FIGURE 2.

An overview of pathological mechanisms implicated in the development of diabetes mellitus or related metabolic complications. Briefly, overnutrition (which may be characterized by increased adipocyte size) and consistent increased levels of glucose (a state of hyperglycemia) may induce detrimental effects in major organs of the body including the skeletal muscle, liver, and kidneys, and thus aggravate metabolic complications through enhanced oxidative stress and exacerbated inflammation. This consequence is predominantly characterized by impaired glucose homeostasis/insulin signaling, ectopic lipid accumulation, mitochondrial dysfunction, endoplasmic reticulum (ER) stress insufficient or decreased antioxidant responses/increased ROS (reactive oxygen species) production and altered actions of inducible nitric oxide synthase (iNOS) and lipid peroxidation/DNA damage. This may occur along with raised pro-inflammatory markers like tumor necrosis factor-alpha (TNF-α), like nuclear factor kappa β (NF-κβ), c-Jun N-terminal kinases (JNK) and interleukin-6 (IL-6).