Association of Region‐Specific Cardiac Adiposity With Dysglycemia and New‐Onset Diabetes

Background Visceral adipose tissue is assumed to be an important indicator for insulin resistance and diabetes beyond overweight/obesity. We hypothesized that region‐specific visceral adipose tissue may regulate differential biological effects for new‐onset diabetes regardless of overall obesity. Methods and Results We quantified various visceral adipose tissue measures, including epicardial adipose tissue, paracardial adipose tissue, interatrial fat, periaortic fat, and thoracic aortic adipose tissue in 1039 consecutive asymptomatic participants who underwent multidetector computed tomography. We explored the associations of visceral adipose tissue with baseline dysglycemic indices and new‐onset diabetes. Epicardial adipose tissue, paracardial adipose tissue, interatrial fat, periaortic fat, and thoracic aortic adipose tissue were differentially and independently associated with dysglycemic indices (fasting glucose, postprandial glucose, HbA1c, and homeostasis model assessment of insulin resistance) beyond anthropometric measures. The superimposition of interatrial fat and thoracic aortic adipose tissue on age, sex, body mass index, and baseline homeostasis model assessment of insulin resistance expanded the likelihood of baseline diabetes (from 67.2 to 86.0 and 64.4 to 70.8, P for ∆ ꭕ 2 : <0.001 and 0.011, respectively). Compared with the first tertile, the highest interatrial fat tertile showed a nearly doubled risk for new‐onset diabetes (hazard ratio, 2.09 [95% CI, 1.38–3.15], P <0.001) after adjusting for Chinese Visceral Adiposity Index. Conclusions Region‐specific visceral adiposity may not perform equally in discriminating baseline dysglycemia or diabetes, and showed differential predictive performance in new‐onset diabetes. Our data suggested that interatrial fat may serve as a potential marker for new‐onset diabetes.

Communication of subcutaneous, visceral, periaortic, epicardial fat and metabolic parameters with arterial stiffness in young people with abdominal obesity

Obesity plays a key role in the epidemic of type 2 diabetes mellitus (DM), cardiovascular and cerebrovascular diseases. Most studies confirm the association of increased arterial stiffness with obesity. However, the interrelation of various fat depots with one of the main indicators of vascular wall stiffness - the cardiovascular vascular index (CAVI) is currently not clear. The purpose of this study is to assess arterial stiffness in people with abdominal obesity without metabolic syndrome (MS) and with MS, the connection of fat depots (visceral, subcutaneous, perivascular, epicardial fat) with the stiffness parameter CAVI. Materials and methods. 68 people with abdominal obesity (AO) at the age of 18-45 years. The study included height, weight, BMI, waist circumference, and biochemical blood tests (fast glucose and glucose tolerance, uric acid, creatinine, GFR - MDRD, lipid profile, insulin, HOMA-IR). 24-hour blood pressure monitoring, computed tomography (Aquilion One Vision Edition, Toshiba, Japan) with the definition of subcutaneous, visceral, perivascular, epicardial fat, and also calculated the ratio subcutaneous to visceral fat. It was determined CAVI on the VaSera 1000 unit (Fukuda Denshi, Japan) to assess arterial stiffness. Abdominal obesity was derteming by cut off waist circumference >80 cm for women and >94 cm for men. As a result, we were formed 2 groups: persons with abdominal obesity and the presence of no more than one additional risk factor (metabolically healthy) - group 1, persons with MS (abdominal obesity in combination with 2 and more extra risk factors) - group 2, the control group consisted of healthy individuals (n=15) without obesity - group 0. Results. There was no statistically significant difference between CAVI groups. Correlations of CAVI with age r=0.340 (p=0.005), with daytime mean systolic blood pressure - SBPm average (r=0.280, p=0.021) and with mean diastolic blood pressure - DBPm average (r=0.329, p=0.006), with night SBPm average (r=0.233, p=0.014) and with DBPm average (r=0.297, p=0.014), with the volume of periaortic fat (r=0.218, p=0.074) were found. An inverse correlation was found between CAVI and BMI (r=-0.279, p=0.021), with subcutaneous fat depot (r=-0.285, p=0.019) and with the ratio of subcutaneous to visceral fat (r=-0.303, p=0.012). According to the multivariate regression analysis, the most significant impact on CAVI is exerted by age, daytime SBPm, BMI, and the volume of periaortic fat