In plain words
Insulin resistance of pregnancy is the normal rise in that happens during pregnancy, mainly in the second half. It is the same process as insulin resistance, now driven by hormones made by the placenta. The change sends more sugar and fat to the baby. Blood sugar after meals stays higher, and the pancreas responds by making more insulin. For most people, this rise is enough to meet the baby's needs. For some, the body cannot make enough extra insulin, and develops. Insulin resistance of pregnancy is not a disease, and it is not caused by anything a mother did. It is usually detected through blood sugar screening rather than a direct test. Ask your provider how your results compare with the usual ranges.
The deeper version
Insulin resistance of pregnancy is the physiologic decline in peripheral insulin sensitivity that begins in the second trimester and peaks in the third. Placental hormones, including , placental growth hormone, progesterone, and cortisol, along with adipokines and cytokines such as TNF-alpha, impair insulin signaling in muscle and adipose tissue. Lain and Catalano (2007) describe the scale of the change, with insulin sensitivity falling by roughly half or more by the third trimester. Gestational diabetes occurs when beta-cell compensation fails. Whether the size of this change should guide screening, and how it relates to later metabolic health, remain open questions.
Where it comes up
- Gestational diabetesPregnancy: Your Body
- Eating with gestational diabetesPregnancy: Eating
- Weight gain in pregnancyPregnancy: Your Body
What mothers here say about insulin resistance of pregnancy
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Sources
- Lain KY, Catalano PM — Metabolic changes in pregnancy. Clinical Obstetrics and Gynecology, 2007