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Daily Endocrinology Research Analysis

3 papers

Three impactful endocrinology papers span mechanistic, translational, and care-delivery science. A Diabetes study uncovers adenylosuccinate (S-AMP) as a key mediator of imeglimin’s β-cell proliferative and antiapoptotic actions across multiple islet systems. A 3-year prospective extension of the 4T program shows durable HbA1c improvements in youth with type 1 diabetes using early CGM plus remote patient monitoring. A translational Obesity study suggests preconception GLP-1RA improves maternal li

Summary

Three impactful endocrinology papers span mechanistic, translational, and care-delivery science. A Diabetes study uncovers adenylosuccinate (S-AMP) as a key mediator of imeglimin’s β-cell proliferative and antiapoptotic actions across multiple islet systems. A 3-year prospective extension of the 4T program shows durable HbA1c improvements in youth with type 1 diabetes using early CGM plus remote patient monitoring. A translational Obesity study suggests preconception GLP-1RA improves maternal lipid metabolism via liver-secreted FGF21.

Research Themes

  • β-cell metabolic resilience and therapeutic mechanisms
  • Early CGM and remote monitoring to sustain glycemic outcomes in youth T1D
  • GLP-1 biology, FGF21 signaling, and maternal-fetal lipid metabolism

Selected Articles

1. Adenylosuccinate Mediates Imeglimin-Induced Proliferative and Antiapoptotic Effects in β-Cells.

84Level VBasic/Mechanistic researchDiabetes · 2025PMID: 40638403

This mechanistic study shows that imeglimin elevates adenylosuccinate (S-AMP) in β-cells and that blocking its synthesis via ADSS inhibition attenuates imeglimin’s proliferative and antiapoptotic effects across mouse, human, porcine islets, and hPSC-derived β-cells. Findings position S-AMP as a metabolic mediator of imeglimin’s β-cell benefits.

Impact: Identifying S-AMP as a mediator links imeglimin to a concrete metabolic pathway, offering actionable targets for β-cell preservation strategies.

Clinical Implications: While preclinical, the S-AMP/ADSS axis could guide biomarker development and combination strategies to enhance β-cell survival in type 2 diabetes and islet transplantation.

Key Findings

  • Imeglimin increases adenylosuccinate (S-AMP) and aspartate content in β-cells/islets.
  • ADSS inhibition blunts imeglimin-induced β-cell proliferation and antiapoptotic effects.
  • Effects are consistent across mouse, human, porcine islets, and hPSC-derived β-cells, indicating broad biological relevance.

Methodological Strengths

  • Multi-system validation across species including human islets and hPSC-derived β-cells
  • Causal probing of pathway via pharmacologic ADSS inhibition

Limitations

  • Preclinical mechanistic work without in vivo clinical endpoints
  • Quantitative dose–response and long-term in vivo β-cell functional outcomes not reported

Future Directions: Test S-AMP/ADSS modulation in vivo with metabolic phenotyping, evaluate translational biomarkers, and explore combination therapies that potentiate imeglimin’s β-cell effects.

2. Sustained HbA1c Improvements Over 36 Months in Youth in the Teamwork, Targets, Technology, and Tight Control (4T) Study.

73Level IICohortThe Journal of clinical endocrinology and metabolism · 2025PMID: 40635651

Starting CGM within the first month of diagnosis and coupling it with intensive education and remote patient monitoring yielded a 1.2% adjusted HbA1c advantage at 3 years versus historical controls. Notably, 68% achieved HbA1c <7.5% and 37% achieved <7% at 3 years, supporting early technology-enabled care models.

Impact: Provides rare 3-year prospective evidence that early CGM plus structured RPM can durably improve glycemia in youth with T1D.

Clinical Implications: Supports early CGM initiation with intensive remote support in the first year post-diagnosis to achieve and sustain HbA1c targets; informs clinic resource allocation and payer policy.

Key Findings

  • Adjusted HbA1c was 1.2% lower at 3 years compared with historical controls (95% CI 0.7–1.7%).
  • At 3 years, 68% achieved HbA1c <7.5% and 37% achieved <7% versus 37% and 20% in controls.
  • Intervention included CGM within 1 month of diagnosis, weekly RPM in year 1, then monthly RPM.

Methodological Strengths

  • Prospective follow-up with predefined CGM-enabled care pathway
  • Objective outcomes (HbA1c and CGM metrics) and 3-year duration

Limitations

  • Nonrandomized design with historical controls may introduce selection and temporal biases
  • Single-center study may limit generalizability

Future Directions: Randomized, multicenter trials comparing early CGM+RPM vs usual care, cost-effectiveness analyses, and identification of subgroups benefiting most.

3. Prepregnancy GLP-1RA use improves maternal lipid metabolism via liver-secreted FGF21 during pregnancy in HFD-fed dams.

69Level IIICohort + Experimental (animal)Obesity (Silver Spring, Md.) · 2025PMID: 40635195

A mixed human–animal study suggests that preconception GLP-1RA use lowers maternal triglycerides, gestational weight gain, and early-pregnancy MASLD likelihood, with rat data indicating hepatic FGF21 and downstream ERK/PPAR-γ and AMPK/SIRT1 pathway activation. Visceral adipose showed increased lipolysis and reduced lipogenesis signatures.

Impact: Links preconception GLP-1RA exposure to improved pregnancy lipid profiles and provides mechanistic support via hepatic FGF21 signaling.

Clinical Implications: For women with obesity planning pregnancy, optimizing metabolic status with GLP-1RA preconception may reduce gestational dyslipidemia and MASLD risk; safety and timing relative to conception must follow current guidelines.

Key Findings

  • In women with obesity (n=42), preconception GLP-1RA use was associated with lower prepregnancy BMI, reduced gestational weight gain, reduced early MASLD proportion, and lower triglycerides.
  • In HFD-fed pregnant rats, GLP-1RA increased plasma FGF21 and adiponectin and improved triglycerides in midgestation.
  • Late-gestation liver showed increased FA oxidation/lipolysis gene expression, decreased lipogenesis genes, and activation of ERK/PPAR-γ and AMPK/SIRT1 pathways; visceral fat showed enhanced lipolysis and reduced lipogenesis with increased p-FGFR1.

Methodological Strengths

  • Translational design combining human retrospective case-control with controlled animal experiments
  • Pathway-level mechanistic readouts (FGF21, ERK/PPAR-γ, AMPK/SIRT1) and tissue-specific analyses

Limitations

  • Small human sample size with retrospective design and potential confounding by weight loss behaviors
  • Animal model translatability and periconception timing relative to human clinical practice require caution

Future Directions: Prospective trials evaluating preconception GLP-1RA timing, safety, and maternal–fetal metabolic outcomes, with biomarker studies of FGF21 signaling.