ライフサイエンスコーパス: visceral fat

1 loss by specifically promoting lipolysis in visceral fat.

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

3 significantly correlated to subcutaneous and visceral fat.

4 in and adiponectin protein expression within visceral fat.

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

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

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

8 increased the effector-memory populations in visceral fat.

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

10 esistance, and steatosis despite having more visceral fat.

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

12 ubcutaneous adipose tissue (SAT), but not in visceral fat.

13 tosterone administration in adults decreases visceral fat.

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

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

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

17 lin sensitivity, and favor subcutaneous over visceral fat.

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

19 trogen use, statin use, smoking, lipids, 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 ion in the liver and chronic inflammation in visceral fat.

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

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

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

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

27 , despite HI subjects having marginally more visceral fat.

28 human tissues and ASCs from subcutaneous and visceral fat.

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

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

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

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

33 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

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

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

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

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

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

39 Excessive visceral fat accumulation is a primary risk factor for m

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

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

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

43 eep white matter in obese subjects with high visceral fat accumulation, independent of common obesity

44 0.8% [95% CI, -1.6% to -0.07%]; P = .03) and visceral fat (adjusted mean difference, -3.9 cm3 [95% CI

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

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

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

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

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

50 Visceral fat and age were strong individual predictors o

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

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

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

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

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

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

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

58 pecially in terms of increased risk of added visceral fat and increased risk of non-communicable dise

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

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

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

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

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

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

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

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

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

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

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

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

71 Lower visceral fat and SCD-1 activity may contribute to the pa

72 In multivariate models, visceral fat and SCD-1 were associated with total fastin

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

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

75 llowing abstinence, drug co-exposure reduced visceral fat and the amount of insulin required to clear

76 Notably, both visceral fat and the pro-inflammatory cytokine tumor nec

77 18 months resulted in significantly reduced visceral fat and truncal obesity, triglycerides, and dia

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

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

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

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

82 whole-body insulin sensitivity, hepatic and visceral fat, and SCD-1 levels.

83 ipid components, fasting plasma glucose, and visceral fat, and there might be possible misclassificat

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

85 tissue specimens containing high amounts of visceral fat are challenging to analyze because of fat d

86 Measures of visceral fat are positively related to arterial inflamma

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

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

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

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

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

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

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

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

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

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

97 Compared with African Americans, the mean visceral fat area was 45% and 73% greater in Japanese Am

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

99 Visceral fat area was measured with computed tomography.

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

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

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

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

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

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

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

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

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

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

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

111 D55 was paradoxically associated with higher visceral fat but lower risk of type 2 diabetes.

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

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

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

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

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

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

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

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

120 -1, e.g. derived from macrophages located in visceral fat, contributes to the development of diet-ind

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

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

123 s aluminum oxide sample slide that minimizes visceral fat delocalization after thaw-mounting of tissu

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

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

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

127 ) mice exhibited accelerated weight gain and visceral fat deposition with age, when compared to wild

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

129 2D show a greater propensity for ectopic and visceral fat deposition.

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

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

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

133 In a condition of dysfunctional visceral fat depots, as in the case of obesity, alterati

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

135 and the pathophysiological contributions of visceral fat depots.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

165 UBSQ and visceral fat increase and decrease proportionately with

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

167 The obesity-asthma link is driven mainly by visceral fat, independent of total fat mass; therefore,

168 Higher visceral fat index, independent of fat mass index, was a

169 organ fat including subcutaneous fat index, visceral fat index, pericardial fat index, and liver fat

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

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

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

173 Excessive visceral fat is associated with insulin resistance and o

174 Although excess visceral fat is associated with noninfectious inflammati

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

176 The visceral fat is highly susceptible to the availability o

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

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

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

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

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

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

183 it obese individuals had significantly lower visceral fat levels than unfit obese peers (-3.0; P = 0.

184 body composition, amount of subcutaneous and visceral fat, liver and heart ectopic fat, adipose tissu

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

186 cible deletion of adipose OGT causes a rapid visceral fat loss by specifically promoting lipolysis in

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

188 Mechanistically, visceral fat maintains a high level of O-GlcNAcylation d

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

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

191 p experienced a ~73% reduction (~0.69 kg) in visceral fat mass (false discovery rate, FDR < 2.0 x 10(

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 icrobiota and diet have been shown to impact visceral fat mass (VFM), a major risk factor for cardiom

196 Visceral fat mass and brain stearic acid, arachidonic ac

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

198 Patients with higher visceral fat mass are at a higher risk of developing sev

199 nsitivity improved (P < 0.001), and body and visceral fat mass decreased in all groups (P < 0.001).

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

201 iR-34c in early onset insulin resistance and visceral fat mass increase, contributing to accelerated

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

203 A was: fat mass R2 = 0.88 male, 0.93 female; visceral fat mass R2 = 0.67 male, 0.75 female.

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

205 Visceral fat mass was the only independent predictor of

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

207 , most of the observed beneficial changes in visceral fat mass, and metabolomic and transcriptomic pr

208 aving three or more risk factors out of high visceral fat mass, high blood pressure, low high-density

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

210 fat, kidney filtration, percentage body fat, visceral fat mass, lean body mass, cardiopulmonary fitne

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

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

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

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

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

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

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

218 gnificantly increased body mass, overall and visceral fat masses, and decreased bone area.

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

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

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

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

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

224 Addition of abdominal visceral fat minimally increased the correlation.

225 Visceral fat necrosis has been associated with severe ac

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

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

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

229 expression itself was down-regulated in the visceral fat of two obese mouse models and obese patient

230 Visceral fat (omentum) and abdominal subcutaneous fat of

231 Acute lipolysis of visceral fat or circulating triglycerides may worsen acu

232 ester lipase (CEL), which may leak into the visceral fat or systemic circulation during pancreatitis

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

234 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

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

236 .5- to 2.0-fold increase in subcutaneous and visceral fat (P < 0.0002) while remaining euglycemic, in

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

263 11beta-HSD-2 gene expression was very low in visceral fat, the viscera released cortisone (P < 0.001)

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

265 Visceral fat tissue primarily consists of adipocytes tha

266 4.3] cm2, P =.07) and the ratio of abdominal visceral fat to abdominal subcutaneous fat improved sign

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

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

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

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

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

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

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

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

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

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

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

278 The primary outcome was abdominal visceral fat volume.

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

280 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

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

282 3DO visceral fat was as precise (%CV = 7.4 for males, 6.8 fo

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

284 subcutaneous adipose tissue as the amount of visceral fat was independent of the level of chimerism.

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.