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Glucose shields RINm5F beta cells against arsenic-induced apoptosis

Rosa Isela Ortiz-Huidobro1, Pablo Pánico1, Ana María Salazar1

  • 1Department of Genomic Medicine and Environmental Toxicology, Instituto de Investigaciones Biomédicas, Universidad Nacional Autónoma de México, Mexico City, Mexico.

Scientific Reports
|November 25, 2025
PubMed

Insights

High glucose levels mitigate arsenic-induced beta-cell apoptosis in Type 2 Diabetes (T2D) research. This study reveals glucose co-treatment alters insulin signaling pathways, impacting cell survival mechanisms.

Area of Science:

  • Endocrinology
  • Toxicology
  • Cell Biology

Background:

  • Type 2 Diabetes (T2D) involves hyperglycemia, beta-cell dysfunction, and insulin resistance.
  • Arsenic exposure and high carbohydrate intake are T2D risk factors, but their interaction mechanisms are unclear.
  • Understanding these interactions is crucial for elucidating beta-cell apoptosis pathways.

Purpose of the Study:

  • To investigate the effects of arsenic and glucose on beta-cell apoptosis.
  • To explore the underlying mechanisms involving insulin signaling pathways.
  • To determine if glucose co-treatment affects arsenic-induced beta-cell apoptosis.

Main Methods:

  • In vitro exposure of RINm5F insulinoma beta-cells to arsenic (As), glucose (Gluc), and their combination (As + Gluc) for 48 and 72 hours.
  • Analysis of apoptosis using flow cytometry and assessment of key signaling pathways (PI3K/Akt, MAPK).
  • Measurement of calpain activity and Bax/Caspase-3 pathway markers.

Main Results:

  • Arsenic alone induced early apoptosis in beta-cells.
  • Glucose co-treatment reduced arsenic-induced apoptosis.
  • As + Gluc altered insulin signaling, increasing Akt/S6K1 activation and decreasing ERK1/2 activation.
  • Increased calpain activity and down-regulation of the Bax/Caspase-3 pathway were observed with As + Gluc compared to As alone.

Conclusions:

  • Glucose co-treatment mitigates the pro-apoptotic effects of arsenic in beta-cells.
  • Calpains play a significant role in this protective response.
  • The Akt/S6K1 signaling axis is notably altered, suggesting its involvement in the protective mechanism against arsenic toxicity.
Keywords:
ApoptosisArsenicCalpainsGlucoseInsulin signalingPancreatic beta-cells

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