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Daily Endocrinology Research Analysis

3 papers

Three impactful endocrinology studies stood out: an international consensus defined standardized outcome criteria for medically treated primary aldosteronism (PAMO), a Lancet Commission proposed diagnostic criteria redefining clinical obesity beyond BMI, and a randomized trial showed the pan-PPAR agonist lanifibranor improves insulin resistance and hepatic steatosis in T2D with MASLD.

Summary

Three impactful endocrinology studies stood out: an international consensus defined standardized outcome criteria for medically treated primary aldosteronism (PAMO), a Lancet Commission proposed diagnostic criteria redefining clinical obesity beyond BMI, and a randomized trial showed the pan-PPAR agonist lanifibranor improves insulin resistance and hepatic steatosis in T2D with MASLD.

Research Themes

  • Standardizing outcome assessment in endocrine hypertension (primary aldosteronism)
  • Redefining clinical obesity diagnosis beyond BMI
  • Metabolic therapeutics targeting insulin resistance and steatosis in T2D with MASLD

Selected Articles

1. Definition and diagnostic criteria of clinical obesity.

86.5Level VSystematic ReviewThe lancet. Diabetes & endocrinology · 2025PMID: 39824205

An international Commission redefines obesity by introducing “clinical obesity” as a chronic illness due to organ/tissue dysfunction from excess adiposity and distinguishes it from “preclinical obesity.” It proposes objective diagnostic criteria that move beyond BMI alone, incorporating adiposity distribution and functional impairment.

Impact: This work challenges BMI-centric diagnosis and offers a field-wide framework likely to influence clinical guidelines, coding, and therapeutic prioritization.

Clinical Implications: Clinicians should assess adiposity distribution and organ dysfunction (e.g., cardiometabolic, renal, hepatic, musculoskeletal) to distinguish preclinical vs clinical obesity and guide treatment intensity beyond BMI thresholds.

Key Findings

  • Defines clinical obesity as a chronic systemic illness due to organ/tissue dysfunction from excess adiposity.
  • Differentiates preclinical obesity (excess adiposity without dysfunction) from clinical obesity (with dysfunction).
  • Establishes objective diagnostic criteria beyond BMI, informed by a 58-member multidisciplinary, international panel including people with lived experience.

Methodological Strengths

  • Multidisciplinary, international consensus process including patients’ perspectives
  • Clear conceptual framework distinguishing disease states with pragmatic diagnostic orientation

Limitations

  • Consensus-based framework requires prospective validation and operationalization in clinical pathways
  • Potential implementation variability across health systems and risk of misclassification without standardized tools

Future Directions: Develop and validate clinical tools and biomarkers integrating organ dysfunction metrics; test health and economic outcomes when applying the new criteria across diverse populations.

2. Outcomes after medical treatment for primary aldosteronism: an international consensus and analysis of treatment response in an international cohort.

82.5Level IIICohortThe lancet. Diabetes & endocrinology · 2025PMID: 39824204

The PAMO criteria standardize biochemical and clinical outcome definitions for medical therapy in primary aldosteronism. In 1,258 patients, 52.9% achieved complete biochemical response and 18.3% complete clinical response; higher spironolactone dose, female sex, fewer antihypertensives, and absence of microalbuminuria/LVH were associated with better outcomes.

Impact: Provides a unified, consensus-based outcome framework and benchmarks that can harmonize clinical care, research endpoints, and quality improvement in primary aldosteronism.

Clinical Implications: Use PAMO criteria to titrate mineralocorticoid receptor antagonist therapy, monitor biochemical/clinical endpoints at 6–12 months, and identify patients needing intensified care.

Key Findings

  • Established PAMO consensus criteria defining complete, partial, and absent biochemical and clinical responses to medical therapy.
  • Among 1,258 patients, 52.9% achieved complete biochemical response and 18.3% achieved complete clinical response at 6–12 months.
  • Higher spironolactone dose (median 40 mg vs 25 mg) and factors such as female sex, fewer baseline antihypertensives, and absence of microalbuminuria/LVH predicted better clinical response.

Methodological Strengths

  • Delphi法による国際専門家パネルの合意形成と明確なアウトカム定義
  • 28施設の大規模実臨床コホートでのベンチマーク提示と外的妥当性

Limitations

  • Observational cohort without randomization; potential confounding in treatment intensity and patient selection
  • Short to intermediate follow-up (6–12 months) with limited data on long-term outcomes

Future Directions: Prospectively validate PAMO in diverse settings; test algorithmic dose-titration strategies; evaluate long-term cardiovascular/renal outcomes and patient-reported measures.

3. Pan-PPAR agonist lanifibranor improves insulin resistance and hepatic steatosis in patients with T2D and MASLD.

76.5Level IIRCTJournal of hepatology · 2025PMID: 39824443

In a randomized, placebo-controlled phase II trial (n=38), lanifibranor reduced intrahepatic triglycerides by ~44–50% versus 12–16% with placebo, with 65–79% achieving ≥30% IHTG reduction and 25% steatosis resolution. Hepatic and peripheral insulin sensitivity improved, adiponectin rose 2.4-fold, and cardiometabolic markers improved, with modest weight gain (+2.7%) and mild adverse events.

Impact: Demonstrates multi-tissue insulin sensitization with substantial hepatic fat reduction in T2D with MASLD, supporting pan-PPAR agonism as a disease-modifying strategy.

Clinical Implications: Lanifibranor may offer a pharmacologic option to target insulin resistance and steatosis beyond weight loss strategies in T2D with MASLD; monitoring for weight gain and hematologic changes is warranted.

Key Findings

  • Lanifibranor reduced intrahepatic triglyceride content by ~44–50% vs. 12–16% with placebo; steatosis resolution occurred in 25% vs. 0%.
  • Improved hepatic and peripheral insulin sensitivity (reduced endogenous glucose production and increased insulin-stimulated Rd); adiponectin increased 2.4-fold.
  • Secondary metabolic markers improved (fasting glucose, insulin, HOMA-IR, HbA1c, HDL-C); modest weight gain (+2.7%) and mild AEs observed.

Methodological Strengths

  • Randomized, placebo-controlled design with tissue-specific insulin sensitivity assessments
  • Clinically meaningful imaging/biochemical endpoints and predefined thresholds (≥30% IHTG reduction)

Limitations

  • Single-center, small sample size (n=38) with 24-week follow-up limits generalizability and long-term inference
  • Weight gain and hemoglobin decrease warrant longer-term safety evaluation

Future Directions: Larger, multicenter phase III trials assessing histologic NASH/MASH endpoints, cardiovascular/renal outcomes, and combination strategies with weight-loss agents.