For a long time, there has been discussion in the medical community about how hormonal changes related to menopause in women could play a role in the development of Type 2 diabetes.
For just as long, though, there have been some unanswered questions — such as how big of a role menopause plays in raising a woman’s diabetes risk compared with other age-related changes, and exactly how losing estrogen might affect the regulation of glucose in your blood.
A new study, published earlier this month in the journal JCI Insight, sheds some light on the relationship between estrogen and blood glucose levels, showing how estrogen can help improve glucose tolerance in both estrogen-deprived mice and human cells.
Estrogen, your pancreas, and your intestines
For their experiment with mice, researchers at the University of Geneva in Switzerland looked at the effects of removing the mice’s ovaries on blood glucose control. When the mice were given an oral glucose tolerance test (OGTT), they had elevated blood glucose compared with mice that still had their ovaries. This suggests that estrogen, at least in mice, plays an important role in glucose metabolism — something researchers have long known or suspected.
What’s different about this study is what it examined, and discovered, at the cellular level. “We were able to isolate intestinal L cells and pancreatic insulin- and glucagon-producing cells, and for the first time show the effects of estrogens on these cells,” says lead researcher Jacques Philippe, MD,, a professor of medicine and chief of the division of endocrinology, diabetes, and nutrition at the University of Geneva.
Estrogen, Philippe notes, acts on hormone-producing cells in your pancreas and intestines in a number of different ways.
“In the pancreas, estrogens directly stimulate secretion of insulin, the hormone which lowers blood glucose after a meal, and inhibit secretion of glucagon, which elevates blood glucose,” says Philippe. Estrogen also stimulates the production of a hormone called GLP-1, which is produced in both the pancreas and the intestines — and GLP-1 acts to stimulate the release of insulin and inhibit the release of glucagon, as well.
When the mice in the study were given estrogen, the effects of estrogen deprivation on their glucose tolerance were reversed — with increased secretion of GLP-1 seen along with the effects on blood glucose levels. Increased GLP-1 secretion was also seen in cells from the mice that were removed and cultured when these cells were exposed to estrogen. The researchers also did the same with human cells from deceased donors, and found the same effect.
Implications for estrogen therapy?
Because this study examined only mice and human cells, it can’t offer any conclusions or recommendations regarding the use of hormone replacement therapy (HRT) to increase estrogen levels in women after menopause.
It does, though, point to mechanisms in both the pancreas and the intestines by which estrogen helps your body regulate glucose — and these processes support the idea that a higher risk of diabetes after menopause is due to estrogen deprivation, not just other age-related changes.
“By these mechanisms, which disappear after menopause, estrogens protect from diabetes,” Philippe emphasizes.
Philippe notes that further studies will be needed to learn how the timing and dosage of supplemental estrogen might reduce the risk of diabetes in postmenopausal women.
What’s clear now, though, is that estrogen plays a vital role in how women’s bodies handle glucose. If you’re going through menopause or have done so recently, it may be worthwhile to discuss this topic with your doctor.
Want to learn more about women’s health and diabetes? Read “Top 10 Health Tips for Women Over 65,” “Pregnant and Pumping,” and “Pregnancy and Type 1 Diabetes.”
