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1 linemia, resulting in insulin resistance and visceral obesity.
2 o regulation of adipose tissue metabolism in visceral obesity.
3 s, diabetes, cancer, metabolic syndrome, and visceral obesity.
4 ain may contribute to insulin resistance and visceral obesity.
5  insulin resistance, lipid accumulation, and visceral obesity.
6  levels are further increased in humans with visceral obesity.
7 erglycemia, with increased susceptibility to visceral obesity.
8 hypertriglyceridemia, hepatic steatosis, and visceral obesity.
9  and help prevent metabolic complications of visceral obesity.
10 eration in states of impaired metabolism and visceral obesity.
11 chronic inflammatory profile associated with visceral obesity.
12 a greater portion of hepatic FFA delivery in visceral obesity.
13 y indicate that MSNA is elevated in men with visceral obesity.
14  cardiovascular diseases in individuals with visceral obesity.
15 g variant of the beta3-adrenoceptor gene and visceral obesity.
16 olesterol and VLDL triglycerides, and marked visceral obesity.
17 ate that sleep loss predisposes to abdominal visceral obesity.
18 ional risk (57%), were overweight (53%), had visceral obesity (62%), had a normal SMI (51%), had a lo
19 OR: 2.35; 95% CI: 1.22, 4.54; P = 0.010) and visceral obesity [adjusted OR: 1.44 (1.09, 1.89); P = 0.
20  SVO compared to patients with sarcopenia or visceral obesity alone at 36 months (39% vs. 14% vs. 8%)
21 e, novel findings indicate that specifically visceral obesity and characteristics of impaired metabol
22    Moreover, whether the association between visceral obesity and CHD risk differs by sex, age, race,
23 hat it could be associated with an increased visceral obesity and could be assessed preoperatively.
24               Excess glucocorticoids produce visceral obesity and diabetes, but circulating glucocort
25 nd, leading to fat redistribution, including visceral obesity and ectopic fat accumulation, promoting
26 tive pathways is an effective way to prevent visceral obesity and insulin resistance induced by high
27 esity and metabolic syndrome and can predict visceral obesity and insulin resistance.
28 lipase activity, an activity associated with visceral obesity and lipoprotein levels in humans.
29                        Obesity, particularly visceral obesity and sarcopenia, are poor prognostic ind
30              This appears to be secondary to visceral obesity and the metabolic syndrome, with increa
31 ivity may be a common molecular etiology for visceral obesity and the metabolic syndrome.
32          A clear relationship exists between visceral obesity and type 2 diabetes, whereas subcutaneo
33 (visceral fat index) was used as a metric of visceral obesity and was calculated as the proportion of
34  percentage who met criteria for sarcopenia, visceral obesity, and SVO were 45%, 42%, and 20%, respec
35                                              Visceral obesity appears to be the most common and predi
36 h changes in T cell function associated with visceral obesity are thought to affect chronic VAT infla
37 lative exposure to estrogen, and overall and visceral obesity, are the most common and strongest pred
38  may be 'spokes on a wheel', with central or visceral obesity as the postulated hub of the wheel.
39 ribution to white adipose tissue, leading to visceral obesity at 2 months of age.
40  only protects against high-fat diet-induced visceral obesity but also regulates insulin action and g
41                                              Visceral obesity, but not BMI, is associated with recurr
42             Mediation analyses proposed that visceral obesity contributes to deep white matter lesion
43                                              Visceral obesity, defined by a high visceral adipose tis
44 issue exhibit a full metabolic syndrome with visceral obesity, dyslipidemia, insulin-resistant diabet
45 is no definition for the metabolic syndrome; visceral obesity, elevated lipids and glucose, and hyper
46 n increase in energy intake and body weight, visceral obesity, fatty liver, elevated insulin levels a
47                                              Visceral obesity has been defined as an important elemen
48 onsisting of systemic arterial hypertension, visceral obesity, impairment of glucose metabolism, and
49 nd for the genetic association of SORLA with visceral obesity in humans.
50 ake as determinants of hepatic steatosis and visceral obesity in overweight adolescents at risk of ty
51  intratumoral NK cell frequencies decline as visceral obesity increases in EAC patients.
52                                              Visceral obesity increases risk of cognitive decline in
53                                              Visceral obesity increases risks for all-cause mortality
54 nd other adiposity indexes, 2) to identify a visceral obesity index that is independent of total adip
55        Metabolic syndrome is associated with visceral obesity, insulin resistance and an increased ri
56 e diet induced metabolic syndrome, including visceral obesity, insulin resistance, proinflammatory ch
57                      The metabolic syndrome (visceral obesity, insulin resistance, type 2 diabetes, a
58 only associated with insulin resistance, and visceral obesity is associated with a chronic, low-grade
59 eater intake of fat and fried foods, whereas visceral obesity is associated with increased consumptio
60                                              Visceral obesity is associated with insulin resistance a
61                                              Visceral obesity is directly linked to increased cardiov
62                                              Visceral obesity is often accompanied by non-alcoholic f
63                          Obesity, especially visceral obesity, is associated with insulin resistance
64 r intake was associated with reduced odds of visceral obesity (OR: 0.82; 95% CI: 0.68, 0.98; P = 0.02
65 tion of soda were positively associated with visceral obesity (OR: 6.4; 95% CI: 1.2, 34.0; P = 0.03).
66 MUST and subcutaneous adiposity (P < 0.001), visceral obesity (P < 0.001), and low skeletal muscle in
67                                              Visceral obesity, possibly via hyperinsulinemia, has als
68                                      Whether visceral obesity predicts coronary heart disease (CHD) r
69 air on Cardiometabolic Risk Working Group on Visceral Obesity summarises the evidence for visceral ad
70                We aimed to define sarcopenic visceral obesity (SVO) using CT-based skeletal muscle in
71 ipose levels of corticosterone and developed visceral obesity that was exaggerated by a high-fat diet
72                     However, with respect to visceral obesity, the association with ankle SBP was mor
73 implicated as one possible factor that links visceral obesity to adverse metabolic consequences; howe
74  contributes to the clinical presentation of visceral obesity, type 2 diabetes, and related cardiomet
75 sured by magnetic resonance spectroscopy and visceral obesity (visceral-to-subcutaneous adipose tissu
76 (2) in men and <39 cm(2) /m(2) in women) and visceral obesity (VSR >= 1.54 in men and >=1.37 in women
77                        Hepatic steatosis and visceral obesity were evident in 43% and 44% of the samp
78 ought to investigate the association between visceral obesity with disease recurrence and survival in
79 pression of this enzyme in fat cells develop visceral obesity with insulin resistance and dyslipidemi