The increased prevalence of diabetes and associated complications presents a major health risk worldwide, and requires an
efficient management protocol. Type-1 and type-2 diabetes have several common pathophysiological denominators including
hyperglycemia, elevated oxidative stress, increased inflammation and apoptosis. These pathological factors are implicated in the progression
and worsening of the disease, and the related cardiometabolic complications associated with it. Despite the advancement in management
of type-1 and type-2 diabetes, the high incidence of diabetes and related complications calls for novel therapeutic strategies. Recent
findings suggest that the pharmacological modulation of the microsomal heme oxygenase (HO) system may be an important
therapeutic avenue to explore. The HO system and related products such as carbon monoxide, bilirubin, biliverdin, biliverdin reductase
and ferritin have been shown to abate inflammation, oxidative stress, and apoptosis and reduce hyperglycemia. In addition, the HO
system also enhances insulin sensitivity and increase pancreatic beta cell insulin production in experimental models of type-1 and type-2
diabetes. This review is an effort to provide evidence of the regulatory and cytoprotective role of the HO system in type-1 and type-2
diabetes, and will highlight the multifaceted mechanisms implicated in the anti-diabetic effects of the HO system.
Keywords: Inflammation, Insulin resistance, Oxidative stress, Pro-inflammatory cytokines, Activation transcription factors, Adiponectin.
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