ライフサイエンスコーパス: caloric intake

1 etofore assumed, simply triggered by reduced caloric intake.

2 IL-13; this co-expression is enhanced after caloric intake.

3 s in skeletal muscle quality correlated with caloric intake.

4 es fat accumulation independent of excessive caloric intake.

5 size cap on SSBs and the potential effect on caloric intake.

6 and cholesterol levels without a decrease in caloric intake.

7 equired for the ability to maintain constant caloric intake.

8 equire parenteral nutrition (PN) to optimize caloric intake.

9 energy homeostasis, especially after excess caloric intake.

10 es in survival and fitness through increased caloric intake.

11 ased leptin expression, resulting in greater caloric intake.

12 ncy questionnaires and standardized to total caloric intake.

13 dergo rapid expansion during times of excess caloric intake.

14 tube dislodgment and may result in improved caloric intake.

15 hat these differences were due to changes in caloric intake.

16 and gut peptides that influence appetite and caloric intake.

17 n equations to describe the cumulative daily caloric intake.

18 adipose tissue mass during states of excess caloric intake.

19 ed weight gain and adiposity despite similar caloric intake.

20 f age, admission and weight-restored BMI, or caloric intake.

21 ioma risk, with adjustment for age and total caloric intake.

22 ic rats, but modified neither chow nor total caloric intake.

23 d with accelerated aging due to chronic high caloric intake.

24 the health benefits of DER without reducing caloric intake.

25 eight by decreasing appetite and spontaneous caloric intake.

26 reasing de novo lipogenesis independently of caloric intake.

27 , wound healing, chemopreventive agents, and caloric intake.

28 hanges explain these diet-induced changes in caloric intake.

29 injury in these mice that are independent of caloric intake.

30 s index, physical activity, time period, and caloric intake.

31 gher ambulatory blood pressure and increased caloric intake.

32 omeostasis in the face of wide variations in caloric intake.

33 body weight, extent of burn area, and daily caloric intake.

34 to loss of body fat in the context of normal caloric intake.

35 diets, comprising as much as 25% of average caloric intake.

36 tissue, and that expression is regulated by caloric intake.

37 er a meal and shows potential for decreasing caloric intake.

38 s subjected to 6 years of a 30% reduction in caloric intake.

39 s of lactoferrin being partly independent of caloric intake.

40 ession, with adjustment for age, gender, and caloric intake.

41 gth z scores were negatively correlated with caloric intake.

42 eppers, is able to induce satiety and reduce caloric intake.

43 lation of LHA glutamatergic neurons enhances caloric intake.

44 eted their fat stores, despite having higher caloric intake.

45 in the first 6 days, and not used to augment caloric intake.

46 fluenced neither cancer nor longevity at two caloric intakes.

47 0%, 95% CI, -12% to +12%; P = .30), or total caloric intake (+117 kcal; 95% CI, -243 to +479; relativ

48 -19.8%, p = 0.49) and in mean per capita SSB caloric intake (-13.3%, p = 0.56) from baseline to post-

49 e rates aimed at maintaining constant hourly caloric intake; 2) rates of responding markedly increase

50 ceived total parenteral nutrition (TPN) with caloric intake 20% to 30% above their resting energy exp

51 p, individuals had lower protein (30.1%) and caloric intake (30.2%) (P = 0.01 and 0.02, respectively)

52 the HF diet exhibited significantly reduced caloric intake (-40%), NPY expression in the arcuate nuc

53 per day orally, providing 33% of total daily caloric intake); 6 received alcohol and irbesartan (5 mg

54 respond differentially to various aspects of caloric intake(8-13) and social stimuli(14,15).

55 nd globally prevalent condition, with excess caloric intake a suspected etiologic factor.

56 ts the animals' ability to maintain constant caloric intake across experimental sessions.

57 urnal awakenings and ingestions, total daily caloric intake after the evening meal, CGI severity rati

58 of nocturnal ingestions and awakenings, and caloric intake after the evening meal.

59 cids) than could be accounted for by reduced caloric intake alone.

60 Excessive caloric intake and a shift in dietary composition toward

61 ration of cardiac aging under TRF, even when caloric intake and activity were unchanged.

62 esult from the interaction of modern dietary caloric intake and ancient mitochondrial genetic polymor

63 resents a promising option for reducing both caloric intake and appetite in humans.

64 tones in postmenopausal women independent of caloric intake and BMI, primarily because of the amount

65 In the whole cohort, after adjustment for caloric intake and cardiovascular disease risk factors,

66 Ad libitum, low-carbohydrate diets decrease caloric intake and cause weight loss.

67 is affects host fitness owing to the loss of caloric intake and colonization resistance (protection f

68 ioral and physiological situations including caloric intake and digestion, breast feeding, poison-avo

69 h reduced volume results in comparable total caloric intake and diminishes the risk of prolonged diar

70 nges of: (1) a significant increase in total caloric intake and dissected fat pad weights; (2) a rise

71 This results in a restricted caloric intake and diversion of bile and pancreatic secr

72 -type mice, the lean AAV mice have increased caloric intake and do not develop age-related obesity or

73 rt term HFD feeding led to a 37% increase in caloric intake and elevated base-line free FAs and insul

74 t is the consequence of an imbalance between caloric intake and energy consumption.

75 Obesity originates from an imbalance between caloric intake and energy expenditure that promotes adip

76 matory pathways results in the uncoupling of caloric intake and energy expenditure, fostering overeat

77 a novel role of PDE10A in the regulation of caloric intake and energy homeostasis.

78 Despite this, the balance between caloric intake and expenditure is tremendously accurate

79 cues, and that maintaining a balance between caloric intake and expenditure may reduce striatal, insu

80 lso imply that maintaining a balance between caloric intake and expenditure over time may reduce stri

81 Long term administration of leptin decreases caloric intake and fat mass and improves glucose toleran

82 iposity, the effect of FGF21 on body weight, caloric intake and fat oxidation were significantly atte

83 ated their metabolic syndrome with increased caloric intake and feed efficiency, reduced oxygen consu

84 First, we determined caloric intake and food choice after bilateral administr

85 libitum breakfast test meal, and their total caloric intake and food preferences were measured.

86 e onset of weight gain in response to excess caloric intake and hyperinsulinemia; however, the mechan

87 e energy expenditure, GLP-1 action to reduce caloric intake and improve glucose control, and GIP acti

88 duced by adipocytes, and it acts to decrease caloric intake and increase energy expenditure.

89 and pharmacologic interventions that reduce caloric intake and increase fatty acid oxidation, it see

90 ts was principally associated with decreased caloric intake and increased diet duration but not with

91 that promoted weight loss through decreased caloric intake and increased physical activity (interven

92 style intervention, which focused on reduced caloric intake and increased physical activity, or usual

93 individuals must make major restrictions in caloric intake and increases in energy expenditure.

94 d obese mice and was found to acutely reduce caloric intake and induce weight loss.

95 These results reveal that caloric intake and liver energy sensors dictate the bloo

96 Restoring energy balance by reducing caloric intake and losing weight are important therapeut

97 All of the models had normal or greater caloric intake and lower to normal metabolic rate, fasti

98 Caloric intake and meal-timing data were collected durin

99 ethods resulted in fat-induced inhibition of caloric intake and normalization of hypothalamic neurope

100 and considers the hypothesis that excessive caloric intake and obesity may be produced by dietary an

101 timescale to adapt to rapid fluctuations in caloric intake and on a chronic timescale to regulate bo

102 t studies exploring the relationship between caloric intake and outcomes in obese patients with under

103 ure secondary to exposure to excessive daily caloric intake and overnutrition.

104 evels were then compared across quintiles of caloric intake and physical activity in linear regressio

105 hours in bed under controlled conditions of caloric intake and physical activity.

106 eep extension under controlled conditions of caloric intake and physical activity.

107 Whereas excessive caloric intake and physical inactivity are likely import

108 of LHA glutamatergic neurons increased daily caloric intake and produced weight gain in mice that had

109 hotosynthesis constitute much of human daily caloric intake and provide the basis for high-energy bio

110 sity and diabetes are associated with excess caloric intake and reduced energy expenditure resulting

111 Caloric intake and REE were correlated with muscle prote

112 dietary switch changed the pattern of daily caloric intake and suppressed HFD-induced adipose macrop

113 a high-fat diet (HFD), which also increases caloric intake and the amount of stored calories.

114 Self-reported daily caloric intake and the measured resting metabolic rate a

115 tritional source for humans due to their low caloric intake and their high content in carbohydrates,

116 ght/dark cycle, despite equivalent levels of caloric intake and total daily activity output.

117 low social rank is associated with increased caloric intake and weight gain.

118 (500-kcal/d deficit from weight-maintaining caloric intake) and then randomly assigned to pioglitazo

119 ions include muscle wasting, anemia, reduced caloric intake, and altered immune function, which contr

120 time of scan, gender, ethnicity, education, caloric intake, and apolipoprotein genotype.

121 relative contribution of physical activity, caloric intake, and BMI to fasting insulin levels.

122 on cycle, provides a percentage of our daily caloric intake, and is a major driver in the renewable c

123 related to age, length of time on PN, total caloric intake, and lipid or glucose overload.

124 genotype, family history of type 1 diabetes, caloric intake, and omega-6 fatty acid intake, omega-3 f

125 Urinary creatinine, total caloric intake, and percentages of nutrient intake from

126 to support informed consumer choice, reduce caloric intake, and potentially encourage restaurant ref

127 ural systems regulating natural and adaptive caloric intake, and those regulating social behaviours,

128 crops that are vital to sustain the world's caloric intake are salt sensitive.

129 hat a restricted HFD intake regimen inhibits caloric intake as a consequence of FA-induced VMH ketone

130 itum, Hcrt-UCP2 transgenic mice had the same caloric intake as their wild-type littermates but had in

131 These changes were not due to aging or caloric intake, as neither these changes nor the MS were

132 d nonobese subjects underwent measurement of caloric intake at maximum satiation; postprandial sympto

133 Greater daily caloric intake attenuates this growth failure.

134 Caloric intake averaged 1168 +/- 801 kcal/day, amounting

135 These changes occur independently of caloric intake because of the effect of fructose on ATP

136 icity, education, apolipoprotein E genotype, caloric intake, body mass index, smoking status, depress

137 Appetite, caloric intake, body weight, and fat mass were measured

138 Adipose tissue expands in response to excess caloric intake, but individuals prone to deposit viscera

139 ability of fat mass to expand with increased caloric intake, but that SMRT also negatively regulates

140 ne week of daily anodal tDCS reduced overall caloric intake by 14% in comparison with sham stimulatio

141 A reduction of caloric intake by 40% for a short period (7 weeks), impl

142 All groups decreased their daily caloric intake by 400 kcal.

143 r day (low-carbohydrate diet) or to restrict caloric intake by 500 calories per day with <30% of calo

144 1.5 fewer HFSS adverts per day and decrease caloric intake by 9.1 kcal (95% UI 0.5-17.7 kcal), which

145 ng humans, can achieve precise regulation of caloric intake by adjusting consumption in response to c

146 of a fat emulsion maintained constant hourly caloric intake by adjusting the number of dry licks in r

147 fructose that supplies approximately 10% of caloric intake by Americans clearly affects absorption o

148 The evidence is accumulating that caloric intake can increase production of reactive oxyge

149 Excess caloric intake can lead to insulin resistance.

150 ivity, other breast cancer risk factors, and caloric intake controlled for (false discovery rate <0.2

151 Increased caloric intake correlated with atrophy in discrete neura

152 Reduced caloric intake decreases arterial blood pressure in heal

153 habditis elegans longevity genes, restricted caloric intake) demonstrate the feasibility of extending

154 e, cigarette smoking, body mass index, total caloric intake, dietary intake of lutein and zeaxanthin,

155 e quality of dietary intake (particularly in caloric intake, dietary protein intake, dietary fiber in

156 High caloric intake disrupted this interaction and decreased

157 A reduction in caloric intake dramatically slows cancer progression in

158 restriction, exhibited a greater increase in caloric intake during sleep restriction (d = 0.62), and

159 ly differ in daily caloric intake, increased caloric intake during sleep restriction, or meal timing.

160 ed by body mass index, menopausal status, or caloric intake during the past year.

161 Age, sex, caloric intake, education status, and UHDRS motor scores

162 iatal region showed increased sensitivity to caloric intake even in the absence of gustatory inputs.

163 or age, sex, education, body mass index, and caloric intake examined the associations between MedDiet

164 Caloric intake exceeded the estimated energy requirement

165 uch reward-related consumption can result in caloric intake exceeding requirements and is considered

166 When caloric intake exceeds expenditure, the surplus is chann

167 Animals exposed to 3 days of high caloric intake exhibited hyperinsulinemia without hyperg

168 In nearly every organism studied, reduced caloric intake extends life span.

169 occurred in the absence of a change in total caloric intake, fat pad weights, and adipose-related mea

170 The overall mean (+/-sd) daily caloric intake for all study participants was 49.4 +/- 2

171 ypercaloric diets (in 75% excess of habitual caloric intake) for 3 days, enriched in unsaturated FA (

172 iations (P < 10(-5)) for percentage of total caloric intake from protein and carbohydrate.

173 nactivity in the past 30 days, proportion of caloric intake from sweetened beverages (24-hour recall)

174 Higher caloric intake further increases the risk of incident st

175 Proper caloric intake goals in critically ill surgical patients

176 th increased physical activity and decreased caloric intake have been proposed to reduce insulin as a

177 ries that help in balancing food choice with caloric intake; however, this metabolic learning or memo

178 parate experiments a significant increase in caloric intake in a subsequent laboratory chow meal.

179 ct of less-healthy food advertising on acute caloric intake in children from a published meta-analysi

180 Long-term caloric intake in excess of energy expenditures, chronic

181 us findings, C75 was ineffective at reducing caloric intake in ketotic rats.

182 ounteracts the negative effects of increased caloric intake in mice fed a diet rich in fat and fructo

183 Average enteral caloric intake in pediatric patients was 15 kcal/kg befo

184 ats lack compensatory mechanisms to increase caloric intake in response to a T3-induced increase in E

185 l-3-yl)pyridine] significantly reduced total caloric intake in these mice during high-fat access.

186 ial sweeteners in rats resulted in increased caloric intake, increased body weight, and increased adi

187 whites did not significantly differ in daily caloric intake, increased caloric intake during sleep re

188 These focused on reducing caloric intake, increasing physical activity, and behavi

189 this epidemic has been attributed to excess caloric intake, induced by ever present food cues and th

190 alent among obese individuals with excessive caloric intake, insulin resistance, and type II diabetes

191 insulin), and the age 9-10 y insulin x total caloric intake interaction predicted IFG and T2DM at age

192 Increased daily caloric intake is a major behavioral mechanism that unde

193 Excessive caloric intake is associated with an increased risk for

194 ntained within a narrow range; even when the caloric intake is excessive, compensatory FA-induced upr

195 igenic gastric peptide hormone secreted when caloric intake is limited.

196 Excess caloric intake is linked to weight gain, obesity, and re

197 Caloric intake is normal in MGAT2-deficient mice, and di

198 Restricting caloric intake is one of the most effective ways to exte

199 s not tested whether an objectively measured caloric intake is positively associated with neural resp

200 In this paradigm, daily caloric intake is restricted to a consistent window of 8

201 nt to diet-induced obesity even though their caloric intake is similar to that of wild-type mice, sug

202 ant flies take larger but fewer meals, their caloric intake is the same as that of wild-type flies.

203 Excessive caloric intake is thought to be sensed by the brain, whi

204 ant proportion of the resulting reduction in caloric intake is unaccounted for by the restrictive and

205 Homeostatic feeding (i.e. titration of caloric intake), is typically associated with hypothalam

206 ikely due to severity of illness rather than caloric intake itself.

207 on and energy expenditure, with no change in caloric intake, locomotor activity, or thyroid hormone l

208 (iii) Restriction of caloric intake lowers steady-state levels of oxidative s

209 were grouped into one of four categories of caloric intake: <25%, 25-49%, 50-74%, and > or =75% of a

210 sought to assess sex and race differences in caloric intake, macronutrient intake, and meal timing du

211 that enhance the desire to eat and increase caloric intake, making it exceedingly difficult for indi

212 ing epidemiological evidence indicating that caloric intake may influence risk for AD and raises the

213 l outcomes but other studies concluding that caloric intake may not be important in determining outco

214 uts, vegetables, and spices, or even reduced caloric intake, may lower age-related cognitive declines

215 all patients with bvFTD had increased total caloric intake (mean, 1344 calories) compared with the A

216 del adjusted for age, CAG repeat length, and caloric intake, MeDi was not associated with phenoconver

217 for health behaviors (drinking, smoking, and caloric intake), medications for hypertension, high chol

218 onal studies suggest that achieving targeted caloric intake might not be necessary since provision of

219 However, the mechanisms by which reduced caloric intake modulates inflammation are poorly underst

220 Appetite, tiredness, nausea, well-being, caloric intake, nutritional status, and function were pr

221 nce appetite, tiredness, nausea, well-being, caloric intake, nutritional status, or function after 2

222 estricted feeding (TRF) regimen in which all caloric intakes occur consistently within </= 12 h every

223 s were fed ad libitum (AL) or a CR diet (60% caloric intake of AL diet).

224 rose ad libitum, Fat/Sucrose pair-fed to the caloric intake of CHO, or Fat/Sucrose at 60% of ad libit

225 t [Triticum aestivum]) providing most of the caloric intake of contemporary humans and their livestoc

226 In contrast, a high-fat diet reduces caloric intake of diabetics to normal, reflected by norm

227 Moderate differences in the caloric intake of meat products provided nontrivial redu

228 erine growth in FASDEL mice by supplementing caloric intake of pregnant dams normalized beta-cell mas

229 libitum, HPD ad libitum, HPD pair-fed to the caloric intake of the BCD, or the HPD at 60% of ad libit

230 the food, is costly, because it reduces the caloric intake of the benefactor vis-a-vis the beneficia

231 lower than those of nonvegetarians and that caloric intake of vegetarians is typically lower than th

232 tionally includes high amounts (30% of total caloric intake) of saturated fat rather than omega-6 fat

233 hGH) gene, GH1, to assess the effect of high caloric intake on expression as well as the local chromo

234 hysical activity muted the effects of excess caloric intake on insulin levels, GH1 promoter hyperacet

235 Insulin could mediate the effect of caloric intake on leptin and could be a determinant of i

236 he first in-depth analysis of the effects of caloric intake on NK cell phenotype and function and pro

237 ed to evaluate the effects of DEDS, DVS, and caloric intake on outcome.

238 rves, independent of changes in body weight, caloric intake or adiposity.

239 lating fatty acids but produced no change in caloric intake or body weight, stimulated novelty-seekin

240 on of high-fructose diets leads to increased caloric intake or decreased energy expenditure, thereby

241 ed by increasing physical activity, reducing caloric intake, or both, should lower insulin levels, pr

242 ned from stores contribute to disparities in caloric intake over time.

243 of physical activity (P < .0001), and lower caloric intake (P < .02) were all independently associat

244 sleep restriction, subjects increased daily caloric intake (P < 0.001) and fat intake (P = 0.024), i

245 2.36; 95% CI, 1.0-5.57; P = .05) and higher caloric intake (P = .04) were associated with risk of ph

246 proportion of patients with low protein and caloric intake (P = 0.02 and 0.01, respectively).

247 DEDS (P = 0.016) and DVS (P = 0.048) but not caloric intake (P = 0.585) significantly predicted outco

248 ta = 201 mg/d, adjusted for age, gender, and caloric intake; P < 0.001).

249 functions including digestion, regulation of caloric intake, pancreatic insulin secretion, and metabo

250 than women due to a larger increase in daily caloric intake, particularly during late-night hours.

251 aracteristics of the Western lifestyle (high caloric intake, physical inactivity, obesity, smoking, a

252 x, television watching, caregiver education, caloric intake, poverty-income ratio, race/ethnicity, se

253 Low caloric intake prior to first birth followed by a subseq

254 hormone levels, resting energy expenditure, caloric intake, pulmonary function, or clinical status.

255 in the lowest physical activity and highest caloric intake quintile (P < .0001).

256 in the highest physical activity and lowest caloric intake quintile compared with insulin levels of

257 regression, adjusted for age, gender, total caloric intake, reason for screening (routine or other),

258 The attenuated caloric intake, reduced food efficiency, and normalizati

259 To avoid increasing caloric intake, regular nut consumption can be recommend

260 iasis, but the role of physical activity and caloric intake remains poorly understood.

261 nate represented 1.4% and 0.08% of the total caloric intake, respectively, developed liver fibrosis a

262 y from 1980-1982 to 1995-1997, while overall caloric intake rose 8% in women but not men.

263 -day study period, the percent of prescribed caloric intake (+/- SE) received by the enteral route wa

264 ggest partial neural mediation of changes in caloric intake seen after RYGB surgery.

265 icity, education, apolipoprotein E genotype, caloric intake, smoking, medical comorbidity index, and

266 In 2004, caloric intake still remained >19% above the EER in both

267 Postnatal ad libitum caloric intake superimposed on intrauterine growth restr

268 to income ratio, sex, serum cotinine level, caloric intake, television watching, and urinary creatin

269 Caloric intake tended to decrease after DB administratio

270 produces a sustained decrease in ad libitum caloric intake that may be mediated by increased central

271 After adjustment for daily caloric intake, the greater likelihood of meeting calciu

272 et refeeding on the respective formulas with caloric intake titrated to achieve weight maintenance.

273 n, but the need for a long-term reduction in caloric intake to achieve these benefits has been assume

274 se or amino acid uptake or require a greater caloric intake to avoid hypoglycemia.

275 The accurate matching of caloric intake to caloric expenditure involves a complex

276 nisms to maintain energy balance by matching caloric intake to caloric expenditure.

277 justment for sex, age, height, weight, total caloric intake, tobacco smoking, and education.

278 CD subjects had increased caloric intake versus controls, but no alterations in to

279 Secondary outcomes included self-reported caloric intake, walking, and moderate physical activity.

280 iduals after adjustment for age, gender, and caloric intake was -6 mg/d (P = 0.95) in the control gro

281 the women were nulliparous, and median daily caloric intake was 1,840 cal (IQR 1,487-2,222).

282 Caloric intake was 61% and 22% of goal for the IEF and C

283 ) or low-fat (LF; 12% Kcal) diets, and equal caloric intake was maintained until euthanasia at 7 mont

284 A higher caloric intake was observed in patients with PD and did

285 A greater reduction in body weight and caloric intake was observed in response to IMC-H7 during

286 Daily caloric intake was recorded for each patient.

287 Caloric intake was similar in the two groups, with the t

288 Evaluating approximately 15% of Americans' caloric intake, we estimate that annual microplastics co

289 Decreases in caloric intake, weight, and BMI correlated with activati

290 ed women with AN, lower DEDS and DVS but not caloric intake were associated with poor outcome.

291 re (PBMR), predicted energy expenditure, and caloric intake were calculated using recommended formula

292 No differences in caloric intake were found.

293 Neither saturated fat nor total caloric intakes were independently associated with obesi

294 an increased drive to eat to restore normal caloric intake whilst reducing thermogenesis in order to

295 o be at lower risk than people with the same caloric intake who consumed smaller amounts of dietary f

296 Excessive caloric intake without a rise in energy expenditure prom

297 PDE10A deficiency produces a decrease in caloric intake without affecting meal frequency, daytime

298 ghrelin plasma concentrations, satiety, and caloric intake.Women (n = 39) were more sensitive toward

299 at stool calories expressed as percentage of caloric intake would increase with underfeeding compared

300 als, the female AT(2)KO mice with equivalent caloric intake (WT: 1424+/-48; AT(2)KO:1456+/-80 kcal) g