---
title: "Asprosin, maternal diabetes, and metabolic outcomes in rat offspring: experimental findings"
id: "pubmed-42758780"
canonical_url: "https://medichelpline.com/clinical-feed/pubmed-42758780"
content_type: "clinical_feed_article"
specialty: "Pharmacology"
source_name: "PubMed / NCBI"
source_url: "https://pubmed.ncbi.nlm.nih.gov/42758780/"
doi: "10.1371/journal.pone.0354870"
published_at: "2026-09-18T00:00:00.000Z"
evidence_level: "Journal Article"
license: "CC-BY-NC-4.0 / Informational Use"
---
# Asprosin, maternal diabetes, and metabolic outcomes in rat offspring: experimental findings
## Provenance & Clinical Metadata
- **Canonical URL:** https://medichelpline.com/clinical-feed/pubmed-42758780
- **Specialty:** [Pharmacology](https://medichelpline.com/clinical-feed/pharmacology.md)
- **Primary Source:** PubMed / NCBI
- **Source URL:** [Original Journal Publication](https://pubmed.ncbi.nlm.nih.gov/42758780/)
- **DOI:** [10.1371/journal.pone.0354870](https://doi.org/10.1371%2Fjournal.pone.0354870)
- **Published At:** 2026-09-18T00:00:00.000Z
- **Evidence Rating:** Journal Article
## Executive GIST (TL;DR)
- Maternal diabetes mellitus (DM) increases risk of metabolic dysfunction in offspring, but mechanisms for intergenerational transmission remain unclear. - The study measured circulating **asprosin** in dams and their male offspring in a Wistar rat model to evaluate a potential mediator role. - Twelve pregnant Wistar rats were randomized to streptozotocin (STZ)-induced diabetic (n = 6) or non-diabetic control (n = 6) groups; DM was confirmed when blood glucose exceeded 250 mg/dL at 72 hours after STZ. - At 16 weeks postnatal, six male offspring per group were euthanized and plasma collected; asprosin quantified with a commercial **ELISA** kit. - Maternal circulating asprosin was significantly higher in diabetic dams versus controls (330.70 ± 78.13 vs 244.00 ± 21.54 pg/mL; P = 0.02). - Offspring circulating asprosin concentrations were comparable between groups (234.50 ± 10.60 vs 235.00 ± 7.23 pg/mL; P = 0.92), indicating no persistent change in offspring asprosin at 16 weeks. - In diabetic mothers, asprosin correlated significantly with atherogenic lipid parameters and indices of glucose homeostasis; such correlations were not observed in offspring of either group. - The authors interpret these preliminary results as suggesting that **asprosin** may not be a key mediator of the intergenerational transmission of diabetes-associated metabolic dysfunction. - Conflict of interest: authors declared no competing interests. Details on sample size justification, additional metabolic measures, or broader mechanistic assays were not reported in the abstract.
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Affiliations Expand ### Affiliations * 1 Department of Biochemistry and Biophysics, TeMS.C., Islamic Azad University, Tehran, Iran. * 2 Department of Physiology, School of Medicine, Iran University of Medical Sciences, Tehran, Iran. * 3 Department of Anatomy, School of Medicine, Iran University of Medical Sciences, Tehran, Iran. * 4 Department of Biochemistry, School of Medicine, Iran University of Medical Sciences, Tehran, Iran. * PMID: **42758780** * DOI: [ 10.1371/journal.pone.0354870 ](https://doi.org/10.1371/journal.pone.0354870) Item in Clipboard # Exploring the link between asprosin and glucose and lipid dysregulation in offspring of diabetic mothers in a rat model Hamidreza Ahmadasadi et al. PLoS One. 2026. Show details Display options Display options Format Abstract PubMed PMID PLoS One Actions * [ Search in PubMed ](https://pubmed.ncbi.nlm.nih.gov/?term=%22PLoS+One%22%5Bjour%5D&sort=date&sort_order=desc) * [ Search in NLM Catalog ](https://www.ncbi.nlm.nih.gov/nlmcatalog?term=%22PLoS+One%22%5BTitle+Abbreviation%5D) * [ Add to Search ](https://pubmed.ncbi.nlm.nih.gov/42758780/) . 2026 Sep 18;21(9):e0354870. doi: 10.1371/journal.pone.0354870. eCollection 2026. ### Authors [Hamidreza Ahmadasadi](https://pubmed.ncbi.nlm.nih.gov/?term=Ahmadasadi+H&cauthor_id=42758780)[ 1 ](https://pubmed.ncbi.nlm.nih.gov/42758780/#short-view-affiliation-1 "Department of Biochemistry and Biophysics, TeMS.C., Islamic Azad University, Tehran, Iran."), [Peyman Rasouli Emamgholi](https://pubmed.ncbi.nlm.nih.gov/?term=Rasouli+Emamgholi+P&cauthor_id=42758780)[ 1 ](https://pubmed.ncbi.nlm.nih.gov/42758780/#short-view-affiliation-1 "Department of Biochemistry and Biophysics, TeMS.C., Islamic Azad University, Tehran, Iran."), [Issa Layali](https://pubmed.ncbi.nlm.nih.gov/?term=Layali+I&cauthor_id=42758780)[ 1 ](https://pubmed.ncbi.nlm.nih.gov/42758780/#short-view-affiliation-1 "Department of Biochemistry and Biophysics, TeMS.C., Islamic Azad University, Tehran, Iran."), [Tina Kianfar](https://pubmed.ncbi.nlm.nih.gov/?term=Kianfar+T&cauthor_id=42758780)[ 2 ](https://pubmed.ncbi.nlm.nih.gov/42758780/#short-view-affiliation-2 "Department of Physiology, School of Medicine, Iran University of Medical Sciences, Tehran, Iran."), [Shahriyar Tork](https://pubmed.ncbi.nlm.nih.gov/?term=Tork+S&cauthor_id=42758780)[ 3 ](https://pubmed.ncbi.nlm.nih.gov/42758780/#short-view-affiliation-3 "Department of Anatomy, School of Medicine, Iran University of Medical Sciences, Tehran, Iran."), [Mobina Jafarpour](https://pubmed.ncbi.nlm.nih.gov/?term=Jafarpour+M&cauthor_id=42758780)[ 4 ](https://pubmed.ncbi.nlm.nih.gov/42758780/#short-view-affiliation-4 "Department of Biochemistry, School of Medicine, Iran University of Medical Sciences, Tehran, Iran."), [Masoume Aliabadi](https://pubmed.ncbi.nlm.nih.gov/?term=Aliabadi+M&cauthor_id=42758780)[ 4 ](https://pubmed.ncbi.nlm.nih.gov/42758780/#short-view-affiliation-4 "Department of Biochemistry, School of Medicine, Iran University of Medical Sciences, Tehran, Iran."), [Hafez Heydari](https://pubmed.ncbi.nlm.nih.gov/?term=Heydari+H&cauthor_id=42758780)[ 4 ](https://pubmed.ncbi.nlm.nih.gov/42758780/#short-view-affiliation-4 "Department of Biochemistry, School of Medicine, Iran University of Medical Sciences, Tehran, Iran.") ### Affiliations * 1 Department of Biochemistry and Biophysics, TeMS.C., Islamic Azad University, Tehran, Iran. * 2 Department of Physiology, School of Medicine, Iran University of Medical Sciences, Tehran, Iran. * 3 Department of Anatomy, School of Medicine, Iran University of Medical Sciences, Tehran, Iran. * 4 Department of Biochemistry, School of Medicine, Iran University of Medical Sciences, Tehran, Iran. * PMID: **42758780** * DOI: [ 10.1371/journal.pone.0354870 ](https://doi.org/10.1371/journal.pone.0354870) Item in Clipboard Cite Display options Display options Format Abstract PubMed PMID ## 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. Copyright: © 2026 Ahmadasadi et al. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. 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