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miR-1a-3p impairs β-cell function in male offspring via disrupted NBR1-dependent mitochondrial function but not apoptosis after maternal high-saturated-fat diet in mice
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DOI：10.1016/j.jnutbio.2026.110480.png)
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Abstract
En 中文
• Maternal high-saturated fat (HSF) diet increases offspring type 2 diabetes risk, but maternal and late-adulthood HFD "two-hit" effects on β-cell function are unclear. • We first report the miRNA profile and miR-1a-3p’ role in maternal metabolic programming of male offspring β-cell function. • Maternal HSF upregulates miR-1a-3p in male offspring islets, impairing β-cell function via NBR1-mediated mitochondrial dysfunction, independent from apoptosis; miR-1a-3p inhibition alleviates HFD-induced β-cell dysfunction. • This study provides a basis for improving perinatal diet to prevent intergenerational diabetes, and identify miR-1a-3p as a clinically translatable biomarker and therapeutic strategy for metabolic diseases.
Keywords:
Maternal high-saturated-fat diet
Male offspring
β-cell dysfunction
miR-1a-3p
Mitochondrial dysfunction
NBR1
GSIS
,
Glucose-stimulated insulin secretion
HFD
,
High fat diet
HSF
,
High-saturated fats
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4.9
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4.5K
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1.4W
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