J Clin Endocrinol Metab. 2026 Sep 15:dgag379. doi: 10.1210/clinem/dgag379. Online ahead of print.
ABSTRACT
Women with diabetes experience substantial fluctuations in insulin sensitivity across the reproductive lifespan, yet clinical guidance on managing these glycemic challenges remains limited. This review synthesizes current evidence on the metabolic impact of key hormonal transitions, including puberty, the menstrual cycle, fertility treatment, pregnancy, and menopause, in women with type 1 (T1DM) and type 2 diabetes (T2DM). Puberty is marked by a physiological decline in insulin sensitivity compounded by behavioral and neurocognitive factors, contributing to dysglycemia and increased cardiometabolic risk. Cyclical variations in estradiol and progesterone influence insulin resistance across the menstrual cycle, but existing data predominantly concern T1DM, leaving major knowledge gaps for T2DM. As fertility treatment becomes more common, understanding the glycemic effects of ovarian stimulation is increasingly important, though current evidence remains sparse. Pregnancy represents a period of pronounced insulin resistance, but advances in diabetes technology, particularly continuous glucose monitoring (CGM) and automated insulin delivery systems, have improved maternal glycemic control and neonatal outcomes and should be integrated into preconception and pregnancy care. In menopause, declining estrogen and relatively preserved androgen levels contribute to increased insulin resistance; menopausal hormone therapy (MHT) may improve glycemia, though evidence in T1DM is limited. Across all life stages, the historical underrepresentation of women in metabolic research has hindered development of evidence-based strategies for managing hormonally driven glucose excursions. Future studies integrating CGM with detailed hormonal profiling, particularly in women with T2DM and those undergoing fertility treatment or MHT, are essential to optimize diabetes care throughout the female lifespan.
PMID:42740693 | DOI:10.1210/clinem/dgag379
