visceral obesity

visceral obesity

a form of obesity due to excessive deposition of fat in the abdominal viscera and omentum, rather than subcutaneously, associated with dyslipidemia (for example, increased plasma triglyceride, low high-density lipoprotein cholesterol); perhaps due to accelerated lipolysis and mobilization of abdominal fatty acids by way of the portal vein; poses greater risk of diabetes mellitus, hypertension, metabolic syndrome, and cardiovascular disease than peripheral obesity does.
Synonym(s): abdominal obesity

vis·cer·al o·be·si·ty

(vis'ĕr-ăl ō-bē'si-tē)
Overweight due to excessive deposition of fat in the abdominal viscera and omentum, rather than subcutaneously, associated with dyslipidemia; poses greater risk of diabetes mellitus, hypertension, metabolic syndrome, and cardiovascular disease than peripheral obesity does.
References in periodicals archive ?
Obesity-related adverse health consequences occur predominately in individuals with upper body fat accumulation, the detrimental distribution, commonly associated with visceral obesity.[3] Abdominal obesity is more common among South Asians than general adiposity in contrast to whites, who have only a slightly higher rate of abdominal adiposity, and blacks who actually have a lower rate of abdominal obesity than general obesity.[4] Abdominal obesity is seen with increased prevalence in South Asians even among those who have a body mass index (BMI) <25 kg/[m.sup.2].
Imaging body composition in cancer patients: visceral obesity, sarcopenia and sarcopenic obesity may impact on clinical outcome.
This means that, according to BMI, the obese patients were not necessarily those with visceral obesity. Figure 2 shows the patients with similar BMI but with visceral fat and subcutaneous fat.
Most mechanisms of sarcopenia are also associated with visceral obesity, which may lead to a vicious cycle of intricate interactions among risk factors.
Obesity, especially visceral obesity, could increase the risk of type 2 diabetes, hypertension, dyslipidemia, and atherosclerosis, suggesting that obese patients with type 2 diabetes are at high risk for cardiovascular diseases [1].
The purpose of this study was to explore whether NAFLD, another accurate indicator for visceral obesity and insulin resistance, could be used as a surrogate for MetS diagnosis in the normal WC population.
Even at supposedly normal BMIs of 23 to 25, there can be hidden fatness observed, particularly in the abdomen (visceral obesity).
The definition of visceral obesity was VFA exceeding 130 [cm.sup.2] [19].
Participants with FTO risk allele (A) had significantly higher odds of being overweight/obese (OR: 0.19 (0.10-0.36), p < 0.001), central obesity (OR: 0.33 (0.15-0.71), p = 0.005), and visceral obesity (OR: 0.12 (0.06-0.23), p < 0.001) than individuals with the T allele only (Table 3).
While certain amounts of WAT are required for survival and health, central or visceral obesity has been linked to the etiology of chronic diseases such as cardiovascular disease, type 2 diabetes, and cancer [2, 3].
Despres, "Pathophysiology of human visceral obesity: an update," Physiological Reviews, vol.