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Beyond the Scale: Metabolic Pathways and the Pathophysiology of Obesity
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Beyond the Scale: Metabolic Pathways and the Pathophysiology of Obesity

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Endocrinology and Metabolism".

Deadline for manuscript submissions: 30 November 2026 | Viewed by 966

Editor

Dr. Marika Crescenzi

E-Mail Website
Guest Editor
Department of Medicine, University of Padova, Via Orus 2/B, 35128 Padova, Italy
Interests: meta-inflammation (inflammation triggered by metabolic abnormalities); adipose and hepatic tissue pathophysiology and interplay; NAMs
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Considering the intricate relationship between obesity, a public health challenge, and its comorbidities, there is an urgent need to understand the molecular mechanisms in order to inform targeted interventions and druggable pathways, and improve management approaches for affected individuals. Obesity is clearly recognized as a dire chronic low-grade inflammatory and endocrine multifactorial disease that disrupts systemic homeostasis in the body, both in adults and in children. Neither the actors responsible for this homeostasis disruption nor the reasons for the imbalance affecting inter-organs connections are fully elucidated.

In this Special Issue “Beyond the Scale: Metabolic Pathways and the Pathophysiology of Obesity", I invite you to contribute with original research articles, reviews, or perspective manuscripts on all aspects related to the topic of obesity, its metabolic pathways and the pathophysiological factors influencing the inter-organ relationships within this complex health condition, especially expert insights into mechanistic, functional, cellular, and biochemical aspects of this topic. The inclusion of NAMs in the research methods is also appreciated.

Dr. Marika Crescenzi
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 250 words) can be sent to the Editorial Office for assessment.

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-anonymized peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. 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

  • meta-inflammation
  • adipokynes
  • purinergic system
  • MASH
  • WAT
  • NAMs
  • gut microbiome

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Published Papers (1 paper)

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Review

14 pages, 900 KB  
Review
Restoring Satiety After GLP-1/GIP Pharmacotherapy: Metabolic Stability, Diet Quality, and the Gut Microbiota
by Lidia Lasik and Natalia Ukleja-Sokołowska
Int. J. Mol. Sci. 2026, 27(11), 4658; https://doi.org/10.3390/ijms27114658 - 22 May 2026
Viewed by 696
Abstract
GLP-1 receptor agonists and dual GLP-1/GIP agonists have significantly transformed the treatment of obesity, enabling clinically meaningful weight reduction and improvements in cardiometabolic parameters. However, clinical trial data indicate that cessation of therapy is associated with biologically driven weight regain and a partial [...] Read more.
GLP-1 receptor agonists and dual GLP-1/GIP agonists have significantly transformed the treatment of obesity, enabling clinically meaningful weight reduction and improvements in cardiometabolic parameters. However, clinical trial data indicate that cessation of therapy is associated with biologically driven weight regain and a partial loss of metabolic benefits. This phenomenon underscores the chronic nature of obesity and the limited durability of effects achieved through pharmacotherapy alone. Nevertheless, structured clinical frameworks describing how to maintain satiety and metabolic stability after GLP-1/GIP dose reduction or discontinuation remain limited. The aim of this narrative review is to discuss the mechanisms underlying weight regain following dose reduction or discontinuation of GLP-1/GIP pharmacotherapy and to present strategies supporting long-term metabolic stabilisation. Weight regain is driven in part by persistent metabolic adaptations, including a reduction in resting energy expenditure (adaptive thermogenesis), alterations in the hunger–satiety axis (increased ghrelin, reduced leptin signalling), and potentially incomplete restoration of adipose tissue and liver-related metabolic function, although direct evidence in this specific setting remains limited. Weight loss is often accompanied by a reduction in fat-free mass, which further lowers energy expenditure and increases susceptibility to a positive energy balance after treatment cessation. It remains unclear whether pharmacological suppression of appetite results in sustained normalisation of endogenous satiety regulation after treatment cessation, and its effects on gut microbiota function remain uncertain. In clinical practice, key priorities include preserving muscle mass (adequate protein intake, resistance training), maintaining dietary nutrient density, stabilising postprandial glycaemia, and ensuring sufficient intake of fermentable fibre to support short-chain fatty acid production and gut–brain signalling. GLP-1/GIP pharmacotherapy should be viewed as a component of an integrated model of obesity treatment. We propose that long-term weight stabilisation may require a transition from pharmacologically induced satiety to satiety supported by diet quality, preserved fat-free mass, and metabolic stability. Further research is needed to define optimal post-treatment strategies and to identify patients in whom therapy can be safely reduced or discontinued. This transition should be regarded as a conceptual framework and forward-looking hypothesis requiring validation in prospective studies. Full article
(This article belongs to the Special Issue Beyond the Scale: Metabolic Pathways and the Pathophysiology of Obesity)
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