ライフサイエンスコーパス: visceral obesity

1 o regulation of adipose tissue metabolism in visceral obesity.

2 s, diabetes, cancer, metabolic syndrome, and visceral obesity.

3 ain may contribute to insulin resistance and visceral obesity.

4 insulin resistance, lipid accumulation, and visceral obesity.

5 levels are further increased in humans with visceral obesity.

6 erglycemia, with increased susceptibility to visceral obesity.

7 hypertriglyceridemia, hepatic steatosis, and visceral obesity.

8 eration in states of impaired metabolism and visceral obesity.

9 chronic inflammatory profile associated with visceral obesity.

10 a greater portion of hepatic FFA delivery in visceral obesity.

11 y indicate that MSNA is elevated in men with visceral obesity.

12 cardiovascular diseases in individuals with visceral obesity.

13 g variant of the beta3-adrenoceptor gene and visceral obesity.

14 olesterol and VLDL triglycerides, and marked visceral obesity.

15 linemia, resulting in insulin resistance and visceral obesity.

16 Moreover, whether the association between visceral obesity and CHD risk differs by sex, age, race,

17 hat it could be associated with an increased visceral obesity and could be assessed preoperatively.

18 Excess glucocorticoids produce visceral obesity and diabetes, but circulating glucocort

19 tive pathways is an effective way to prevent visceral obesity and insulin resistance induced by high

20 esity and metabolic syndrome and can predict visceral obesity and insulin resistance.

21 lipase activity, an activity associated with visceral obesity and lipoprotein levels in humans.

22 This appears to be secondary to visceral obesity and the metabolic syndrome, with increa

23 ivity may be a common molecular etiology for visceral obesity and the metabolic syndrome.

24 A clear relationship exists between visceral obesity and type 2 diabetes, whereas subcutaneo

25 Visceral obesity appears to be the most common and predi

26 h changes in T cell function associated with visceral obesity are thought to affect chronic VAT infla

27 may be 'spokes on a wheel', with central or visceral obesity as the postulated hub of the wheel.

28 ribution to white adipose tissue, leading to visceral obesity at 2 months of age.

29 only protects against high-fat diet-induced visceral obesity but also regulates insulin action and g

30 Visceral obesity, defined by a high visceral adipose tis

31 issue exhibit a full metabolic syndrome with visceral obesity, dyslipidemia, insulin-resistant diabet

32 n increase in energy intake and body weight, visceral obesity, fatty liver, elevated insulin levels a

33 Visceral obesity has been defined as an important elemen

34 onsisting of systemic arterial hypertension, visceral obesity, impairment of glucose metabolism, and

35 ake as determinants of hepatic steatosis and visceral obesity in overweight adolescents at risk of ty

36 nd other adiposity indexes, 2) to identify a visceral obesity index that is independent of total adip

37 Metabolic syndrome is associated with visceral obesity, insulin resistance and an increased ri

38 e diet induced metabolic syndrome, including visceral obesity, insulin resistance, proinflammatory ch

39 The metabolic syndrome (visceral obesity, insulin resistance, type 2 diabetes, a

40 only associated with insulin resistance, and visceral obesity is associated with a chronic, low-grade

41 eater intake of fat and fried foods, whereas visceral obesity is associated with increased consumptio

42 Visceral obesity is often accompanied by non-alcoholic f

43 Obesity, especially visceral obesity, is associated with insulin resistance

44 r intake was associated with reduced odds of visceral obesity (OR: 0.82; 95% CI: 0.68, 0.98; P = 0.02

45 tion of soda were positively associated with visceral obesity (OR: 6.4; 95% CI: 1.2, 34.0; P = 0.03).

46 Visceral obesity, possibly via hyperinsulinemia, has als

47 Whether visceral obesity predicts coronary heart disease (CHD) r

48 ipose levels of corticosterone and developed visceral obesity that was exaggerated by a high-fat diet

49 implicated as one possible factor that links visceral obesity to adverse metabolic consequences; howe

50 contributes to the clinical presentation of visceral obesity, type 2 diabetes, and related cardiomet

51 sured by magnetic resonance spectroscopy and visceral obesity (visceral-to-subcutaneous adipose tissu

52 Hepatic steatosis and visceral obesity were evident in 43% and 44% of the samp

53 pression of this enzyme in fat cells develop visceral obesity with insulin resistance and dyslipidemi