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The Potential Roles of Oral Hypoglycemic Agents to Modulate Mitochondrial Function in Type 1 Diabetes Mellitus: A

Su-Ann Cheng1, Jeong Hoon Lim1,2

  • 1Department of Medicine, National University Hospital, 5 Lower Kent Ridge Road, Singapore 119074, Singapore.

Life (Basel, Switzerland)
|July 28, 2026
PubMed

Insights

Oral hypoglycemic agents (OHAs) may offer adjunctive benefits for type 1 diabetes mellitus (T1DM) by improving mitochondrial function. Research suggests metformin and empagliflozin could enhance mitochondrial quality control, though clinical evidence is still limited.

Area of Science:

  • Endocrinology
  • Metabolic Diseases
  • Mitochondrial Biology

Background:

  • Type 1 diabetes mellitus (T1DM) involves autoimmune destruction of pancreatic beta cells, leading to absolute insulin deficiency.
  • Mitochondrial dysfunction is a key factor in T1DM pathogenesis and complications, impacting energy production and cellular health.
  • Oral hypoglycemic agents (OHAs) are primarily studied in type 2 diabetes but may influence mitochondrial pathways relevant to T1DM.

Purpose of the Study:

  • To review the current evidence on the role of OHAs in T1DM.
  • To specifically investigate the impact of OHAs on mitochondrial function in the context of T1DM.
  • To synthesize findings on mitochondrial dysfunction mechanisms and potential OHA interventions.

Main Methods:

  • Systematic literature review adhering to PRISMA guidelines.
  • Inclusion of studies on T1DM mitochondrial dysfunction and OHA effects on mitochondria in T1DM.
  • Screening of 997 articles, with 24 studies meeting inclusion criteria.

Main Results:

  • Twenty studies detailed T1DM mitochondrial dysfunction, including oxidative stress, impaired ATP production, disrupted proteostasis, apoptosis, and altered dynamics.
  • Four preclinical studies indicated metformin and empagliflozin may improve mitochondrial quality control via adenosine monophosphate-activated protein kinase (AMPK) pathways.
  • These agents potentially enhance mitochondrial biogenesis and reduce fission in T1DM models.

Conclusions:

  • Certain OHAs show potential in modulating mitochondrial dysfunction observed in T1DM.
  • Mechanisms may involve AMPK-dependent enhancement of mitochondrial quality control.
  • Clinical application of OHAs as adjunctive therapy for T1DM requires further investigation and validation.
Keywords:
mitochondriaoral hypoglycemic agenttype 1 diabetes mellitus

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