Sagittal abdominal diameter and visceral adiposity: correlates of beta-cell function and dysglycemia in severely obese women

• Authors: Nana Gletsu-Miller, Purdue University; Henry Kahn, Centers for Disease Control and Prevention; Danijela Gasevic, Simon Fraser University; Zhe Liang, Emory University; Jennifer K. Frediani, Emory University; William E Torres, Emory University; Thomas R Ziegler, Emory University; Lawrence S Phillips, Emory University; Edward Lin, Emory University
• Journal Title: Obesity Surgery
• Volume: Volume 23, Number 7
• Publisher: Springer Verlag (Germany) | 2013-07, Pages 874-881
• Type of Work: Article | Post-print: After Peer Review
• Publisher DOI: http://doi.org/10.1007/s11695-013-0874-6
• Subjects: Health Sciences, Nutrition; Health Sciences, Medicine and Surgery
• Keywords: Obesity; Type 2 diabetes; Waist circumference; Anthropometry; Intra-abdominal fat; Insulin resistance; Sagittal abdominal diameter

Abstract

Background In the context of increasing obesity prevalence, the relationship between large visceral adipose tissue (VAT) volumes and type 2 diabetes mellitus (T2DM) is unclear. In a clinical sample of severely obese women (mean body mass index [BMI], 46 kg/m2) with fasting normoglycemia (n=40) or dysglycemia (impaired fasting glucose+diabetes; n=20), we sought to determine the usefulness of anthropometric correlates of VAT and associations with dysglycemia. Methods VAT volume was estimated using multi-slice computer tomography; anthropometric surrogates included sagittal abdominal diameter (SAD), waist circumference (WC) and BMI. Insulin sensitivity (Si), and beta-cell dysfunction, measured by insulin secretion (AIRg) and the disposition index (DI), were determined by frequently sampled intravenous glucose tolerance test. Results Compared to fasting normoglycemic women, individuals with dysglycemia had greater VAT (P<0.001) and SAD (P=0.04), but BMI, total adiposity and Si were similar. VAT was inversely associated with AIRg and DI after controlling for ancestry, Si, and total adiposity (standardized beta, −0.32 and −0.34, both P<0.05). In addition, SAD (beta=0.41, P=0.02) was found to be a better estimate of VAT volume than WC (beta=0.32, P=0.08) after controlling for covariates. Receiver operating characteristic analysis showed that VAT volume, followed by SAD, outperformed WC and BMI in identifying dysglycemic participants. Conclusions Increasing VAT is associated with beta-cell dysfunction and dysglycemia in very obese women. In the presence of severe obesity, SAD is a simple surrogate of VAT, and an indicator of glucose dysregulation.