Exploring the link between asprosin and glucose and lipid dysregulation in offspring of diabetic mothers in a rat model.

Maternal diabetes mellitus (DM) is a known risk factor for offspring metabolic dysfunction, predisposing them to DM later in life. While this association is established, the molecular mechanisms underlying the intergenerational transmission of DM risk are not fully understood. This study investigated the effects of in utero exposure to maternal DM on circulating levels of asprosin in offspring, aiming to clarify the potential role of asprosin in this pathological cascade. Twelve pregnant Wistar rats were randomized into two groups: a streptozotocin (STZ)-induced diabetic group (n = 6) and a non-diabetic control group (n = 6). DM was confirmed via blood glucose measurements (>250 mg/dL) 72 hours post-STZ administration. At 16 weeks postnatal, six male offspring per group were euthanized for plasma collection. Asprosin levels were measured using a commercial ELISA kit. Statistical analyses were performed to compare group means and determine the relationship between asprosin and variables. Maternal asprosin levels were significantly higher in the DM group compared to controls (330.70 ± 78.13 vs. 244.00 ± 21.54 pg/mL, P = 0.02). However, offspring of both groups showed comparable circulating asprosin concentrations (234.50 ± 10.60 vs 235.00 ± 7.23 pg/mL, P = 0.92). In contrast to diabetic mothers, in whom asprosin was significantly correlated with atherogenic lipid parameters and glucose homeostasis indices, no significant correlations were observed between asprosin and these parameters in offspring of either group. These preliminary findings suggest that asprosin may not be a critical mediator in the intergenerational transmission of diabetes-associated metabolic dysfunction.