ライフサイエンスコーパス: caloric intake

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

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

3 equired for the ability to maintain constant caloric intake.

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

5 energy homeostasis, especially after excess caloric intake.

6 es in survival and fitness through increased caloric intake.

7 ased leptin expression, resulting in greater caloric intake.

8 ncy questionnaires and standardized to total caloric intake.

9 dergo rapid expansion during times of excess caloric intake.

10 tube dislodgment and may result in improved caloric intake.

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

12 and gut peptides that influence appetite and caloric intake.

13 gth z scores were negatively correlated with caloric intake.

14 n equations to describe the cumulative daily caloric intake.

15 adipose tissue mass during states of excess caloric intake.

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

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

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

19 the health benefits of DER without reducing caloric intake.

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

21 eight by decreasing appetite and spontaneous caloric intake.

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

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

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

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

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

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

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

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

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

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

32 lation of LHA glutamatergic neurons enhances caloric intake.

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

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

35 s of lactoferrin being partly independent of caloric intake.

36 etofore assumed, simply triggered by reduced caloric intake.

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

38 s in skeletal muscle quality correlated with caloric intake.

39 es fat accumulation independent of excessive caloric intake.

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

41 and cholesterol levels without a decrease in caloric intake.

42 fluenced neither cancer nor longevity at two caloric intakes.

43 0%, 95% CI, -12% to +12%; P = .30), or total caloric intake (+117 kcal; 95% CI, -243 to +479; relativ

44 -19.8%, p = 0.49) and in mean per capita SSB caloric intake (-13.3%, p = 0.56) from baseline to post-

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

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

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

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

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

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

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

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

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

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

55 Excessive caloric intake and a shift in dietary composition toward

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

90 Caloric intake and meal-timing data were collected durin

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

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

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

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

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

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

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

98 Whereas excessive caloric intake and physical inactivity are likely import

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

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

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

102 Caloric intake and REE were correlated with muscle prote

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

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

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

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

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

108 (500-kcal/d deficit from weight-maintaining caloric intake) and then randomly assigned to pioglitazo

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

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

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

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

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

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

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

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

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

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

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

120 Greater daily caloric intake attenuates this growth failure.

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

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

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

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

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

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

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

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

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

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

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

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

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

134 Excess caloric intake can lead to insulin resistance.

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

136 Increased caloric intake correlated with atrophy in discrete neura

137 Reduced caloric intake decreases arterial blood pressure in heal

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

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

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

141 High caloric intake disrupted this interaction and decreased

142 A reduction in caloric intake dramatically slows cancer progression in

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

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

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

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

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

148 Caloric intake exceeded the estimated energy requirement

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

150 When caloric intake exceeds expenditure, the surplus is chann

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

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

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

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

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

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

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

158 Higher caloric intake further increases the risk of incident st

159 Proper caloric intake goals in critically ill surgical patients

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

176 Excessive caloric intake is associated with an increased risk for

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

221 2.36; 95% CI, 1.0-5.57; P = .05) and higher caloric intake (P = .04) were associated with risk of ph

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

242 Postnatal ad libitum caloric intake superimposed on intrauterine growth restr

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

244 Caloric intake tended to decrease after DB administratio

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

260 Daily caloric intake was recorded for each patient.

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

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

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

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

265 No differences in caloric intake were found.

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

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

268 Excessive caloric intake without a rise in energy expenditure prom

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

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

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