William E. Torres
Current Organizations / Institutes
The organizations/institutes from the scholar's latest article
Research Subjects
William E. Torres has a total of 8 co-authors. Here are the top co-authors by number of shared publications:
- Danijela Gasevic
School of Public Health and Preventive Medicine, Monash University, Melbourne, Victoria, Australia
1 shared publication - Edward Lin
Emory University
1 shared publication - Henry S. Kahn
Emory University School of Medicine, Atlanta, Georgia
1 shared publication - Jennifer K. Frediani
Nell Hodgson Woodruff School of Nursing, Emory University, Atlanta, Georgia, USA
1 shared publication - Lawrence S. Phillips
Emory University School of Medicine, Department of Medicine, Division of Endocrinology, Metabolism, and Lipids, Atlanta VA Health Care System, Atlanta, GA 30322, USA
1 shared publication - Nana Gletsu-Miller
Department of Nutrition Science, Purdue University, 700 W. State Street, Stone Hall, Room 208, West Lafayette, IN, 47907, USA.
1 shared publication
Latest Publications
- 14 February 2013
- Published by Springer Nature in Obesity Surgery
- Vol. 23 (7) , 874-881
Sagittal Abdominal Diameter and Visceral Adiposity
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.
- 14 February 2013
- Published by Springer Nature in Obesity Surgery
- Vol. 23 (7) , 874-881
Sagittal Abdominal Diameter and Visceral Adiposity
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.