Telomeres are shorter in placentas from pregnancies with uncontrolled diabetes

The intrauterine environment, including the placenta, is influenced by a variety of factors, among which is diabetes during pregnancy. These factors can affect lifetime morbidity. Senescence is a state of cellular metabolic arrest, known to be correlated with age-related diseases and is usually accompanied by short telomeres. This study evaluated telomere characteristics in placentas and in cord blood from term pregnancies complicated by uncontrolled diabetes mellitus.

Placental biopsies and cord blood were collected from 16 pregnancies with poorly controlled diabetes and from 16 healthy controls. Senescence-associated heterochromatin foci (SAHF) and senescence-associated β-galactosidase (SAβ-Gal) staining were evaluated. Apoptosis was evaluated using tunel staining. Telomere length and aggregate formation were assessed in placentas and in cord blood using Q-FISH.

Increased SAHF (19.28% ± 7.93 vs. 7.78% ± 5.31, P < 0.001) and SAβ-Gal (7.1% ± 1.32 vs. 0.8% ± 0.41, P < 0.001), but not apoptosis were present in placentas from diabetic pregnancies compared to controls. Higher percentage of trophoblasts with short telomeres (24.42% ± 12.6 vs. 4.92% ± 6.4, P = 0.013) and noticeably more aggregate formation (2.75% ± 1.14 vs. 0.62% ± 0.87, P < 0.001) were observed in diabetic placentas compared to controls. These differences were not observed in cord blood samples.

Poorly controlled diabetes is related to increased senescence and shorter telomeres in placentas. Those findings may partially explain increased long-term, related morbidity.