Exploring the link between asprosin and glucose and lipid dysregulation in offspring of diabetic mothers in a rat model
4 affiliations
- 1Department of Biochemistry and Biophysics, TeMS.C., Islamic Azad University, Tehran, Iran
- 2Department of Physiology, School of Medicine, Iran University of Medical Sciences, Tehran, Iran
- 3Department of Anatomy, School of Medicine, Iran University of Medical Sciences, Tehran, Iran
- 4Department of Biochemistry, School of Medicine, Iran University of Medical Sciences, Tehran, Iran
Abstract
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.
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BibTeX
@article{ahmadasadi2026exploring,
title = {{Exploring the link between asprosin and glucose and lipid dysregulation in offspring of diabetic mothers in a rat model}},
author = {Hamidreza Ahmadasadi and Peyman Rasouli Emamgholi and Issa Layali and Tina Kianfar and Shahriyar Tork and Mobina Jafarpour and Masoume Aliabadi and Hafez Heydari},
journal = {PLOS One},
year = {2026},
month = sep,
doi = {10.1371/journal.pone.0354870},
url = {https://doi.org/10.1371/journal.pone.0354870},
note = {CC BY 4.0},
}
RIS
TY - JOUR
TI - Exploring the link between asprosin and glucose and lipid dysregulation in offspring of diabetic mothers in a rat model
AU - Hamidreza Ahmadasadi
AU - Peyman Rasouli Emamgholi
AU - Issa Layali
AU - Tina Kianfar
AU - Shahriyar Tork
AU - Mobina Jafarpour
AU - Masoume Aliabadi
AU - Hafez Heydari
PY - 2026
DA - 2026/09/18
JO - PLOS One
DO - 10.1371/journal.pone.0354870
UR - https://doi.org/10.1371/journal.pone.0354870
AB - 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.
SN - 1932-6203
ER -