1471-P: Visceral and Subcutaneous Adipose Tissue Attenuation Differs by Type 1 and Type 2 Diabetes Status

Abstract

Adipose tissue (AT) volume and quality may contribute to cardiovascular risk. AT volume and attenuation can be derived from computed tomography (CT) scans, with greater attenuation indicating poor AT quality and increased fibrosis. We examined whether AT quantity and quality were associated with coronary artery calcium (CAC) in a sample of adults without diabetes (non-DM), with type 1 diabetes (T1D), and with type 2 diabetes (T2D). 294 non-DM adults (mean age±SD 55±9 years), 226 adults with T1D (mean age±SD 52±9 years), and 52 adults with T2D (mean age±SD 53±9 years) completed CT scans for CAC measurement and abdominal CT scans at lumbar 4-5 for visceral (VAT) and subcutaneous (SAT) AT volume and attenuation measurement. Adults with T2D had significantly more VAT and SAT when adjusting for age and sex compared with T1D and non-DM adults, but after adjusting for BMI there was no difference in VAT volume by diabetes status. Adults with T2D had significantly lower SAT volume when adjusted for BMI as compared with both non-DM and T1D adults (157 cm3 vs. 177 cm3 and 183 cm3, p=0.0008). Adults with T1D had significantly higher SAT attenuation as compared with non-DM and T2D adults (p<0.0001 for both). Square root-transformed CAC volume was significantly higher in both T1D (mean volume±SD 10.4±14.7) and T2D (mean volume±SD 9.6±15.9) compared to non-DM adults (mean volume±SD 4.5±8.2). Greater attenuation of VAT and SAT was associated with increased CAC (p=0.03 for both), but there was no association between AT volume and CAC in this sample. AT attenuation was significantly higher in T1D and independently associated with subclinical atherosclerosis in a sample of non-DM, T1D, and T2D adults. AT fibrosis is associated with metabolic dysfunction, decreased angiogenesis, and increased inflammation; our results suggest that despite similar AT volume, T1D adults have adverse fat quality that may indicate fibrosis. This may be a mechanism through which T1D is associated with greater levels of CAC. Disclosure A. Keshawarz: None. A.C. Alman: None. C.C. Low Wang: Advisory Panel; Spouse/Partner; Bayer Healthcare, LLC, CSL Behring, Genentech/Roche, Hema Biologics, Novo Nordisk Pharmaceuticals, Inc, Octapharma Pharmazeutika, Shire. Speaker's Bureau; Self; Medical Education Resources. S. Mitchell: None. I.E. Schauer: Other Relationship; Spouse/Partner; Kestrel Labs. J.E.B. Reusch: Board Member; Self; American Diabetes Association. Other Relationship; Self; Merck & Co., Inc. J.G. Regensteiner: None. J.K. Snell-Bergeon: None. Funding American Diabetes Association (7-13-CD-10 to J.K.S-B.)