Sex hormones have been shown to impact glucose metabolism and homeostasis; in some cases, the effect is so prominent as to induce glucose intolerance, or even full blown type 2 diabetes. The molecular pathways responsible for these changes are being revealed as of 2011 and continue to indicate a role for estrogen in excessive insulin production in the pancreas, in some cases exhausting the insulin-secreting Beta cells, thus leading to disease.
Pancreatic Insulin Regulation
A 2008 study from the University of Bremen-Germany demonstrated the presence of estrogen receptors on pancreatic Beta cells, which are responsible for insulin production in your body. The study looked at the effect of long-term exposure to normal levels of estrogen on Beta cells; the researchers found increased insulin content, insulin gene expression and insulin release from the cells. These adaptations occurred without hypertrophy of the pancreas; in other words, the increases are due to increased activity in each individual cell, rather than just an increase in total cell number.
Effect of Estrogen on Diabetes Risk
A 2002 study published by the American Diabetes Association examined the association between estrogen use in postmenopausal women and insulin/glucose levels in these individuals. The researchers also investigated the effect of estrogen therapy on the risk of developing type 2 diabetes. The data indicates that estrogen use in postmenopausal American Indian women is associated with a decrease in glucose tolerance; the probability of disease increased with the duration of estrogen therapy. This study suggests that estrogen not only increases insulin production but it clearly increases release and ultimately produces low blood glucose levels. Over time, this excessive insulin stimulation leads to a loss of glucose tolerance as the supply of insulin deteriorates and the patient develops type 2 diabetes.
Insulin Resistance
Excess levels of estrogen production, or the presence of an environmental estrogen such as BPA, have been shown to produce an increase in insulin signaling. A 2009 review from the "Journal of Molecular and Cellular Endocrinology" describes how the excess of insulin may be so high as to induce insulin resistance in liver and muscle throughout the body; this may be accompanied by exhaustion of the Beta cells, which ultimately leads to glucose intolerance. When your pancreas is unable to produce insulin, your blood sugar will be highly variable and will fluctuate based on diet. This condition is referred to as type 2 diabetes and requires management with diet or medication.
Applications
The higher levels of estrogen in women may partially account for higher proportions of fat in women; the increased insulin secretion will induce fat storage. Evolutionarily, this adaptation makes sense; the presence of female hormones in the blood will automatically induce fat storage, conceivably for maintaining high energy levels during pregnancy.
References
- "PLoS One"; Pancreatic Insulin Content Regulation by the Estrogen Receptor ER-alpha; Paloma Alonso-Magdalena, et.al; 2008
- "Diabetes Care"; The Effect of Estrogen Use on Levels of Glucose and Insulin and the Risk of Type 2 Diabetes in American Indian Postmenopausal Women; Ying Zhang, et al.; 2002
- "Molecular and Cellular Endocrinology"; The pancreatic Beta-cell as a target of estrogens and xenoestrogens: Implications for blood glucose homeostasis and diabetes; Angel Nadal, et al.; 2009
