Nano-Enabled Regulation of Adipokines and Cytokine Signaling in Obesity-Induced Inflammatory Pathways
Winniefred Nankya
Department of Clinical Pharmacy Kampala International University Uganda
Email:winniefred.nankya@studwc.kiu.ac.ug
ABSTRACT
Obesity is characterized by an imbalance in energy homeostasis, leading to an increase in adiposity and the subsequent release of adipokines and cytokines, which play a pivotal role in the pathogenesis of obesity associated inflammation. This inflammation is a critical factor in the development of obesity-related comorbidities, such as type 2 diabetes, cardiovascular disease, and certain cancers. Recent advancements in nanotechnology have opened new therapeutic avenues to regulate adipokines and cytokines, offering promising strategies for modulating obesity-induced inflammatory pathways. Nano-enabled approaches, including nanomaterials, nanoparticles, and nanostructures, have demonstrated their potential in enhancing the bioavailability, stability, and targeted delivery of therapeutic agents. Moreover, these nanomaterials can interact with adipocytes, immune cells, and the extracellular matrix to modulate the expression and secretion of proinflammatory adipokines and cytokines. This review explores the current understanding of nano-enabled regulation of adipokines and cytokine signaling, highlighting the mechanisms through which nanoparticles influence key inflammatory pathways. Furthermore, the article examines the applications of nano-based
therapies in controlling obesity-induced inflammation and their potential for mitigating obesity-related diseases. Finally, the challenges, limitations, and future directions of nanotechnology in obesity management are discussed.
Keywords: Obesity, Adipokines, Cytokines, Nano-therapy, Inflammation.
CITE AS: Winniefred Nankya (2026). Nano-Enabled Regulation of Adipokines and Cytokine Signaling in Obesity-Induced Inflammatory Pathways. NEWPORT INTERNATIONAL JOURNAL OF SCIENTIFIC AND EXPERIMENTAL SCIENCES, 7(2):54-59.
https://doi.org/10.59298/NIJSES/2026/72.5459