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Nutrients
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Nutrition, Adipose Tissue, and Human Health
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Nutrition, Adipose Tissue, and Human Health

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

Deadline for manuscript submissions: closed (15 October 2025) | Viewed by 12171

Special Issue Editor

Dr. Dimiter Avtanski

E-Mail Website
Guest Editor
1. Friedman Diabetes Institute, Lenox Hill Hospital, Northwell Health, New York, NY 10022, USA
2. Feinstein Institutes for Medical Research, Hempstead, NY 11030, USA
3. Donald and Barbara Zucker School of Medicine at Hofstra/Northwell, Hempstead, NY 11549, USA
Interests: adipose tissue; obesity; inflammation; diabetes; breast cancer
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Adipose tissue, once viewed simply as an energy storage depot, is now recognized as a complex endocrine organ. It releases a wide range of bioactive molecules that influence systemic metabolism, inflammation, and overall health. Disruptions in adipose tissue function, often associated with obesity, can trigger chronic inflammation and contribute to the development of metabolic diseases such as type 2 diabetes, cardiovascular disease, dyslipidemia, and liver disease.

Nutrition plays a crucial role in modulating adipose tissue function. Dietary patterns, specific nutrients, and bioactive food components can either exacerbate or mitigate adipose tissue dysfunction and related inflammation. This Special Issue aims to explore the latest research on the intersection of adipose tissue, nutrition, inflammation, and chronic disease. We welcome original research articles, reviews, and perspectives that address the following topics:

Mechanisms linking adipose tissue dysfunction to metabolic disease.
The impact of dietary components on adipose tissue inflammation and endocrine functions.
Nutritional interventions for targeting adipose tissue-related inflammation and metabolic health.
The role of the gut microbiome in the adipose–nutrition axis.
Novel strategies for assessing adipose tissue function and its response to nutritional interventions.

Dr. Dimiter B. Avtanski
Guest Editor

Manuscript Submission Information

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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. Nutrients is an international peer-reviewed open access semimonthly 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 2900 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

  • adipose tissue
  • nutrition
  • obesity
  • inflammation
  • metabolic disease
  • type 2 diabetes
  • dyslipidemia
  • liver disease
  • cardiovascular disease
  • endocrine function
  • gut microbiome

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Published Papers (4 papers)

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Research

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16 pages, 577 KB  
Article
Liver Fibrosis Is Positively and Independently Associated with Leptin Circulating Levels in Individuals That Are Overweight and Obese: A FibroScan-Based Cross-Sectional Study
by Nicole Cerabino, Martina Di Chito, Davide Guido, Vincenza Di Stasi, Caterina Bonfiglio, Giuseppe Lisco, Endrit Shahini, Marianna Zappimbulso, Raffaele Cozzolongo, Valeria Tutino, Arianna Diciolla, Rosanna Mallamaci, Dolores Stabile, Anna Ancona, Sergio Coletta, Pasqua Letizia Pesole, Gianluigi Giannelli and Giovanni De Pergola
Nutrients 2025, 17(11), 1908; https://doi.org/10.3390/nu17111908 - 1 Jun 2025
Cited by 5 | Viewed by 1476
Abstract
Background: Metabolic dysfunction-associated steatotic liver disease (MASLD) is strongly correlated with the severity of obesity, and the extent of liver fibrosis is associated with a higher risk of liver-related complications, cardiovascular events, and overall mortality. Leptin circulating levels are directly correlated with the [...] Read more.
Background: Metabolic dysfunction-associated steatotic liver disease (MASLD) is strongly correlated with the severity of obesity, and the extent of liver fibrosis is associated with a higher risk of liver-related complications, cardiovascular events, and overall mortality. Leptin circulating levels are directly correlated with the amount of adipose tissue. Aims: In the present study, we investigated the association between circulating leptin levels and liver steatosis and fibrosis. Methods: Eighty-six patients (41.7 ± 12.6 yrs, 35 men, 41%), naïve to medications, who attended the Nutrition Center for the Research and Care of Obesity and Metabolic Diseases at the National Institute of Gastroenterology “Saverio de Bellis” for weight management, were cross-sectionally evaluated. Demographic, anthropometric, clinical, and laboratory data were collected and analyzed. All patients underwent liver ultrasonographic assessment by FibroScan to diagnose liver steatosis (controlled attenuation parameter, CAP > 275 dBm) and fibrosis (liver stiffness measurement, LSM > 8.2 kPa). Results: Sixty-three individuals (73.3%) had liver steatosis, and 17 (19.8%) had liver fibrosis. The mean leptin levels were 22.3 ± 14.1 ng/mL, while the BMI and waist circumference were 36.7 ± 7.2 kg/m2 and 114.5 ± 16.4 cm, respectively. CAP values exhibited no correlation with leptin (r = 0.09, p = 0.436), while a significant connection was seen between leptin and LSM (β = 0.065; p = 0.038). Specifically, for each unit increase in leptin, LSM values were varied by +0.065 units (p = 0.038). This association was independent of gender, age, insulin resistance, adiponectin, RBP4, and visfatin. This is the first study showing these results by using FibroScan assessment in patients naïve to medications. Conclusions: Circulating leptin concentrations are independently correlated with hepatic fibrosis in individuals with a BMI ≥ 25 kg/m2. These findings indicate a function for leptin in promoting liver fibrosis; however, longitudinal studies are required to elucidate the causal nature of this interaction. Full article
(This article belongs to the Special Issue Nutrition, Adipose Tissue, and Human Health)
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14 pages, 6952 KB  
Article
Chronic Low-Grade Inflammation and Brain Structure in the Middle-Aged and Elderly Adults
by Yujia Bao, Xixi Chen, Yongxuan Li, Shenghao Yuan, Lefei Han, Xiaobei Deng and Jinjun Ran
Nutrients 2024, 16(14), 2313; https://doi.org/10.3390/nu16142313 - 18 Jul 2024
Cited by 14 | Viewed by 5006
Abstract
Low-grade inflammation (LGI) mainly acted as the mediator of the association of obesity and inflammatory diet with numerous chronic diseases, including neuropsychiatric diseases. However, the evidence about the effect of LGI on brain structure is limited but important, especially in the context of [...] Read more.
Low-grade inflammation (LGI) mainly acted as the mediator of the association of obesity and inflammatory diet with numerous chronic diseases, including neuropsychiatric diseases. However, the evidence about the effect of LGI on brain structure is limited but important, especially in the context of accelerating aging. This study was then designed to close the gap, and we leveraged a total of 37,699 participants from the UK Biobank and utilized inflammation score (INFLA-score) to measure LGI. We built the longitudinal relationships of INFLA-score with brain imaging phenotypes using multiple linear regression models. We further analyzed the interactive effects of specific covariates. The results showed high level inflammation reduced the volumes of the subcortex and cortex, especially the globus pallidus (β [95% confidence interval] = −0.062 [−0.083, −0.041]), thalamus (−0.053 [−0.073, −0.033]), insula (−0.052 [−0.072, −0.032]), superior temporal gyrus (−0.049 [−0.069, −0.028]), lateral orbitofrontal cortex (−0.047 [−0.068, −0.027]), and others. Most significant effects were observed among urban residents. Furthermore, males and individuals with physical frailty were susceptive to the associations. The study provided potential insights into pathological changes during disease progression and might aid in the development of preventive and control targets in an age-friendly city to promote great health and well-being for sustainable development goals. Full article
(This article belongs to the Special Issue Nutrition, Adipose Tissue, and Human Health)
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Review

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28 pages, 602 KB  
Review
Nutrient-Induced Remodeling of the Adipose-Cardiac Axis: Metabolic Flexibility, Adipokine Signaling, and Therapeutic Implications for Cardiometabolic Disease
by Nikola Pavlović, Petar Todorović, Mirko Maglica, Marko Kumrić and Joško Božić
Nutrients 2025, 17(24), 3945; https://doi.org/10.3390/nu17243945 - 17 Dec 2025
Viewed by 975
Abstract
Insulin resistance, dyslipidemia, hypertension, and visceral adiposity are the leading causes of the growing worldwide health burden associated with metabolic syndrome, obesity, and cardiovascular diseases (CVDs). Despite the “obesity paradox,” which emphasizes the varied cardiovascular outcomes among obese people, obesity is now acknowledged [...] Read more.
Insulin resistance, dyslipidemia, hypertension, and visceral adiposity are the leading causes of the growing worldwide health burden associated with metabolic syndrome, obesity, and cardiovascular diseases (CVDs). Despite the “obesity paradox,” which emphasizes the varied cardiovascular outcomes among obese people, obesity is now acknowledged as an active contributor to cardiometabolic dysfunction through endocrine, inflammatory, and metabolic pathways. Growing evidence indicates that nutrition is a key determinant of cardiometabolic risk, highlighting the need to understand diet-mediated mechanisms linking adipose tissue to cardiac function. Adipokines, including adiponectin, leptin, TNF-α, and resistin, which regulate systemic inflammation, metabolic homeostasis, and myocardial physiology, are secreted by adipose tissue, which is no longer thought of as passive energy storage. Its heterogeneous phenotypes, white, brown, and beige adipose tissue, exhibit distinct metabolic profiles that influence cardiac energetics and inflammatory status. Nutrient-driven transitions between these phenotypes further underscore the intricate interplay between diet, adipose biology, and cardiac metabolism. Central nutrient-sensing pathways, including mTOR, AMPK, SIRT1, PPAR-γ, and LKB1, integrate macronutrient and micronutrient signals to regulate adipose tissue remodeling and systemic metabolic flexibility. These pathways interact with hormonal mediators such as insulin, leptin, and adiponectin, forming a complex regulatory network that shapes the adipose-cardiac axis. This review synthesises current knowledge on how nutrient inputs modulate adipose tissue phenotypes and signaling pathways to influence cardiac function. By elucidating these mechanisms, we highlight emerging opportunities for precision nutrition and targeted therapeutics to restore metabolic balance, strengthen cardiac resilience, and reduce the burden of cardiometabolic disease. Full article
(This article belongs to the Special Issue Nutrition, Adipose Tissue, and Human Health)
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31 pages, 5869 KB  
Review
Lipid Metabolism–Signaling Crosstalk in Metabolic Disease and Aging: Mechanisms and Therapeutic Targets
by Paalki Sethi, Awdhesh Kumar Mishra, Shampa Ghosh, Krishna Kumar Singh, Samarth Sharma, Radoslav Stojchevski, Dimiter Avtanski and Jitendra Kumar Sinha
Nutrients 2025, 17(23), 3699; https://doi.org/10.3390/nu17233699 - 26 Nov 2025
Cited by 3 | Viewed by 3900
Abstract
Lipid metabolism and lipid-derived signaling together ensure cellular and systemic homeostasis. Their dysregulation causes obesity, type 2 diabetes, cardiovascular disease, NAFLD/MASH, and neurodegeneration throughout life. This review integrates central pathways, such as ACC–FASN-mediated de novo lipogenesis, lipid-droplet lipolysis, and mitochondrial and peroxisomal β-oxidation, [...] Read more.
Lipid metabolism and lipid-derived signaling together ensure cellular and systemic homeostasis. Their dysregulation causes obesity, type 2 diabetes, cardiovascular disease, NAFLD/MASH, and neurodegeneration throughout life. This review integrates central pathways, such as ACC–FASN-mediated de novo lipogenesis, lipid-droplet lipolysis, and mitochondrial and peroxisomal β-oxidation, and their regulation by insulin–PI3K–Akt, glucagon–cAMP–PKA, SREBPs, PPARs, and AMPK. We emphasize the mechanisms by which bioactive lipids like diacylglycerols, ceramides, eicosanoids, and endocannabinoids serve as second messengers linking nutrient state to insulin signaling, inflammation, and stress response; pathologic accumulation of these species enhances insulin resistance and lipotoxicity. Aging disrupts these axes via diminished catecholamine-stimulated lipolysis, defective fatty-acid oxidation, mitochondrial failure, and adipose depot redistribution, facilitating ectopic fat and postprandial dyslipidemia. We suggest a pathway-to-phenotype paradigm that connects lipid species and tissue environment to clinical phenotypes, allowing for mechanism-to-intervention alignment. Therapeutic avenues range from lipid lowering for atherogenic risk to novel agents targeting ACLY, ACC, FASN, CPT1, and nuclear receptors, with precision lifestyle intervention in diet and exercise. Translation is still heterogeneous because of isoform-dependent effects, safety trade-offs, and inconsistent adherence. We prioritize harmonization of lipidomics with multi-omics for stratifying patients, enriching responders, and bridging gaps between mechanistic understanding and clinical outcome, with focus on age-sensitive prevention and treatment for lipid-mediated metabolic disease. Full article
(This article belongs to the Special Issue Nutrition, Adipose Tissue, and Human Health)
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