Why do sugars go high during pregnancy?

Normally in pregnancy the placental steroid and peptide hormones (e.g. estrogens, progesterone, and chronic somatomammotropin) raise linearly throughout the second and third trimesters. In pregnancy, human placental lactogen, which is structurally similar to growth hormone, and tumor-necrosis factor-alpha induce changes in the insulin receptor and in post-receptor signaling.

Changes in the beta-subunit of the insulin receptor, decreased phosphorylation of tyrosine kinase on the insulin receptor, and alterations in insulin receptor substrate-1 (IRS-1) and the intracytoplasmic phosphatidylinositol 3-kinase (PI3K) appear to be involved in reducing glucose uptake in skeletal muscle tissue.

As a consequence, there is an increase in tissue insulin resistance; there is an increase in insulin secretion with feeding which escalates progressively during pregnancy. By the third trimester, 24-hour mean insulin levels are 50% higher than in the nonpregnant state. In normoglycemic pregnant women, there is a tendency for hypoglycemia (plasma glucose mean = 65–75 mg/dL) in fasting and postabsorptive phases. This is because the fetus continues to transfer glucose across the placenta from the maternal bloodstream, even during periods of fasting irrespective of maternal glucose. Hypoglycemia becomes increasingly severe in postabsorptive state as pregnancy progresses as the glucose demand of the fetus increases. In contrast to this, in glucose intolerant pregnant women as in polycystic ovary syndrome (PCOS) or metabolic syndrome, the beta cells may fail to meet this demand leading to impaired glucose tolerance. This typically manifests as recurrent postprandial hyperglycemic episodes. These postprandial episodes are the most significant source of the accelerated growth exhibited by the fetus.