Glucose metabolism in lymphoid and inflammatory cells and tissues.

PURPOSE OF REVIEW: To examine the role of glucose as a fuel for immune cells and the influence of glucose supply on immune-cell functional responses. RECENT
FINDINGS: Immune cells express the insulin receptor and a range of glucose-transporter isoforms. Glucose transporters are responsive to both immune stimulation and insulin. The pattern of glucose-transporter upregulation differs among different types of immune cell. In-vitro studies reveal that both hypo- and hyperglycaemia impair immune-cell functions and promote inflammatory responses. Clamp studies have revealed proinflammatory effects of hyperglycaemia and antiinflammatory and immune-promoting effects of insulin.
SUMMARY: Glucose is readily utilized by cells of the immune system and is used to generate energy and biosynthetic precursors. Activation of immune cells is associated with increased glucose utilization and this is facilitated, in part, by increased expression of glucose transporters. Immune cells express the insulin receptor and respond to insulin. Both hypo- and hyperglycaemia impair immune-cell functions and promote inflammatory responses. Insulin therapy in hyperglycaemic subjects may be of benefit through effects of both insulin itself and lowered glucose concentration. Excessive lowering of blood glucose concentration may also be harmful to the immune response.