Insulin resistance occurs normally in pregnancy to ensure that nutrients are provided to the growing fetus.1–3 Pregnancy is considered a test for β-cell reserve. If there is good function, insulin resistance will be overcome; if not, gestational diabetes will occur.
Lipid deposition in muscle fibres (intramyocellular) could be one of the possible mechanisms of insulin resistance in gestational diabetes mellitus.3,4 A poor insulin-release response, possible fat deposition in the skeletal muscle, or ectopic fat deposition may cause dysfunctional homeostasis in gestational diabetes mellitus,4 which may in turn influence the fine tuning of the metabolic machinery of a growing fetus. Offspring may thus be more prone to glucose intolerance and ectopic lipid deposition.
The finding in Blotsky and colleagues’ article in CMAJ that children born to mothers with gestational diabetes mellitus are prone to glucose intolerance5 may be a sign that the β-cell function of such children should be monitored.
Footnotes
Competing interests: None declared.