What is the clinical evidence from this study?

Study design: Cross-Sectional. Population: Type 2 Diabetes and Obesity (n=40). Intervention: Type 2 Diabetes and Diabetic Kidney Disease vs. Normal weight controls and obesity without T2D. Primary outcome: Cardiac and aortic structure, hemodynamics, and tissue properties (p=<0.05).

What does this research mean for the field?

In young adults with type 2 diabetes, obesity drives cardiac hypertrophy, whereas diabetic kidney disease is associated with vascular stiffness and myocardial edema, indicating that albuminuria is a key biomarker for subclinical heart failure risk. Novelty: ClaimNovelty.INCREMENTAL. Consensus alignment: ConsensusAlignment.NEUTRAL.

What question did this study set out to answer?

This research aims to clarify the contributions of obesity and diabetic kidney disease to early cardiac remodeling in young adults with type 2 diabetes.

June 7, 2026

1404-P: Obesity Drives Cardiac Hypertrophy while Diabetic Kidney Disease Links to Myocardial Edema and Vascular Stiffness in Young Adults with Type 2 Diabetes

Q: What are the key findings of this study?

In young adults, obesity is associated with cardiac hypertrophy, while diabetic kidney disease correlates with vascular stiffness and myocardial edema (p<0.05).

Q: What does this research mean for the field?

In young adults with type 2 diabetes, obesity drives cardiac hypertrophy, whereas diabetic kidney disease is associated with vascular stiffness and myocardial edema, indicating that albuminuria is a key biomarker for subclinical heart failure risk. Novelty: ClaimNovelty.INCREMENTAL. Consensus alignment: ConsensusAlignment.NEUTRAL.

Q: What question did this study set out to answer?

This research aims to clarify the contributions of obesity and diabetic kidney disease to early cardiac remodeling in young adults with type 2 diabetes.

Key Result

In young adults, obesity is associated with cardiac hypertrophy, while diabetic kidney disease correlates with vascular stiffness and myocardial edema (p<0.05).

Key Points

This research aims to clarify the contributions of obesity and diabetic kidney disease to early cardiac remodeling in young adults with type 2 diabetes.
Conducted multiparametric cardiac MRI on young adults with type 2 diabetes, obesity, and normal weight controls (n=40 total).
Assessed kidney function using UACR and estimated GFR.
Analyzed metrics like left ventricular thickness and aortic pulse wave velocity across groups.
Young adults with type 2 diabetes showed increased left ventricular myocardial wall thickness versus normal weight controls (p<0.05).
Higher albuminuria correlated with decreased right ventricular volumes and elevated myocardial T2* (p<0.05).
Diabetic kidney disease links to increased vascular stiffness and myocardial edema, suggesting a pro-inflammatory cardiac phenotype.

Study Design

Type

Cross-Sectional (n=40)

Structured PICO

Do obesity and diabetic kidney disease drive early cardiac remodeling in young adults with type 2 diabetes?

Population

40 young adults (26 with T2D, 11 with obesity, 3 normal weight controls) evaluated with multiparametric cardiac MRI to assess early cardiac remodeling.

Comparator

Normal weight controls (n=3) and obesity controls (n=11)

Outcome

Cardiac and aortic structure, hemodynamics, and tissue properties assessed by multiparametric cardiac MRI with native T1/T2* mappingsurrogate

In young adults with type 2 diabetes, obesity is associated with cardiac hypertrophy, while diabetic kidney disease (albuminuria and lower eGFR) is linked to vascular stiffness and myocardial edema, suggesting early pro-inflammatory cardiac remodeling.

Main Result

p-value: p=<0.05

Abstract

Introduction and Objective: Young-onset T2D has an aggressive phenotype including premature heart failure. However, contributions of obesity vs. diabetic kidney disease (DKD) to early cardiac remodeling remain unclear. We used multiparametric cardiac MRI (CMR) with native T1/T2* mapping to investigate drivers of cardiac and aortic structure, hemodynamics, and tissue properties in young adults (YA). Methods: YA with T2D (n=26), obesity (OC; n=11), and normal weight controls (NWC; n=3) underwent CMR (Phillips 3T). Kidney function was assessed by UACR (first AM void), estimated (eGFR, CKD-EPI creatinine and cystatin C) and measured GFR (mGFR, iohexol clearance). Results: YA with T2D (24±6 years, BMI 35±9 kg/m2, A1c 8.5±3.1%, UACR 11 8, 661 mg/g, eGFR 110±39 ml/min/1.73m2, 62% male) and OC (25±9 years, BMI 37±8 kg/m2, UACR 5 4, 15 mg/g, eGFR 125±22 ml/min/1.73m2, 64% male) had higher peak aortic wall shear stress and left ventricular (LV) myocardial wall thickness vs. NWC (all p0.05). LV and right ventricular (RV) cardiac output and LV myocardial walls were higher in T2D vs. NWC (all p0.05). Native T1 was higher in T2D vs. OC, suggesting fibrosis or inflammation, and RV end systolic and diastolic volumes (ESV and EDV) were lower in T2D vs. OC (all p0.05). Higher A1c, BMI and lower eGFR associated with LV myocardial thickness. Lower eGFR (r:-0.62, p0.0001) and mGFR (r:-0.53, p=0.002) correlated with higher aortic pulse wave velocity. Higher UACR correlated with lower RVESV (r:-0.39, p=0.02), RVEDV (r:-0.40, p=0.01), and higher myocardial T2* (r:0.35, p=0.03). T2D and OC with severe albuminuria (UACR ≥300 mg/g; n=7) had higher T2* vs. without severe albuminuria (p0.05). Conclusion: While obesity associates with cardiac hypertrophy, DKD is linked with vascular stiffness and myocardial edema. The association between albuminuria and elevated myocardial T2* suggests that early DKD signals a potential “pro-inflammatory” cardiac phenotype, highlighting UACR as a key biomarker for subclinical heart failure risk. Disclosure Y. Choi: None. S. Park: None. S. Ramesh: None. L. Pyle: None. I. de Boer: Consultant; Current; Boehringer Ingelheim International GmbH, Novo Nordisk, GlaxoSmithKline plc., Lilly. Consultant; Ended; Dexcom, Inc. Research Support; Current; Novo Nordisk, Dexcom, Inc. Consultant; Ended; AstraZeneca. Consultant; Current; Roche Diabetes Care. Consultant; Ended; Lexicon Pharmaceuticals, Inc. K. Tommerdahl: Advisory Panel; Current; Sanofi. D. van Raalte: Consultant; Current; AstraZeneca. Research Support; Current; AstraZeneca. Consultant; Current; Boehringer Ingelheim International GmbH. Research Support; Current; Boehringer Ingelheim International GmbH. Consultant; Current; Eli Lilly and Company. Research Support; Current; Eli Lilly and Company. Consultant; Current; Merck Current; Merck Current; Novo Nordisk. Research Support; Current; Novo Nordisk. M. Kelsey: Research Support; Current; Rhythm Pharmaceuticals, Inc. K. Bornfeldt: Advisory Panel; Current; ESPERION Therapeutics, Inc. E.K. Englund: None. J. Snell-Bergeon: None. F. Persson: None. D.I. Casillas: None. L.M. Laffel: Other - Travel support for scientific presentations; Ended; Boehringer Ingelheim International GmbH. Other - DSMB Chair; Ended; Janssen Pharmaceuticals, Inc. Consultant; Current; Dexcom, Inc. Advisory Panel; Current; Medtronic, Sequel, Tandem Diabetes Care, Inc. Consultant; Current; Roche Diabetes Care, Sinocare. Advisory Panel; Ended; Sanofi. Advisory Panel; Current; MannKind Corporation. J. Kanter: None. M.L. Granda: None. B. Ariens: None. A.J. Kula: None. D. Cherney: Consultant; Current; Boehringer Ingelheim-Lilly, Merck, AstraZeneca, Sanofi, Mitsubishi-Tanabe, Abbvie, Janssen, AMGEN, Bayer, Prometic, BMS, Maze, Gilead, CSL-Behring, Otsuka, Novartis, Youngene, Lexicon, Inversago, GSK,. Research Support; Current; Boehringer Ingelheim-Lilly, Merck, Janssen, Sanofi, AstraZeneca, CSL-Behring, Lexicon, Novo-Nordisk, Bayer. A. Caldwell-McGee: None. C.L. Birznieks: None. T.J. Dobbs: None. J. Romanowicz: None. N. Bansal: Consultant; Current; AstraZeneca. L. Browne: None. K.J. Nadeau: None. A. Barker: None. P. Bjornstad: Consultant; Current; Bayer AG, Boehringer Ingelheim International GmbH, Lilly, Novo Nordisk. Funding Horizon PharmaChildren's Hospital of Colorado, NIH/NIDDK

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