ライフサイエンスコーパス: visceral fat

1 in and adiponectin protein expression within visceral fat.

2 at was dramatically lower in those with more visceral fat.

3 ult abdominal fat appeared to be specific to visceral fat.

4 ity-based sample with and without respect to visceral fat.

5 increased the effector-memory populations in visceral fat.

6 than birth weight alone, leads to increased visceral fat.

7 the ER stress-induced TRIP-Br2 expression in visceral fat.

8 esistance, and steatosis despite having more visceral fat.

9 ER) stress-induced inflammatory responses in visceral fat.

10 ninefold higher (P < 0.01) in liver than in visceral fat.

11 tosterone administration in adults decreases visceral fat.

12 but did not differ in the amount of body or visceral fat.

13 , despite HI subjects having marginally more visceral fat.

14 y balance, whereas the opposite is seen with visceral fat.

15 at diets, with lower body weight and reduced visceral fat.

16 lin sensitivity, and favor subcutaneous over visceral fat.

17 , and may even influence the accumulation of visceral fat.

18 trogen use, statin use, smoking, lipids, and visceral fat.

19 human tissues and ASCs from subcutaneous and visceral fat.

20 increased lean mass and reduced truncal and visceral fat.

21 l B- and T-cell development, and accumulated visceral fat.

22 ter body mass index, waist circumference, or visceral fat.

23 besity are best predicted by the quantity of visceral fat.

24 se in subcutaneous adipose tissue but not in visceral fat.

25 riginates from the nonsplanchnic UB fat, not visceral fat.

26 ex, total cholesterol, triglyceride, LDL and visceral fat.

27 le or with liver or were similar to those in visceral fat.

28 ntent, aortic pulse wave velocity (PWV), and visceral fat.

29 re a type of lymphoid tissue associated with visceral fat.

30 cantly elevated levels of PDFF and total and visceral fat.

31 ing blood pressure, triglyceride levels, and visceral fat.

32 significantly correlated to subcutaneous and visceral fat.

33 men not on HRT and in the lowest quartile of visceral fat (0.96 mg/liter).

34 bdominal visceral fat (HAVF; n=13, abdominal visceral fat=118.1+/-15.8 cm2) compared with their age-

35 ), skeletal muscle fat (117-221%; P < 0.05), visceral fat (24-31%; P < 0.05), blood triglycerides (32

36 re (-4.9 mm Hg; 95% CI, -9.5 to -0.3 mm Hg), visceral fat (-250.19 g; 95% CI, -459.9 to -40.5 g), and

37 d among HRT users in the highest quartile of visceral fat (4.29 mg/liter) compared with women not on

38 used statins (31% versus 19%), and had more visceral fat (69.4 versus 62.1 cm3) and lower HDL choles

39 Black men had less visceral fat (73.1+/-35.9 cm2) than white men (99.3+/-40

40 r abdominal visceral fat levels (LAVF; n=13, visceral fat= 73.0+/-6.0 cm2).

41 e three depots did not differ between meals; visceral fat accounted for only approximately 5% of meal

42 hypertrophic obesity combined with increased visceral fat accumulation and insulin resistance.

43 splanchnic cortisol production contribute to visceral fat accumulation and the hepatic insulin resist

44 he relationship between indices of abdominal visceral fat accumulation and the most commonly used bio

45 In adults, visceral fat accumulation is associated with insulin res

46 beta-HSD-1(-/-) mice also exhibited reduced visceral fat accumulation upon high-fat feeding.

47 Thus, obesity, visceral fat accumulation, and ethnicity in children may

48 oinflammatory cytokine production, stimulate visceral fat accumulation, enhance adipose tissue insuli

49 y in mice (pol eta(-/-)) causes obesity with visceral fat accumulation, hepatic steatosis, hyperlepti

50 were more insulin resistant, independent of visceral fat accumulation.

51 0.8% [95% CI, -1.6% to -0.07%]; P = .03) and visceral fat (adjusted mean difference, -3.9 cm3 [95% CI

52 ed a reversal of food aversion and sustained visceral fat after 5 weeks of allergy.

53 The reduction in visceral fat after RYGB appeared largely because of food

54 in chronic inflammation associated with less visceral fat after surgery may contribute to the reducti

55 subcutaneous fat and 0.9 +/- 0.1 kg (16.1%) visceral fat (all P < 0.0001 compared with baseline valu

56 r 6 months was associated with reductions in visceral fat and additionally with modest reductions in

57 idence for strong genetic effects underlying visceral fat and android/gynoid ratio.

58 Males have proportionally more visceral fat and are more likely to develop complication

59 onged SNS activation, favors accumulation of visceral fat and contributes to the clinical presentatio

60 The HFD increased body weight and visceral fat and decreased the length of the small intes

61 Calorie-restricted aged mice contain less visceral fat and displayed reduced cytokine levels, prot

62 d EWS aversion that was associated with less visceral fat and high levels of anti-Ova IgE antibodies

63 AR-gamma agonist, has been shown to decrease visceral fat and improve metabolic and inflammatory para

64 lic effects such as reducing weight gain and visceral fat and increasing glucose-stimulated insulin r

65 Excess visceral fat and insulin resistance, but not general adi

66 adiposity phenotype, characterized by excess visceral fat and insulin resistance, may contribute to d

67 ontrols, significant reductions in total and visceral fat and intrahepatic lipid were observed in bot

68 erized by selective loss of subcutaneous and visceral fat and is associated with hypertriglyceridemia

69 White women lost significantly more visceral fat and less SAAT than did African American wom

70 men would display higher levels of total and visceral fat and lower levels of physical activity than

71 males, but not males, had significantly less visceral fat and lower total serum and high density lipo

72 at for 3 mo did not differentially influence visceral fat and metabolic syndrome in a low-processed,

73 igher and PPARgamma level was lower in human visceral fat and mouse epididymal fat compared with thei

74 lipid accumulation in subcutaneous layer and visceral fat and not in the liver.

75 ons, with the strongest associations between visceral fat and Oscillospira members.

76 PM(2.5) induced YFP cell accumulation in visceral fat and potentiated YFP cell adhesion in the mi

77 en shown to reduce accumulation of abdominal visceral fat and protect against insulin resistance in l

78 Obese adolescents with a high proportion of visceral fat and relatively low abdominal subcutaneous f

79 thnicity influenced the relationship between visceral fat and risk factors.

80 provide a potential mechanistic link between visceral fat and systemic inflammation in people with ab

81 nhibited Sirt1 expression, and the deficient visceral fat and Th2 responses in Chi3l1 null mice were

82 18 months resulted in significantly reduced visceral fat and truncal obesity, triglycerides, and dia

83 release from nonhepatic tissues (presumably visceral fat) and nonhepatic fractional spillover (R = 0

84 and high proportion of deep subcutaneous and visceral fat) and skeletal muscle (low percentage of lea

85 ic effects, including increased body weight, visceral fat, and blood glucose levels and decreased lep

86 olling for age, sex, and change in fat mass, visceral fat, and fat-free mass; and was similar in chil

87 er UCP1 in all types of white fat, including visceral fat, and promoted additional browning in brown

88 LDL cholesterol, insulin sensitivity (S(i)), visceral fat, and subcutaneous abdominal adipose tissue

89 In conclusion, visceral fat appears metabolically unique in children, b

90 groups showed similar decreases in abdominal visceral fat (approximately 25%; P < 0.001 for all).

91 Measures of visceral fat are positively related to arterial inflamma

92 Central obesity and the accumulation of visceral fat are risk factors for the development of typ

93 at cells residing in the stromal fraction of visceral fat are the primary source of PAI-1.

94 ify each other within the vasculature and in visceral fat, are key processes that drive the initiatio

95 ith placebo induced significant decreases in visceral fat area (-13 cm2 vs +3 cm2, respectively; P =

96 hereas gluteal adipocyte size was related to visceral fat area (P=0.002), which suggests that these 2

97 weighted MR images (rho = 0.75), and average visceral fat area (rho = 0.77) (all P < .01) but poorly

98 ch, we compared computed tomography-acquired visceral fat area (VFA) and plasma adipocytokines, analy

99 act electrode system for measuring abdominal visceral fat area (VFA).

100 s on opposed-phase T1-weighted MR images and visceral fat area may be used as biomarkers for the pres

101 A visceral fat area of greater than or equal to 73.8 cm(2)

102 Visceral fat area was measured at three levels on water-

103 Visceral fat area was measured with computed tomography.

104 take, protein intake, physical activity, and visceral fat area, we found that Chinese elderly with T2

105 taneous fat area (TFA [total fat area], VFA [visceral fat area], and SFA [subcutaneous fat area], res

106 Abdominal subcutaneous fat, but not visceral fat, area was higher in ELBW survivors compared

107 are consistent with the hypothesized role of visceral fat as a unique, pathogenic fat depot.

108 However, the potential role of abdominal visceral fat as an important adipose tissue depot linkin

109 Individuals with higher measures of visceral fat as well as elevated arterial inflammation a

110 Most of these results involve visceral fat associations, with the strongest associatio

111 Lifestyle reduced visceral fat at L2-L3 (men -24.3%, women -18.2%) and at

112 t, waist circumference, and subcutaneous and visceral fat at L2-L3 and L4-L5 by computed tomography w

113 Abdominal visceral fat (AVF), abdominal subcutaneous fat (ASF), an

114 nge in birth weight) = -0.09, P = 0.002] and visceral fat (B = -0.07, P = 0.01) but not between birth

115 NT-proBNP remained inversely associated with visceral fat (beta coefficient = -0.08; p < 0.0001) and

116 ed atherosclerosis triggered by inflammatory visceral fat but had no protective effect on atheroscler

117 ids; and/or highest sex-specific quartile of visceral fat by computed tomography scan (in lieu of wai

118 onclude that UFAs generated via lipolysis of visceral fat by pancreatic lipases convert mild AP to SA

119 teriovenous concentration differences across visceral fat, by obtaining portal vein and radial artery

120 ession is significantly upregulated in human visceral fat compared with subcutaneous fat in obese ind

121 surrogate marker for tracking changes in the visceral fat compartment in black women.

122 Intramuscular, subcutaneous, and visceral fat compartments were delineated manually.

123 nt C57Bl/6J mice fed a high fat diet reduced visceral fat content and body weight.

124 diture; oxidation rates of lipid; ectopic or visceral fat content; or inflammatory and metabolic biom

125 Our data suggest that excessive abdominal visceral fat contributes to increased plasma IL-6, which

126 -1, e.g. derived from macrophages located in visceral fat, contributes to the development of diet-ind

127 etermining the factors related to children's visceral fat could result in interventions to improve ch

128 These include increased total and visceral fat, decreased muscle mass and aerobic capacity

129 res of aging, such as caloric restriction or visceral fat depletion, have succeeded in improving insu

130 her receptor pool showed extensive abdominal visceral fat deposition and weight gain compared with wi

131 (Ln) with T2D exhibit increased ectopic and visceral fat deposition and whether these are linked to

132 Both show stronger links between ectopic and visceral fat deposition, and an increased cardiometaboli

133 2D show a greater propensity for ectopic and visceral fat deposition.

134 icant relationships were observed in UBSQ or visceral fat depot.

135 ary obesity in the stromal vascular cells of visceral fat depots from mice.

136 of an accumulation in both subcutaneous and visceral fat depots with very little change in body weig

137 s in both upper-body subcutaneous (UBSQ) and visceral fat depots.

138 and the pathophysiological contributions of visceral fat depots.

139 oxemia; p = 0.013) and significantly reduced visceral fat-derived messenger RNA expression of interle

140 Furthermore, mice transplanted with visceral fat developed significantly more atherosclerosi

141 en and estrogen receptor (ER)-alpha suppress visceral fat development through actions in several orga

142 sical induction cocktail, whereas those from visceral fat differentiate poorly but can be induced to

143 ces in pancreatic, hepatic, subcutaneous and visceral fat distribution compared to NBW participants.

144 rage, but sex differences in this process in visceral fat do not account for sex differences in visce

145 Changes in food intake and visceral fat do not seem to explain improvements in insu

146 ge, height, body weight, BMI, fat-free mass, visceral fat, energy expenditure, respiratory quotient,

147 In vitro culture of visceral fat explants from naive dietary restricted mice

148 ipose tissue macrophages (F4/80(+) cells) in visceral fat expressing higher levels of tumor necrosis

149 were as follows: body weight, BMI, fat mass, visceral fat, fat-free mass, resting metabolic rate (RMR

150 results indicate that hens mainly mobilized visceral fat for egg formation and PCBs were deposited i

151 ween the decrease in FMD and the increase in visceral fat gain (rho=-0.42, p=0.004), but not with sub

152 Although UBSQ and visceral fat gains were completely reversed after 8 wk o

153 index < or =35 kg/m2) with higher abdominal visceral fat (HAVF; n=13, abdominal visceral fat=118.1+/

154 ation in the s.c. adipose tissue, but not in visceral fat, identified the metabolic syndrome in equal

155 was not associated with changes in body fat, visceral fat, IGF-I, androgens, or estradiol.

156 circumference, and total, subcutaneous, and visceral fat in 759 participants in the Quebec Family St

157 has limited potential to accurately estimate visceral fat in a clinical setting.

158 t stature homeobox 2) is higher in s.c. than visceral fat in both rodents and humans and that levels

159 ated after adjustment for percentage fat and visceral fat in both whites (P = 0.051) and blacks (P =

160 d, the increased (p<0.05) sizes of liver and visceral fat in high-fat dietary hamsters compared to th

161 patic FFA delivery increases with increasing visceral fat in humans and that this effect is greater i

162 he innate and adaptive immune systems within visceral fat in mice.

163 propensity to be released from hypertrophied visceral fat in MUO individuals and that this is the key

164 IP-Br2 expression is selectively elevated in visceral fat in obese humans, suggests that this transcr

165 Increased visceral fat in obesity leads to adiposopathy, due to th

166 n resistance and inflammatory changes in the visceral fat in response to high fructose.

167 ght due to the reduction of subcutaneous and visceral fat in the Dm-dNK(+/-)Tk2(-/-) mice was the onl

168 This is consistent with an involvement of visceral fat in the occurrence of coronary artery calciu

169 t, abdominal subcutaneous fat, and abdominal visceral fat in univariate and multivariate regression a

170 to almost 50% and increased as a function of visceral fat in women (r = 0.49, P = 0.002) and in men (

171 mutant mice acquired many key properties of visceral fat, including decreased thermogenic and increa

172 UBSQ and visceral fat increase and decrease proportionately with

173 However, as the proportion of visceral fat increased across tertiles, BMI and percenta

174 of the endothelium and is protective against visceral fat inflammation in obese mice.

175 ral fat, which may explain relations between visceral fat, insulin resistance, and vascular disease.

176 are consistent with the idea that abdominal visceral fat is an important adipose tissue depot linkin

177 These data suggest that visceral fat is an important site for IL-6 secretion and

178 Excessive visceral fat is associated with insulin resistance and o

179 Although excess visceral fat is associated with noninfectious inflammati

180 Reduced visceral fat is consistent with a role for increased myo

181 e been postulated; however, we now know that visceral fat is only one of many ectopic fat depots used

182 ctious inflammation, it is not clear whether visceral fat is simply associated with or actually cause

183 health burden, the accumulation of abdominal visceral fat is the specific cardio-metabolic disease ri

184 Increased intraabdominal (visceral) fat is associated with a high risk of diabetes

185 the effects of physical activity on adults' visceral fat, it was hypothesized that, after accounting

186 rway reactivity was significantly related to visceral fat leptin expression (rho = -0.8; P < 0.01).

187 .8 cm(2), P>0.05) peers with lower abdominal visceral fat levels (LAVF; n=13, visceral fat= 73.0+/-6.

188 and less insulin resistance, including lower visceral fat, liver fat, and homeostasis model assessmen

189 Despite similar visceral fat loss, S(I) improved less in old ( increase

190 nal subcutaneous fat mass (1650-1850 cm(3)), visceral fat mass (1350-1650 cm(3)), and total body weig

191 M:I was associated with Kf independently of visceral fat mass (B coefficient 3.13 [95% CI 0.22-6.02]

192 In multivariable analysis, higher baseline visceral fat mass (odds ratio [OR] per 1 SD [1.4 kg], 2.

193 e explained exclusively by associations with visceral fat mass (P=0.002), with no association seen be

194 were strong correlation between HOMA-IR and visceral fat mass (r = 0.570, 95% confidence interval(CI

195 Visceral fat mass and brain stearic acid, arachidonic ac

196 macronutrient and food profiles, may affect visceral fat mass and metabolic syndrome.

197 Normalization of visceral fat mass in the weight-reduced obese was accomp

198 m adiponectin was positively associated with visceral fat mass in young (r = 0.596, p</=0.001) and ad

199 und to induce significant weight loss in the visceral fat mass of HFD-fed hyperlipidemic rats without

200 dose TREN also reduced total adiponectin and visceral fat mass to a similar magnitude as TE, while in

201 Visceral fat mass was the only independent predictor of

202 In regression modeling, A1C, visceral fat mass, and M:I explained 38% of the variance

203 r and size, beta cell hyperplasia, decreased visceral fat mass, improved glucose tolerance, and enhan

204 ssed skeletal muscle microvascular function, visceral fat mass, physical activity levels, fitness, an

205 ) neurons reduced POMC neurons and increased visceral fat mass, suggesting a critical role of GnRH ce

206 lar exchange capacity (Kf), independently of visceral fat mass.

207 tely 5% of meal fat disposal irrespective of visceral fat mass.

208 ived PAI-1 protects against expansion of the visceral fat mass.

209 ndices, and the strongest association is for visceral fat mass.

210 tly associated with baseline measurements of visceral fat mass; levels of fasting glucose, insulin, a

211 Metabolism of chylomicron triglycerides in visceral fat may be an important source of portal venous

212 Findings suggest that visceral fat may be one potential pathway through which

213 Suppression of PPARgamma by FABP4 in visceral fat may explain the reported role of FABP4 in t

214 -term T cell depletion protocols specific to visceral fat may represent an additional strategy to man

215 ined after adjustment for percentage fat and visceral fat (mean race difference = 4.95 ng/mL; P < 0.0

216 Addition of abdominal visceral fat minimally increased the correlation.

217 Visceral fat necrosis has been associated with severe ac

218 nts and activity were noted in the extensive visceral fat necrosis of dying obese mice.

219 role of pancreatic lipases in SAP-associated visceral fat necrosis, the inflammatory response, local

220 , we also confirmed that white adipocytes in visceral fat of metabolically unhealthy obese (MUO) indi

221 L cholesterol (HDL-C) concentration; whether visceral fat or Si was independently related to lipids;

222 icant differences were observed in abdominal visceral fat or total fat mass; however, the average inc

223 at (OR: 1.38; 95% CI: 1.04, 1.84), abdominal visceral fat (OR: 1.35; 95% CI: 1.03, 1.76) but not with

224 ower BCF, due to a lower AIR, and increasing visceral fat over time.

225 .5- to 2.0-fold increase in subcutaneous and visceral fat (P < 0.0002) while remaining euglycemic, in

226 01) insulin and C-peptide concentrations and visceral fat (P < 0.05), fasting EGP and glucose disposa

227 sociated with a 13.03-cm(2) higher amount of visceral fat (P = 0.04).

228 In contrast, the sexes were monomorphic for visceral fat (P =.24).

229 ied the association between birth weight and visceral fat (P for interaction = 0.01).

230 educed adiponectin protein expression within visceral fat (p<0.05).

231 eased macrophage content of the transplanted visceral fat pad and reduced plasma monocyte chemoattrac

232 ssue depot, as opposed to an increase in all visceral fat pad depots evident after insulin replacemen

233 manifested in peripheral tissues such as the visceral fat pad, but not in the spleen.

234 Subcutaneous fat, visceral fat, paraspinous musculature, and vertebral cro

235 circumference, which may be a poor marker of visceral fat, particularly for African-American women.

236 ATMs from lean and obese visceral fat process and present major histocompatibilit

237 n resistance, proinflammatory changes in the visceral fat (production of proinflammatory adipokines a

238 To evaluate the hypothesis that visceral fat promotes systemic inflammation by secreting

239 -0.73, P < 0.01) but not when adjusting for visceral fat (r = - 0.54, P < 0.08).

240 osely associated with the level of abdominal visceral fat (r=0.65, P<0.05) than total fat mass (r=0.3

241 Increased visceral fat, rather than subcutaneous fat, during the o

242 leasing hormone analog, specifically targets visceral fat reduction but its effects on liver fat are

243 of improvement of hepatic insulin action by visceral fat removal (VF-).

244 d for differences in percentage body fat and visceral fat, Si no longer differed between groups.

245 d that aging was accompanied by increases in visceral fat similar to that seen in young obese (ob/ob

246 s had higher (p<0.05) weight gains, relative visceral-fat sizes, serum/liver lipids, and serum cardia

247 lusion, overeating SFAs promotes hepatic and visceral fat storage, whereas excess energy from PUFAs m

248 duced storage proteins in those with greater visceral fat suggest that the storage factors we measure

249 at in both humans and rodents, and in humans visceral fat Tbx15 expression is decreased in obesity.

250 Women lost more visceral fat than did men relative to total-body fat los

251 on of fat in their lower body, and much less visceral fat than do lean males at the same body mass in

252 Of note, Mito-Ob female mice developed more visceral fat than male mice.

253 s 626 [39] cm2, p=0.04), and slightly higher visceral fat than the controls (70 [11] vs 47 [6] cm2, p

254 are more closely associated with changes in visceral fat than with changes in other adipose tissue d

255 in that it may help to assess a component of visceral fat that other measures miss.

256 cular regulators of inflammatory response in visceral fat that-given that these pathways are conserve

257 waist-to-hip ratio, waist circumference, or visceral fat, the gender difference in CAC was not signi

258 11beta-HSD-2 gene expression was very low in visceral fat, the viscera released cortisone (P < 0.001)

259 After adjustment for either total body or visceral fat, time was not related to any outcome variab

260 ice have increased adiponectin expression in visceral fat tissue and in serum.

261 Visceral fat tissue primarily consists of adipocytes tha

262 4.3] cm2, P =.07) and the ratio of abdominal visceral fat to abdominal subcutaneous fat improved sign

263 The data suggest that the contribution of visceral fat to inflammation may not be completely accou

264 adolescents and grouped them by MRI-derived visceral fat to visceral adipose tissue (VAT) plus SAT (

265 ect on atherosclerosis in the absence of the visceral fat transplantation.

266 oric fructose restriction on DNL, liver fat, visceral fat (VAT), subcutaneous fat, and insulin kineti

267 To examine whether the accumulation of visceral fat (VF) could play a direct role in the pathop

268 tered body composition, especially increased visceral fat (VF) mass, could be a significant contribut

269 We directly examined whether visceral fat (VF) modulates hepatic insulin action by ra

270 Sexual dimorphism in visceral fat (VF) was attributable to elevated adipose t

271 classical risk factors of CVD, namely excess visceral fat (VF), elevated blood pressure, insulin resi

272 c restriction (CR) or by surgical removal of visceral fat (VF-).

273 at via dual-energy x-ray absorptiometry, and visceral fat via magnetic resonance, analyzed by intenti

274 factors upregulate TRIP-Br2 specifically in visceral fat via the ER stress pathway.

275 cently, the deleterious metabolic effects of visceral fat [visceral adipose tissue (VAT)] deposition

276 The primary outcome was abdominal visceral fat volume.

277 al-energy X-ray absorptiometry (DXA)-derived visceral-fat-volume measurements, in a subset of TwinsUK

278 of [1-(14)C]oleate stored in UBSQ, LBSQ, and visceral fat was 6.7 +/- 3.2, 4.9 +/- 3.4, and 1.0 +/- 0

279 is, the association between birth weight and visceral fat was apparent only in individuals with the h

280 Specifically, we determined whether visceral fat was associated with fasting insulin, insuli

281 t area, leptin decreased by 0.044 ng/mL when visceral fat was controlled for.

282 ssessed by dual-energy X-ray absorptiometry, visceral fat was determined by computed tomography, and

283 The relation between MSNA and abdominal visceral fat was independent of total body fat (r=0.61,

284 djusting for total fat, sex, and ethnicity), visceral fat was independently related to TG (P < 0.05)

285 Abdominal visceral fat was reduced (-19.2 [36.6] cm2 vs 2.3 [24.3]

286 observed for most of the PCB congeners when visceral fat was used.

287 eling, subcutaneous fat (P <0.0001), but not visceral fat, was significantly associated with leptin s

288 ines into the portal circulation that drains visceral fat, we determined adipokine arteriovenous conc

289 Collapsed across groups, changes in visceral fat were associated with changes in intrahepati

290 atic venous blood was sampled; and liver and visceral fat were biopsied in subjects undergoing bariat

291 However, changes in visceral fat were inversely related to increases in O(2)

292 P2-transcript levels in visceral fat were positively correlated with serum free

293 Fat-free mass and abdominal visceral fat were the primary end points after 1 year of

294 ated with components of the MetS, especially visceral fat, which appears to predict fibrosis as well

295 nd T-cell costimulatory molecules on ATMs in visceral fat, which correlated with an induction of T-ce

296 periarteriolar fat and both periarterial and visceral fat, which may explain relations between viscer

297 cantly more likely to have larger amounts of visceral fat while also having less muscle.

298 ected expansion of adipose tissue T cells in visceral fat with aging that includes a significant indu

299 cells led to an increase in CD11c(+) ATMs in visceral fat with high fat diet feeding.

300 -based measurements of abdominal, especially visceral, fat with total brain volume.