ライフサイエンスコーパス: salt intake

1 in rats during sodium deprivation and after salt intake.

2 ring various ingestive activities, including salt intake.

3 n calcium retention as a function of dietary salt intake.

4 neration increased (P < 0.05) 30 to 40% with salt intake.

5 that was independent of the level of dietary salt intake.

6 regulation of insulin sensitivity to dietary salt intake.

7 al P-450 isoform regulated by excess dietary salt intake.

8 c) were studied for BP response to increased salt intake.

9 precede the hypertension resulting from high salt intake.

10 tenance of normal blood pressure during high salt intake.

11 ment a coherent, workable strategy to reduce salt intake.

12 o optimise potential policy to reduce actual salt intake.

13 ndings underrepresent the population's total salt intake.

14 hypertension that was unaffected by dietary salt intake.

15 its sodium content may help lower population salt intake.

16 ous benefits of population-wide reduction in salt intake.

17 g lifestyle, genetics, sex, age, and dietary salt intake.

18 accurate estimation of actual discretionary salt intake.

19 where home cooking remains a major source of salt intake.

20 to sustaining individual dietary control of salt intake.

21 es input to centers in the brain, amplifying salt intake.

22 mic magnocellular system during chronic high-salt intake.

23 nary salt intake from observed discretionary salt intake.

24 in mice and humans across various levels of salt intake.

25 y involved in the vascular responses to high salt intake.

26 ly consumed processed pork products to total salt intake.

27 en the knockout and control mice during high salt intake.

28 d with health outcomes obtained with current salt intake.

29 reby influencing BP under conditions of high salt intake.

30 were challenged to a normal- or chronic high-salt intake (1% NaCl).

31 In populations with high salt intake, a modest reduction in salt intake lowers bl

32 Even a modest reduction in salt intake across the whole population will lead to a m

33 gramme needs further strengthening to reduce salt intake across the whole population, including schoo

34 Excess dietary salt intake acts as a risk factor for autoimmune disease

35 increased in Pkd1 knockout mice during high salt intake; administration of NS-398, a selective cyclo

36 Salt intake affects male body shape by increasing BMI-ad

37 one of the mechanisms underlying how dietary salt intake affects the activity of VP neurons via ENaC

38 Here we show that high salt intake affects the gut microbiome in mice, particul

39 eted subjects displayed significantly larger salt intakes after their second experience with sodium d

40 health challenge due to factors such as high salt intake, air pollution, poor diets, limited healthca

41 r methods for estimating daily discretionary salt intake among females of reproductive age (FRA) in t

42 ension produced by the combination of a high salt intake and administration of angiotensin II, the An

43 and family members was effective in lowering salt intake and blood pressure.

44 ere is a causal relationship between dietary salt intake and blood pressure.

45 g evidence for a causal relationship between salt intake and blood pressure.

46 consistently shown a direct relation between salt intake and cardiovascular risk, and a reduction in

47 hat there is a J-shaped relationship between salt intake and cardiovascular risk, i.e. both high and

48 ciation with an inverse relationship between salt intake and heart rate, indicating intact barorecept

49 observations regarding the relation between salt intake and its reduction on blood pressure have eme

50 endocrine mechanisms that regulate water and salt intake and loss.

51 Avoidance of excessive salt intake and maintenance of vascular health may help

52 tting based on their contribution to dietary salt intake and relevance to ongoing revision in the Mal

53 oordinating homeostatic responses to dietary salt intake and suggest a complex pathophysiology for hy

54 o-parent approach, was effective in lowering salt intake and systolic blood pressure in adults, but t

55 The relationship between dietary salt intake and the associated risk of hypertension and

56 a(+)] and osmolality rise in proportion with salt intake and thus promote release of vasopressin (VP)

57 l by the gustatory system is fundamental for salt intake and tissue homeostasis.

58 h urine collections, a population's habitual salt intake and to explore the potential of using the ra

59 distribution of risk factors associated with salt intake and tobacco use, and to model the effects on

60 SRA mice exhibited an increase in water and salt intake and urinary volume, which were significantly

61 opulations, and the importance of concurrent salt intake and what constitutes K+ supplementation.

62 ntly increased-183% by losartan, 212% by low salt intake, and 227% by the combination of the two-comp

63 ude Helicobacter pylori infection, age, high salt intake, and diets low in fruit and vegetables.

64 ndocrine secretion, cardiovascular function, salt intake, and nociception.

65 youngest vs. oldest: 24% vs. 7%, p = 0.001), salt intake, and other dietary measures (21% vs. 9%, p =

66 elevated plasma angiotensin II and increased salt intake (AngII-salt).

67 ed that the major contributors to Malaysia's salt intake are cooked food and processed foods.

68 urate and precise estimates of discretionary salt intake are essential to the design of salt fortific

69 r pylori (H. pylori) infection and excessive salt intake are known as important risk factors for stom

70 The cardiovascular benefits of reduced salt intake are on par with the benefits of population-w

71 cobacter pylori infection and a high dietary salt intake are risk factors for the development of gast

72 cardiovascular risk, i.e. both high and low salt intakes are associated with an increased risk.

73 ake, studies specifically designed to assess salt intake as an endpoint are needed.

74 ethodologically robust studies with accurate salt intake assessment have shown that a lower salt inta

75 Mean salt intake at baseline was 5.5 g/day (standard deviatio

76 ally involved in the control of need-induced salt intake; (b) negative feedback from the stomach and

77 ered on what basis (eg, sex, ethnicity, age, salt intake, baseline renin, ACE or aldosterone, and gen

78 ly marginal, if any, effects of amiloride on salt intake behavior, highlighting the importance of con

79 eceptors were significantly increased by low salt intake but were significantly decreased by losartan

80 sources of sodium to reduce adult population salt intake by approximately 30% toward the optimal WHO

81 neuroanatomical basis for the modulation of salt intake by the CeA.

82 Also after salt intake, c-Fos activation increased within pontine n

83 mation regarding the feasibility of reducing salt intake, call for renewed efforts in this area as a

84 gy, we examine evidence that the lowering of salt intake can combat hypertension.

85 els that may occur in human blood after high-salt intake can potentiate, in serum-free culture condit

86 In decoy rats, high salt intake caused a greater positive sodium balance.

87 We show that high dietary salt intake caused an increase in the expression and act

88 Primary outcome was the difference in salt intake change (measured by 24 hour urinary sodium e

89 Dietary salt intake controls epithelial Na+ channel (ENaC)-media

90 In adults, salt intake decreased in both intervention and control g

91 A 6-g/d increase in salt intake decreased the level of rhythmical mineraloco

92 was moderate-certainty evidence that reduced salt intake decreased the risk for all-cause mortality i

93 In conditions of high salt intake, defective uromodulin processing predisposes

94 e unexpected observation that long-term high salt intake did not increase water consumption in humans

95 up had greater improvements in self-reported salt intake (difference, 15.4 [95% CI, 4.4 to 26.0]; P =

96 Mice with high dietary salt intake display enhanced induction of Th17 response

97 The salt intake distribution of single-day measurements was

98 Predicting habitual salt intake distribution using single-day measurements w

99 To estimate a population's salt intake distribution, it is important to correct 24-

100 n-person variance significantly narrowed the salt intake distribution-the proportion with salt intake

101 zed clinical and MRI follow-up, suggest that salt intake does not influence MS disease course or acti

102 identified various mechanisms by which high salt intake drives disease in the kidney, brain, vascula

103 ity, and inaccurate and biased estimation of salt intake, e.g. from a single spot urine sample with f

104 Thus, salt intake enhances generation of O(2)(.-) accompanied

105 After 4 weeks of high-salt intake, ES rats still showed a lower mean serum cre

106 id not decrease food intake after fasting or salt intake following salt depletion; inactivation incre

107 High dietary salt intake for 7 days caused an increase in expression

108 rnative or complementary measure to reducing salt intake for lowering of BP.

109 On the normal salt intake for the UK population, supine blood pressure

110 'hidden' salt in processed foods disconnects salt intake from discretionary control.

111 participants to estimate usual discretionary salt intake from observed discretionary salt intake.

112 ave shown that the formulas used to estimate salt intake from spot urine cause a spurious J-curve.

113 A reduction in salt intake from the current world average of ~10 g/day

114 Across all 3 levels of salt intake, half-weekly and weekly rhythmical mineraloc

115 Excessive salt intake has been associated with hypertension and in

116 erson's long-term salt taste preference, and salt intake has been associated with increased risk of c

117 Hyperosmolality due to high dietary salt intake has been linked to pathological inflammatory

118 However, excessive salt intake has often been held responsible for numerous

119 Global targets to reduce salt intake have been proposed, but their monitoring is

120 rmine how, in the face of chronic changes in salt intake, humans maintain volume and osmotic homeosta

121 Here we show that chronic high salt intake impairs baroreceptor inhibition of rat VP ne

122 ection of senktide (NK3r agonist) attenuates salt intake in DOCA-treated animals.

123 time that 20-HETE excretion is regulated by salt intake in hypertension.

124 ulatory adjustments, could reduce population salt intake in Malaysia.

125 hich are recognised as major contributors to salt intake in Malaysian diets.

126 from the home would reduce total population salt intake in New Zealand by 35% (from 8.4 to 5.5 g/d)

127 otective in the setting of low sugar and low salt intake in our past, today, the combination of diets

128 he amygdala (CeA) has been shown to modulate salt intake in response to aldosterone, so we investigat

129 a promising policy option to discourage high salt intake in the out-of-home food sector.

130 We selected two interventions: to reduce salt intake in the population by 15% and to implement fo

131 on observed in response to increased dietary salt intake in these animals.

132 A 6-g/d increase in salt intake increased urine osmolyte excretion, but redu

133 The exact mechanism by which salt intake increases blood pressure and cardiovascular

134 The idea that increasing salt intake increases drinking and urine volume is widel

135 High salt intake increases the risk of cardiovascular disease

136 We show that high salt intake increases the spontaneous firing rate of VP

137 rone-acetate (DOCA) in combination with high salt intake induced arterial hypertension of similar mag

138 Excess dietary salt intake induces the activity of the kidney arachidon

139 roaches we tested whether increased maternal salt intake influences fetal kidney development to rende

140 thogenicity is a central player linking high-salt-intake influences to immunopathophysiology of diabe

141 ate that osmotic balance in response to high salt intake involves a complex regulatory process that i

142 High salt intake is a major risk factor for hypertension.

143 nance of osmotic balance in response to high salt intake is a passive process that is mediated largel

144 High salt intake is a top dietary risk factor.

145 logical studies have shown that high dietary salt intake is also a risk factor for gastric cancer.

146 Salt intake is an established response to sodium deficie

147 lt intake assessment have shown that a lower salt intake is associated with a reduced risk of cardiov

148 vascular risk, and a reduction in population salt intake is associated with a reduction in cardiovasc

149 However, excessive salt intake is associated with high blood pressure.

150 Reducing salt intake is considered an important public health str

151 ovascular morbidity and mortality, excessive salt intake is estimated to cause ~5 million deaths per

152 ies, support the judgment that habitual high salt intake is one of the quantitatively important, prev

153 dy was to examine whether changes in dietary salt intake lead to compensatory changes in expression o

154 A modest reduction in salt intake leads to a fall in blood pressure in both no

155 High salt intake leads to high blood pressure, even when occu

156 e feeding of HCl in the presence of a normal salt intake led to a degree of metabolic acidosis not si

157 r surplus reduced fluid intake at the 12-g/d salt intake level.

158 ys' duration, we exposed 10 healthy men to 3 salt intake levels (12, 9, or 6 g/d).

159 INTERSALT showed that high salt intake, low potassium intake, excess alcohol consum

160 with high salt intake, a modest reduction in salt intake lowers blood pressure and diminishes cardiov

161 ed blood pressure, and a modest reduction in salt intake lowers blood pressure, which is predicted to

162 The proportion with salt intake <6 g/d was 5% and 13% in 2006-2011 and 22% a

163 salt intake distribution-the proportion with salt intake <6 g/d was overestimated by 3-13 percentage

164 ation in mice and in humans and that chronic salt intake may exacerbate gastritis by increasing H. py

165 Furthermore, elevated salt intake may potentiate H. pylori-associated carcinog

166 fference between the two groups in change in salt intake measured by 24 hour urinary sodium during th

167 d 5.8% of stroke cases might be prevented if salt intake meets the recommended maximum intake.

168 Thus, increased dietary salt intake might represent an environmental risk factor

169 ix education sessions on salt reduction, and salt intake monitoring by seven day weighed record of sa

170 Lifelong environmental factors (eg, salt intake, obesity, alcohol) and genetic factors clear

171 r six risk factors (tobacco and alcohol use, salt intake, obesity, and raised blood pressure and gluc

172 r six risk factors (tobacco and alcohol use, salt intake, obesity, and raised blood pressure and gluc

173 ervention designed to achieve a reduction in salt intake of 3 g per day would save 194,000 to 392,000

174 We tested the hypothesis that an increase in salt intake of 6 g/d would change fluid balance in men l

175 and 3) adherence to the recommended maximum salt intake of 6 g/d.

176 ction with slow sodium and placebo to give a salt intake of either 10 g (equivalent to the normal amo

177 World Health Organization recommends a daily salt intake of less than 5.0 g.

178 During the study, salt intake of the children increased in both interventi

179 Reduced salt intake, omega-3 LC-PUFA use, and folate supplementa

180 We aimed to investigate the impact of higher salt intake on asthma incidence in humans and to evaluat

181 To elucidate the potential effect of high salt intake on autoimmune diabetes, nonobese diabetic (N

182 Compelling evidence of the role of salt intake on blood pressure and on other risk factors

183 nt study, we evaluated the effect of dietary salt intake on ENaC regulation and activity in VP neuron

184 a systematic study of the effects of dietary salt intake on glomerular filtration rate (GFR) and tubu

185 l and observational studies on the effect of salt intake on renal and cardiovascular outcomes.

186 , little information exists on the impact of salt intake on type 1 diabetes.

187 ly to the effect of dietary sodium chloride (salt) intake on BP.

188 d adverse lifestyle practices such as higher salt intake or less physical activity may account for so

189 here are no data on regulation of 20-HETE by salt intake or on a role for this compound in SS hyperte

190 tion, nor do they justify advice to increase salt intake or to decrease its concentration in the diet

191 ficantly elevated by losartan treatment, low salt intake, or a combination of the two, compared with

192 creased incrementally two- to threefold with salt intake (P < 0.001), whereas prostaglandin E(2) was

193 s between the observed and ML-predicted mean salt intake (p<0.001).

194 Increased dietary salt intake promotes an early and uniform expansion of e

195 Estimates of the mean +/- SD discretionary salt intake ranged from 6.8 +/- 1.9 g/d (WFR usual intak

196 t alternatives would lead to slightly higher salt intake reductions and thus to more health gain.

197 ion of these actions, coupled with increased salt intake, shifts mice from being salt-resistant to sa

198 Thus, sodium deficiency and salt intake stimulate separate subpopulations of neurons

199 valuate the mechanisms and safety of reduced salt intake, studies specifically designed to assess sal

200 significantly more effective at discouraging salt intake than the control, with mean perceived messag

201 rongly encouraged to achieve the low dietary salt intake that is recommended for all children.

202 During high-salt intake, the sik1(+/+) mice exhibited an increase in

203 ibited reduced arterial pressure during high salt intake; this associated with an increased natriuret

204 blood pressure development triggered by high-salt intake through the modulation of the contractile ph

205 data suggest that animals exposed to chronic salt intake to a level close to that reported for human'

206 To review the evidence that relates salt intake to blood pressure and cardiovascular disease

207 An increase in salt intake to greater than or equal to 3.0% NaCl increa

208 Our results connect high salt intake to the gut-immune axis and highlight the gut

209 -sectional study that assessed discretionary salt intake using 5 approaches: 1) 1-d WFRs; 2) duplicat

210 In 2006-2011 the average habitual salt intake was 10.6 g/d (men) and 8.5 g/d (women); in 1

211 Habitual salt intake was also estimated using single-day measurem

212 lth outcomes were obtained in 2 steps: after salt intake was modeled into blood pressure levels, the

213 Higher salt intake was not associated with decreased time to re

214 Salt intake was predicted from data for 24-h urinary sod

215 Salt intake was reported to be associated with increased

216 Postpartum BP response to high salt intake was studied in women with prior preeclampsia

217 The difference in mean discretionary salt intake was the smallest between the replicate diet

218 The country-specific predicted mean salt intake was within reasonable difference from the be

219 Increased physical activity, a reduced salt intake, weight loss, moderation of alcohol intake,

220 he countries with the highest predicted mean salt intake were in the Western Pacific.

221 (daily fruits and vegetable consumption) and salt intake were obtained from study participants by rec

222 . Finland, the UK, have successfully reduced salt intake, which has resulted in falls in population b

223 ional interventions, especially reduction of salt intake, which is rather high in the Western world.