1.5 Pathophysiology

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1.5 Pathophysiology^{1, 2, 4-6}

1.5.1 Type 1 diabetes

It is mostly caused by autoimmune destruction of the beta cells in the pancreas, resulting in a severe reduction in insulin production. Genetic susceptibility, an environmental factor like viral infection and autoimmunity, in combination, plays an important role in the development of T1DM. Some T1DM cases are idiopathic in nature.

1.5.2 Type 2 diabetes

Insulin resistance and beta cell failure represent the main pathophysiologic defects in T2DM. Subjects with T2DM are maximally insulin resistant and have lost approximately 50% of their beta cell function. The degree of insulin resistance and beta cell loss defer from one type to another type and that is why the presentation of T2DM is heterogeneous. Gradual loss of beta cell function is characteristic of T2DM over the course of time. In addition, muscle (impaired glucose disposal), liver (increased glucose production), beta cell (reduced insulin production), fat cell (accelerated lipolysis), gastrointestinal tract (incretin deficiency/resistance), alpha cell (hyperglucagonemia), kidney (increased glucose reabsorption), and brain (insulin resistance) – all play important roles in the development of glucose intolerance in T2DM individuals. Collectively, these eight pathways comprise the ominous octet.

1.5.3 Gestational diabetes mellitus

This type of diabetes is caused by placental hormones, namely beta hCG, human placental lactogen, estrogen, progesterone, etc. antagonizing the action of insulin.