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The Toll-like receptor 4 (TLR4) system emerges as the principal lipopolysaccharide (LPS) recognition apparatus, executing transmembrane signaling through myeloid differentiation primary response 88 (MyD88)-dependent phosphorylation cascades (Poltorak et al., 1998)

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Further understanding of the complex mechanisms that regulate metabolic homeostasis and how these become dysregulated during metabolic diseases, which are currently a major global burden, will likely lead to the development of new highly desirable more effective therapeutic strategies to combat metabolic diseases such as T2D

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