Diabetes and Its Link with Cancer: Providing the Fuel and Spark to Launch an Aggressive Growth Regime

Figure 1

Under normal conditions, insulin is secreted from pancreatic β-cells in response to an increase in plasma glucose levels. It promotes glucose uptake into skeletal muscle and adipose tissue while suppressing hepatic glucose output, resulting in maintenance of blood glucose concentration to ~5 mM (a). In insulin resistant individuals, an increased amount of insulin is required to compensate for diminished effects on insulin-target organs, giving rise to hyperinsulinaemia. As insulin resistance worsens, blood glucose level gradually increases despite increased insulin secretion and a prediabetic state is established (b). In susceptible individuals, relative insulin deficiency progressively develops due to failure of β-cells to secrete adequate levels of insulin, resulting in loss of glucose homeostasis if exogenous insulin is not provided (c).

(a)

(b)

(c)