Stress and Carbohydrate Metabolism

The essential end product of carbohydrate metabolism in the body is glucose. Although the carbohydrates we ingest can be in different forms such as sucrose, lactose, maltose, and starches, in the end they all are broken down to glucose. The glucose may then undergo glycogenesis or lipogenesis for storage or utilized for energy via aerobic (citric acid cycle) or anaerobic pathways.

Like many other processes in the body, stress also effects carbohydrate metabolism. Hypothalamic activation causes an increase in sympathetic nervous system tone resulting in secretion of catecholamines from the adrenal glands and glucagon from the pancreas. Catecholamines act on Beta-2 receptors to increase glycogenolysis, hepatic gluconeogenesis, glucagon release, and inhibit glycogen production. Hypothalamic activation also results in CRH release stimulating glucocorticoid release (i.e. cortisol) from the adrenal glands. Cortisol stimulates gluconeogenesis in addition to causing increased insulin resistance.

The release of cortisol, catecholamines, and glucagon along with the increased peripheral resistance to insulin result in increased endogenous glucose production and hyperglycemia as the body is trying to maximize available substrates for energy production.

Updated definition 2020:

Overall goal is to increase glucose availability for carbohydrate metabolism:

• Increased peripheral glucose uptake via facilitated diffusion across insulin vs non-insulin mediated (GLUT)receptors and secondary active transport

• Hyperlactatemia occurs under anaerobic conditions after the metabolism of pyruvate, a glycolic pathway end product. Lactate dehydrogenase is the enzyme that does this.

• Increased glucose production or gluconeogenesis occurs via increased activity of phosphoenol pyruvate carbohydrates kinase(PEPCK), pyruvate carboxylase, fructose 1,6 bis phosphatase (FBPase) and glucose 6 phosphatase. Usually regulated by glucocorticoids.

• Decreased glycogenesis in liver and skeletal muscles. Stress causes inhibition if glycogen synthase by phosphorylation by glycogen synthase kinase 3 (GSK 3)

• Glucose intolerance and insulin resistance that is partly thought to be due to glucocorticoids preventing translocation of glucose transporters to the plasma membrane.