This review highlights metabolic inflammation's role in insulin resistance in type 2 diabetes mellitus, suggesting improved therapeutic approaches.
Aim: This review summarizes current understanding of metabolic inflammation and immune metabolism in Type 2 Diabetes Mellitus (T2DM). Methods: A comprehensive review of the literature was conducted in PubMed using keywords like diabetes, metabolic inflammation, immune metabolism, β- cell dysfunction, and insulin resistance to identify published research articles. Peer-reviewed articles on humans or animal models published in English and focusing on the mechanism of β-cell disruption, reduced insulin responsiveness, and the interplay of metabolic and immune pathways with respect to type 2 diabetes mellitus (T2DM) were included. In contrast, those focusing solely on Type 1 or gestational diabetes were excluded. Titles and abstracts were screened for relevance, and the data were qualitatively synthesized to highlight the interplay among immune cells, inflammatory pathways, and metabolic dysfunction in T2DM. Result: Type 2 diabetes mellitus (T2DM) is increasingly recognized as a disease characterized by chronic low-grade inflammation and intricate connections between immune and metabolic pathways. Metabolic inflammation promotes insulin resistance and β-cell dysfunction through immune cell infiltration and cytokine-mediated signaling in metabolic tissues. These processes lead to the generation of pro-inflammatory cytokines that worsen insulin resistance and accelerate β-cell death, creating a self-perpetuating cycle of immune activation and metabolic stress. Conclusions: The immune system and metabolism are intricately intertwined, as metabolic processes influence immune cell activity and vice versa. The interplay between immune system cells and metabolic processes may exacerbate insulin resistance and complicate T2DM therapy. A multidisciplinary strategy that integrates immunology, endocrinology, and metabolic research is critical for developing comprehensive and more effective T2DM treatment approaches.
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Pandey et al. (2026) studied this question.
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