Search for Articles:
Title / Keyword
Author / Affiliation / Email
Journal
Article Type
 
 
Advanced Search
 
Section
Special Issue
Volume
Issue
Number
Page
 
9.3
4.8
Journals
Biomolecules
Special Issues
Metabolic Inflammation and Insulin Resistance in Obesity
share announcement

Metabolic Inflammation and Insulin Resistance in Obesity

A special issue of Biomolecules (ISSN 2218-273X). This special issue belongs to the section "Lipids".

Deadline for manuscript submissions: closed (30 November 2025) | Viewed by 15110

Special Issue Editor

Dr. Bingxian Xie

E-Mail Website
Guest Editor
Vascular Medicine Institute, University of Pittsburgh, Pittsburgh, PA 15260, USA
Interests: metabolism; glucose; T cells; fatty acids metabolism

Special Issue Information

Dear Colleagues,

Obesity remains one of the most urgent public health challenges facing society today, especially in developed countries. Both obesity and its related conditions impose substantial economic and workforce burdens on healthcare systems worldwide. Over recent decades, research has increasingly demonstrated that obesity contributes not only to systemic insulin resistance but also to chronic, low-grade inflammation. This obesity-associated inflammation is thought to be primarily driven by the remodeling and redistribution of adipose tissue. Additionally, the complex interplay between adipose cells and immune cells in this process indicates a multifactorial mechanism that requires further investigation to fully understand the underlying inflammatory pathways.

We are pleased to introduce our Special Issue, “Metabolic Inflammation and Insulin Resistance in Obesity,” which aims to showcase novel research into the molecular mechanisms of obesity-related inflammation—its origins, progression, and potential therapeutic interventions. We encourage submissions that incorporate animal models or clinical studies, as these provide valuable insights with translational relevance. Through this issue, we hope to deepen understanding in this area and help guide future research directions.

While obesity is a major driver of metabolic inflammation, it is important to acknowledge that other factors, such as stress, aging, and gut dysbiosis, also play significant roles. We hope our future Special Issues will provide more opportunities to explore these related areas.

Dr. Bingxian Xie
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-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Biomolecules 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 2700 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

  • obesity-linked inflammation
  • insulin resistance
  • adipose tissue

Benefits of Publishing in a Special Issue

  • Ease of navigation: Grouping papers by topic helps scholars navigate broad scope journals more efficiently.
  • Greater discoverability: Special Issues support the reach and impact of scientific research. Articles in Special Issues are more discoverable and cited more frequently.
  • Expansion of research network: Special Issues facilitate connections among authors, fostering scientific collaborations.
  • External promotion: Articles in Special Issues are often promoted through the journal's social media, increasing their visibility.
  • Reprint: MDPI Books provides the opportunity to republish successful Special Issues in book format, both online and in print.

Further information on MDPI's Special Issue policies can be found here.

Published Papers (5 papers)

Download All Papers
Order results
Result details
Show export options expand_more Show export options expand_less
Select all
Export citation of selected articles as:

Research

Jump to: Review

17 pages, 1053 KB  
Article
Plausible Obesity-Related Chronometabolic and Nutrigenetic Nexus Concerning Dinner Glycemic Index and the FAAH C385A Variant
by Barbara Vizmanos, Alejandra Betancourt-Núñez, Erika Sierra-Ruelas, Juan José López Gómez, Daniel Rico, J. Alfredo Martínez and Daniel A. De Luis
Biomolecules 2026, 16(2), 274; https://doi.org/10.3390/biom16020274 - 9 Feb 2026
Viewed by 743
Abstract
The interaction between chrono-nutrition (dinner intake), glycemic index (GI), and the C358A variant of the endocannabinoid-degrading enzyme fatty acid amide hydrolase (FAAH), along with its impact on morning fasting insulin and glycemia, has not been previously explored. This study provides new insights into [...] Read more.
The interaction between chrono-nutrition (dinner intake), glycemic index (GI), and the C358A variant of the endocannabinoid-degrading enzyme fatty acid amide hydrolase (FAAH), along with its impact on morning fasting insulin and glycemia, has not been previously explored. This study provides new insights into chronometabolic and nutrigenetic interactions. This study aims to analyze the association between the dinner GI and the C385A variant in the FAAH gene with respect to fasting glucose, insulin levels, and HOMA-IR in adults with obesity. It was hypothesized that the dinner GI, probably influenced by the FAAH variant, could be associated with glycemic homeostasis in adults with obesity. This is a secondary analysis of a cross-sectional study focused on 189 adults with obesity (129 women; mean age, 41 ± 12 years; mean BMI, 38.0 ± 5.2 kg/m2). Dietary intake was assessed through two 24 h food records, enabling the calculation of GI and macronutrient composition at each meal, especially dinner. Fasting-parameter setting and genotyping were done during the study. The lineal regression analyses were adjusted by age, sex, BMI, energy intake and dinner protein. Participants with lower fasting glucose levels had higher total GI and dinner GI values than those with higher fasting glucose levels, whereas no differences in dinner GI were observed across groups stratified by insulin or HOMA-IR levels. In fully adjusted regression models, dinner GI values remained inversely associated with fasting glucose levels (β = −0.172, 95%CI −0.298 to −0.045; p = 0.008). The FAAH C385A variant independently predicted lower insulin (β = −2.674, 95%CI −5.185 to −0.164; p = 0.037) and lower HOMA-IR (β = −0.731, 95%CI −1.364 to −0.099; p = 0.024) levels. No statistically significant interaction between dinner GI and the FAAH genotype was detected with respect to glycemia, insulin, and HOMA-IR. Overall, these findings indicate that the dinner GI influences fasting glucose levels in adults with obesity; the FAAH variant predicted lower insulin and HOMA-IR levels, supporting a plausible chrono-nutrigenetic interaction between carbohydrate quality, mealtime intake, and FAAH variation in metabolic regulation, which must be further studied. Full article
(This article belongs to the Special Issue Metabolic Inflammation and Insulin Resistance in Obesity)
►▼ Show Figures

Graphical abstract

23 pages, 1286 KB  
Article
Obesogenic Inflammatory Memory: A New Concept Related to the Dangerous Effects of Weight Cycling
by María del Carmen Navarro, María Dolores Hinchado, Elena Bote, Isabel Gálvez, Eduardo Otero, Miguel Palomino-Segura, Leticia Martín-Cordero and Eduardo Ortega
Biomolecules 2026, 16(2), 193; https://doi.org/10.3390/biom16020193 - 27 Jan 2026
Viewed by 834
Abstract
Obesity is associated with profound metabolic, inflammatory, and neurobehavioral dysfunctions. Dietary interventions leading to weight loss are commonly employed, yet it remains unclear whether all obesity-related alterations are fully reversed upon reaching normal body weight. Poor adherence to dietary regimens often results in [...] Read more.
Obesity is associated with profound metabolic, inflammatory, and neurobehavioral dysfunctions. Dietary interventions leading to weight loss are commonly employed, yet it remains unclear whether all obesity-related alterations are fully reversed upon reaching normal body weight. Poor adherence to dietary regimens often results in weight cycling, or yo-yo dieting, characterized by repeated episodes of weight gain and loss, a phenomenon linked to adverse health outcomes. Here, we investigated the consequences of weight cycling in C57BL/6J mice. The Control Group was maintained on a standard chow diet throughout the protocol, whereas the experimental group underwent two alternating cycles of high-fat diet feeding (weight gain) and standard diet reversion (weight loss), until the end of the protocol where both groups reached 80 weeks of age. Despite achieving a final body weight and glucose and lipid metabolic profile comparable to lean controls, weight-cycled mice exhibited impaired sensorimotor function, increased anxiety-like behavior (evaluated through behavioral tests), and persistent inflammation, including a peritoneal macrophage pro-inflammatory profile and adipose tissue infiltration. We define this phenomenon as “obesogenic inflammatory memory”, highlighting that obesity leaves an immunological imprint that sustains inflammation even after normalization of weight and metabolic parameters. These findings demonstrate that weight cycling is associated with chronic macrophage-mediated inflammatory states, linked to long-term behavioral and neurological manifestations, and opening new avenues for future investigation and therapeutic approaches. Full article
(This article belongs to the Special Issue Metabolic Inflammation and Insulin Resistance in Obesity)
►▼ Show Figures

Figure 1

15 pages, 3999 KB  
Article
Kisspeptin-10 Ameliorates Obesity-Diabetes with Diverse Effects on Ileal Enteroendocrine Cells and Pancreatic Islet Morphology in High-Fat Fed Female Mice
by Ananyaa Sridhar, Dawood Khan, Rithiga Muthukumar, Swetha Sampathkumar, Nigel Irwin, Peter R. Flatt and R. Charlotte Moffett
Biomolecules 2025, 15(11), 1591; https://doi.org/10.3390/biom15111591 - 13 Nov 2025
Viewed by 3188
Abstract
Kisspeptin is a neuropeptide recognised for a pivotal role within the reproductive system, but potentially important endocrine metabolic effects are less well understood. We examined effects of twice-daily intraperitoneal administration of saline vehicle or kisspeptin-10 (25 nmol/kg), for 21 days, on glucose homeostasis, [...] Read more.
Kisspeptin is a neuropeptide recognised for a pivotal role within the reproductive system, but potentially important endocrine metabolic effects are less well understood. We examined effects of twice-daily intraperitoneal administration of saline vehicle or kisspeptin-10 (25 nmol/kg), for 21 days, on glucose homeostasis, energy balance, circulating hormones as well as the morphology-function of enteroendocrine and islet cells in high-fat diet (HFD) fed female mice, with normal diet (ND) mice as an additional control group. Kisspeptin-10 decreased body weight, blood glucose and energy intake to ND levels. HFD increased circulating follicle-stimulating hormone (FSH) levels, which were further enhanced by kisspeptin-10 along with luteinising hormone (LH) concentrations. Neither HFD nor kisspeptin-10 affected progesterone or corticosterone. In the ileum, kisspeptin-10 decreased crypt depth and restored villi length to ND control levels, as well as increasing the proportion of glucose-dependent insulinotropic polypeptide (GIP) positive cells when compared to HFD mice and glucagon-like peptide-1 (GLP-1) positive cells compared to ND mice. Peptide YY (PYY) immunoreactivity was unaltered by HFD or kisspeptin-10. Plasma GIP was unchanged but circulating GLP-1 and PYY were reduced to ND levels. Within the pancreas, total islet, beta- and alpha-cell areas were similar in all mice, but kisspeptin-10 intervention restored relative insulin area to ND levels. Glucagon radius, an indicator of peripherally located alpha-cells, was reduced in HFD mice but normalised by kisspeptin-10 alongside elevated glucagon-islet area. Notably, beta-cell proliferation was increased by kisspeptin-10 with no alteration in beta-cell apoptosis. Overall, we reveal a previously uncharacterised diverse metabolic role for kisspeptin in directly modulating the gut–pancreatic axis. Full article
(This article belongs to the Special Issue Metabolic Inflammation and Insulin Resistance in Obesity)
►▼ Show Figures

Figure 1

Review

Jump to: Research

18 pages, 969 KB  
Review
Obesity-Mediated Inflammation and Its Influence on Inflammatory Bowel Disease: Pathophysiology, Clinical Impact, and Therapeutic Implications
by Diego Casas-Deza, Santiago García-López, Vanesa Bernal-Monterde, Cristina Polo-Cuadro, Carmen Yagüe-Caballero and José M. Arbones-Mainar
Biomolecules 2025, 15(8), 1185; https://doi.org/10.3390/biom15081185 - 18 Aug 2025
Cited by 7 | Viewed by 3964
Abstract
Obesity and inflammatory bowel disease (IBD) are two chronic conditions whose prevalence continues to rise globally. Emerging evidence suggests a bidirectional interplay between them, mediated by shared pathophysiological pathways. This narrative review explores the mechanisms Ilinking obesity to IBD development and progression, focusing [...] Read more.
Obesity and inflammatory bowel disease (IBD) are two chronic conditions whose prevalence continues to rise globally. Emerging evidence suggests a bidirectional interplay between them, mediated by shared pathophysiological pathways. This narrative review explores the mechanisms Ilinking obesity to IBD development and progression, focusing on the role of adipose tissue dysfunction. Both diseases exhibit intestinal dysbiosis, low-grade systemic inflammation, and impaired epithelial barrier integrity, contributing to immune activation. Visceral adiposity, particularly mesenteric fat, acts as an immunometabolic organ producing cytokines and adipokines that may exacerbate intestinal inflammation. In Crohn’s disease, mesenteric fat expansion, or “creeping fat”, is associated with transmural inflammation, fibrosis, and luminal narrowing. Epidemiological data on obesity as a risk factor for IBD remain inconsistent due to methodological heterogeneity and confounders. Similarly, the impact of obesity on IBD outcomes, including disease activity, phenotype, and the need for surgery, is debated. While mesenteric surgical approaches like Kono-S anastomosis showed initial promise in reducing recurrence, recent randomized trials offer conflicting results. Finally, metabolic drugs such as statins, metformin, and GLP-1 receptor agonists have demonstrated anti-inflammatory properties with potential utility in IBD management. Prospective studies are warranted to elucidate the clinical significance of obesity and metabolic dysfunction in IBD and evaluate targeted therapeutic strategies. Full article
(This article belongs to the Special Issue Metabolic Inflammation and Insulin Resistance in Obesity)
►▼ Show Figures

Figure 1

30 pages, 1661 KB  
Review
Gut Hormones and Inflammatory Bowel Disease
by Jonathan Weng and Chunmin C. Lo
Biomolecules 2025, 15(7), 1013; https://doi.org/10.3390/biom15071013 - 14 Jul 2025
Cited by 3 | Viewed by 5428
Abstract
Obesity-driven inflammation disrupts gut barrier integrity and promotes inflammatory bowel disease (IBD). Emerging evidence highlights gut hormones—including glucagon-like peptide-1 (GLP-1), glucagon-like peptide-2 (GLP-2), glucose-dependent insulinotropic polypeptide (GIP), peptide YY (PYY), cholecystokinin (CCK), and apolipoprotein A4 (APOA4)—as key regulators of metabolism and mucosal immunity. [...] Read more.
Obesity-driven inflammation disrupts gut barrier integrity and promotes inflammatory bowel disease (IBD). Emerging evidence highlights gut hormones—including glucagon-like peptide-1 (GLP-1), glucagon-like peptide-2 (GLP-2), glucose-dependent insulinotropic polypeptide (GIP), peptide YY (PYY), cholecystokinin (CCK), and apolipoprotein A4 (APOA4)—as key regulators of metabolism and mucosal immunity. This review outlines known mechanisms and explores therapeutic prospects in IBD. GLP-1 improves glycemic control, induces weight loss, and preserves intestinal barrier function, while GLP-2 enhances epithelial repair and reduces pro-inflammatory cytokine expression in animal models of colitis. GIP facilitates lipid clearance, enhances insulin sensitivity, and limits systemic inflammation. PYY and CCK slow gastric emptying, suppress appetite, and attenuate colonic inflammation via neural pathways. APOA4 regulates lipid transport, increases energy expenditure, and exerts antioxidant and anti-inflammatory effects that alleviate experimental colitis. Synergistic interactions—such as GLP-1/PYY co-administration, PYY-stimulated APOA4 production, and APOA4-enhanced CCK activity—suggest that multi-hormone combinations may offer amplified therapeutic benefits. While preclinical data are promising, clinical evidence supporting gut hormone therapies in IBD remains limited. Dual GIP/GLP-1 receptor agonists improve metabolic and inflammatory parameters, but in clinical use, they are associated with gastrointestinal side effects that warrant further investigation. Future research should evaluate combination therapies in preclinical IBD models, elucidate shared neural and receptor-mediated pathways, and define optimal strategies for applying gut hormone synergy in human IBD. These efforts may uncover safer, metabolically tailored treatments for IBD, particularly in patients with coexisting obesity or metabolic dysfunction. Full article
(This article belongs to the Special Issue Metabolic Inflammation and Insulin Resistance in Obesity)
►▼ Show Figures

Figure 1

Show export options expand_more Show export options expand_less
Select all
Export citation of selected articles as:
 
Displaying articles 1-5
Back to TopTop