“Stressed” is “desserts” spelled backwards: Why weight gain is due to stress

The increased incidence of diabetes in society today is well-known.  According to the Centers for Disease Control and Prevention (CDC), more than one-third of U.S. adults are obese and 11.3% of U.S. adults have diabetes.  What is less known is the role that norepinephrine can play in insulin release and the development of metabolic syndrome and type 2 diabetes.

Figure 1. Normal function of a pancreatic beta cell involves insulin granules docking at the edge of the cell to release insulin in the extracellular space (Gribble, 2010).

Figure 1. Normal function of a pancreatic beta cell involves insulin granules docking at the edge of the cell to release insulin in the extracellular space (Gribble, 2010).

Normally, insulin granules are docked at the edge of pancreatic beta cells to release insulin in response to protein and glucose in the blood (Figure 1).  Insulin causes muscles and fat tissue to absorb glucose from the blood.  Too much glucose in the blood can be toxic and is a hallmark sign of diabetes and metabolic syndrome.

Some individuals have too many α2A-adrenergic receptors that norepinephrine binds to on the pancreatic beta cells that produce insulin (Figure 2). These additional receptors block the insulin granules from docking at the edge of the beta cells, which reduces the amount of insulin released.  Too much norepinephrine activity can lead to less insulin release in individuals who are genetically wired with too many receptors.  Less insulin released can’t regulate blood glucose, leading to higher glucose levels (hyperglycemia) and the development of adrenergic diabetes.  When α2A-adrenergic receptors are blocked by antagonists, insulin granules begin docking again and insulin release returns to normal.

Figure 2. The susceptible genotype for adrenergic diabetes has increased numbers of α2A-adrenergic receptors on pancreatic beta cells.  This inhibits the docking of insulin granules preventing the release of insulin (Gribble, 2010).

Figure 2. The susceptible genotype for adrenergic diabetes has increased numbers of α2A-adrenergic receptors on pancreatic beta cells. This inhibits the docking of insulin granules preventing the release of insulin (Gribble, 2010).

One clinical result of excess α2A-adrenergic receptors is stress-induced hyperglycemia.  Stress-induced hyperglycemia is characterized by elevated blood glucose in response to stress.  This could be caused by increased norepinephrine being released as a response to stress decreasing the amount of insulin that would control blood sugar.  Genetic differences that cause varying levels of the α2A-adrenergic receptors aid our understanding why one patient may be susceptible to stress-induced hyperglycemia, while another may not.

Remember these connections the next time you or a patient is experiencing chronic stress and consider addressing a patient’s stress response as a primary therapy in cases of stress-induced hyperglycemia or as part of your comprehensive blood sugar management approach.  Excessive norepinephrine release from a stress response can lead to metabolic issues due to subsequent decreased insulin release.

References:
http://www.cdc.gov/diabetes/pubs/pdf/ndfs_2011.pdf
http://www.cdc.gov/obesity/data/adult.html
Gribble FM. Phil D.  (2010). a2A adrenergic receptors and type 2 diabetes.  New Eng J Med, 4: 361-362.
Kyrou I. Tsigos C. (2007). Stress mechanisms and metabolic complications.  Horm Metab Res, 39(6): 430-8.
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