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Visceral fat

Excess visceral fat increases T2DM risk

Excess visceral fat and insulin resistance could contribute to cardiovascular disease among obese individuals
Understanding the biological differences between visceral and subcutaneous fat could assist in the battle against obesity
Dr Ian Neeland (left) and Dr James de Lemos (Credit: UT Southwestern Medical Center)

People with excess visceral fat have an increased risk for the development of type 2 diabetes, according to a new study by researchers at UT Southwestern Medical Center, Texas.

“Among obese individuals, it is not necessarily how much fat a person has, but rather where the fat is located on a person that leads to diabetes,” said Dr James de Lemos, professor of internal medicine at UT Southwestern, and senior author of the study.

The study, one of the largest of its kind to assess a multi-ethnic population of obese people in the US using extensive imaging of adipose tissue, also reported that people with excess abdominal subcutaneous fat were not at higher risk for the onset of diabetes.

“We found that individuals who developed pre-diabetes and diabetes had evidence of early cardiovascular disease years before the onset of diabetes,” said Dr Ian Neeland, a cardiology fellow and first author of the paper. “This finding suggests that excess visceral fat and insulin resistance may contribute to cardiovascular disease among obese individuals.”


The purpose of the investigation was to examine the association between adiposity phenotypes and risk for incident pre-diabetes and diabetes in a multi-ethnic, population-based cohort of obese adults.

A total of 6,101 obese participants (BMI≥30) aged 30 to 65 years without diabetes or cardiovascular disease were enrolled in the Dallas Heart Study between 2000 and 2002.

Body composition was measured by dual energy x-ray absorptiometry and magnetic resonance imaging; circulating adipokines and biomarkers of insulin resistance, dyslipidemia, and inflammation; and subclinical atherosclerosis and cardiac structure and function by computed tomography and magnetic resonance imaging.

By determining the location and function of body fat, the researchers were able to identify obese persons who are at a higher risk for developing type 2 diabetes years before the disease appears.

The main outcome measures were the incidence of diabetes through a median 7.0 years (interquartile range, 6.6-7.6) of follow-up.


At seven years, the researchers found that 732 participants (mean age, 43 years; 65% women; 71% non-white), 84 (11.5%) had developed diabetes. In multivariable analysis, higher baseline visceral fat mass (odds ratio [OR] per 1 SD [1.4kg], 2.4; 95% CI, 1.6-3.7), fructosamine level (OR per 1 SD [1.1μmol/L], 2.0; 95% CI, 1.4-2.7), fasting glucose level (OR per 1 SD [1.1μmol/L], 1.9; 95% CI, 1.4-2.6), family history of diabetes (OR, 2.3; 95% CI, 1.3-4.3), systolic blood pressure (OR per 10mmHg, 1.3; 95% CI, 1.1-1.5), and weight gain over follow-up (OR per 1 kg, 1.06; 95% CI, 1.02-1.10) were independently associated with diabetes, with no associations observed for BMI, total body fat or abdominal subcutaneous fat.

Among the 512 participants with normal baseline glucose values, the composite outcome of pre-diabetes or diabetes occurred in 39.1% and was independently associated with baseline measurements of visceral fat mass; levels of fasting glucose, insulin and fructosamine; older age; non-white race; family history of diabetes; and weight gain over follow-up (all p<0.05), but not with measurements of general adiposity.

Therefore, those patients who developed pre-diabetes and diabetes had higher amounts of visceral fat and greater insulin resistance, compared with those who remained healthy.

“Understanding the biological differences between visceral fat and subcutaneous fat may help doctors to more effectively battle the obesity epidemic occurring in the US,” said Dr de Lemos. “The risk for diabetes varies widely among different obese individuals, and this study suggests that by predicting who will get diabetes, it may be possible to target intensive lifestyle, medical, and surgical therapies for those at a higher risk.”

This research, funded by the Donald W Reynolds Foundation, involved numerous noted UT Southwestern scientists and physicians, including Dr Helen Hobbs, director of the Eugene McDermott Center for Human Growth and Development, and Dr Eric Olson, chairman of molecular biology.

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