, [...] Read more.
Background and Objectives: Metabolic dysfunction-associated steatotic liver disease (MASLD) is a progressive liver disorder associated with metabolic risk factors such as obesity, type 2 diabetes, and cardiovascular disease. If left untreated, the accumulation of excess hepatic fat can lead to inflammation, fibrosis, cirrhosis, hepatocellular carcinoma, and ultimately liver failure. Capsaicin (CAP), the primary pungent compound in chili peppers, has previously been shown to prevent weight gain in high-fat diet (HFD)-induced obesity models. In this study, we investigated the potential of dietary CAP to prevent HFD-induced MASLD. Methods: C57BL/6 mice were fed an HFD (60% kcal from fat) with or without 0.01% CAP supplementation for 26 weeks. We evaluated CAP’s effects on hepatic fat accumulation, inflammation, and mitochondrial function to determine its role in preventing MASLD. Results: CAP acts as a potent and selective agonist of the transient receptor potential vanilloid 1 (TRPV1) channel. We confirmed TRPV1 expression in the liver and demonstrated that CAP activates hepatic TRPV1, thereby preventing steatosis, improving insulin sensitivity, reducing inflammation, and enhancing fatty acid oxidation. These beneficial effects were observed in wild-type but not in TRPV1 knockout mice. Mechanistically, CAP-induced TRPV1 activation promotes calcium influx and activates AMPK, which leads to SIRT1-dependent upregulation of PPARα and PGC-1α, enhancing mitochondrial biogenesis and lipid metabolism. Conclusions: Our findings suggest that dietary CAP prevents MASLD through TRPV1 activation. TRPV1 signaling represents a promising therapeutic target for the prevention and management of MASLD in individuals with metabolic disorders. Full article
(This article belongs to the Special Issue Mechanisms and Pathophysiology of Obesity)
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