IL1B and diabetes mellitus: They also trigger two major inflammatory pathways, known as stress-activated pathways, the Nuclear Factor kappa beta (NF-κB), mitogen-activated protein kinase (MAPK), and Jun N-terminal kinases (JNK), leading to the increased production of pro-inflammatory cytokines including IL-6, IL-1, and TNF-α from hypertrophic adipocytes [15,16,17], contributing to obesity-induced blocked insulin receptor activation, insulin resistance, and diabetes.