Figure 2.

Defects in glucose transport in IR. a) Increased expression of inflammatory cytokines (TNF-a, IL −1, IL6) dependent on TLR4/MYD88 activation are negatively involved in downstream insulin signaling (marked with red crosses). Furthermore, an imbalance in the production of microbiota-derived metabolites, including SCFAs and BAs, is indirectly related to insulin resistance through the modulation of their receptors. b) Hyperglycemia is a consequence of over-demand of insulin requirements; indeed, β-cells improve the restoration of glucose homeostasis through increased insulin biosynthesis. Over time, apoptosis exceeded the rate of replication, resulting in loss of β-cells and a reduction in β-cell mass. Created with BioRender.com.