***TASK*** the task is to summarize an input biomedical literature in six sentences 
    ***INPUT*** the input is a biomedical literature 
    ***OUTPUT*** the output is the summary of an input biomedical literature in six sentences 
    ***DOCUMENTATION*** 
    ***EXAMPLES*** 
    Input: Low-salt ( LS ) diet activates the renin-angiotensin-aldosterone and sympathetic nervous systems , both of which can increase insulin resistance ( IR ) . We investigated the hypothesis that LS diet is associated with an increase in IR in healthy subjects . Healthy individuals were studied after 7 days of LS diet ( urine sodium < 20 mmol/d ) and 7 days of high-salt ( HS ) diet ( urine sodium > 150 mmol/d ) in a r and om order . Insulin resistance was measured after each diet and compared statistically , unadjusted and adjusted for important covariates . One hundred fifty-two healthy men and women , aged 39.1 ± 12.5 years ( range , 18 - 65 ) and with body mass index of 25.3 ± 4.0 kg/m(2 ) , were included in this study  . Mean ( SD ) homeostasis model assessment index was significantly higher on LS compared with HS diet ( 2.8 ± 1.6 vs 2.4 ± 1.7 , P < .01 ) . Serum aldosterone ( 21.0 ± 14.3 vs 3.4 ± 1.5 ng/dL , P < .001 ) , 24-hour urine aldosterone ( 63.0 ± 34.0 vs 9.5 ± 6.5 μg/d , P < .001 ) , and 24-hour urine norepinephrine excretion ( 78.0 ± 36.7 vs 67.9 ± 39.8 μg/d , P < .05 ) were higher on LS diet compared with HS diet . Low-salt diet was significantly associated with higher homeostasis model assessment index independent of age , sex , blood pressure , body mass index , serum sodium and potassium , serum angiotensin II , plasma renin activity , serum and urine aldosterone , and urine epinephrine and norepinephrine . Low-salt diet is associated with an increase in IR . The impact of our findings on the pathogenesis of diabetes and cardiovascular disease needs further investigation Our recent studies have indicated that severe salt restriction aggravates vascular insulin resistance in younger normotensive and hypertensive subjects . However , whether the extent of dietary salt restriction commonly advocated adversely affects vascular insulin resistance is unknown . To determine whether moderate dietary salt restriction might affect vascular and systemic sensitivity to insulin , we studied eight subjects after 1 week of a normal sodium diet ( 235 mEq/day ) and 1 week of a moderate salt restriction ( 75 meq/day ) .  Systemic insulin resistance as assessed by the fasting plasma glucose-to-insulin ratio was aggravated by dietary sodium restriction ( normal sodium : 1.2 + /- 0.1 mmol/mIU ; low sodium 0.6 + /- 0.1 , P < .05 ) . Salt restriction significantly reduced maximal insulin-mediated vasodilation ( normal sodium : 51 % + /- 5 % of maximum nitroglycerin-mediated response ; low sodium : 28 % + /- 6 % , P < .01 ) . In contrast , no alterations in nitroglycerin-mediated vasodilation nor phenylephrine-mediated vasoconstriction were noted . These studies demonstrate that moderate salt restriction aggravates both systemic and vascular insulin resistance . This impairment of the vasodilating effect of insulin could be a factor attenuating the blood pressure lowering effect of a low sodium diet To assess the effects of sodium reduction on insulin sensitivity in hypertension , we examined the change of insulin sensitivity after two degrees of dietary sodium restriction by the euglycemic hyperinsulinemic glucose clamp method in 12 subjects with primary hypertension . A controlled period of 1 week , when the subjects were taking a normal sodium diet , was followed by a r and omized crossover study in which the subjects were placed on either moderate or strict reduced sodium diets for 1 week . The result of the 1-week moderate dietary sodium reduction from 200 to 100 mmol/day showed significant decreases in systolic and diastolic blood pressure by 6.5 and 5.0 mm Hg , respectively . Strict dietary sodium reduction to 30 mmol/day for 1 week result ed in no further decrease in blood pressure , but it increased plasma insulin by 40.6 % without changing plasma glucose . There were no changes in glucose infusion rate ( GIR ) or insulin sensitivity index ( ISI ) , which is a measure of GIR divided by plasma insulin , after moderate dietary sodium reduction . However , strict dietary sodium reduction induced decreases in GIR by 19.8 % ( from 1318+/-189 to 1057+/-173 micromol/m2/ min ; P < .01 ) , and ISI by 20.5 % ( from 16.6+/-2.1 to 13.2+/-1.9 micromol/m2/min/microU/mL ; P < .01 ) with a paralleled increase of plasma norepinephrine by 90.0 % ( from 150.5+/-61.6 to 287.3+/-114.9 pg/mL ; P < .01 ) . These results indicate that dietary sodium restriction leads to a deterioration of insulin sensitivity when plasma norepinephrine levels increase , and suggest that moderate dietary sodium reduction may lower blood pressure without a distinct adverse effect on glucose metabolism in subjects with primary hypertension OBJECTIVES To investigate the relationship between salt sensitivity and hyperinsulinaemia in rural black African subjects . DESIGN An intervention study where 27 subjects were divided into two groups ; group 1 was initially salt loaded ( 300 mmol Na+/day ) , while group 2 was salt restricted ( 25 mmol Na+/day ) , each for 4 days , after which a cross-over study was done . SETTING Chidamoyo , a rural area 383 km north of Harare , Zimbabwe . SUBJECTS Twenty-seven rural volunteers ( 16 women , 11 men ) . OUTCOME MEASURES Systolic and diastolic blood pressures , salt sensitivity , insulin and glucose levels , body mass index and mean arterial pressure . RESULTS Mean arterial pressure , which was 91 + /- 2 mmHg on a low-salt diet , increased significantly ( P < 0.01 ) to 105 + /- 3 mmHg on high-salt diet in the salt-sensitive subjects . In the same salt-sensitive subjects , the fasting insulin level was 8.4 + /- 0.8 microU/ml on a low-salt and 6.1 + /- 1.0 microU/ml on a high-salt diet . The difference was not statistically significant . CONCLUSIONS Although salt pressor sensitivity was demonstrated in the subjects , there was no accompanying increase but rather a decrease in fasting insulin levels , suggesting that in the short term , salt sensitivity and hyperinsulinaemia are not linked in raising blood pressure in this sample of rural Zimbabwean subjects Dietary salt restriction lowers blood pressure and has been advocated as a population -based strategy to reduce the cardiovascular morbidity associated with hypertension . However , the effect of lowering salt intake on metabolic vascular risk factors such as insulin resistance and levels of atherogenic lipids and fasting insulin is uncertain . We have studied the short-term effect of moderate dietary salt restriction on insulin resistance and serum lipids in 34 nonobese ( body mass index [ mean + /- SD ] 23.4 + /- 1.8 kg/m2 ) , normotensive young white men . Subjects were maintained on a low salt diet ( < 80 mmol/day ) for the 2-week study period . In a r and omized , cross-over , double-blind fashion , each subject also received 120 mmol of sodium chloride per day during one of the study weeks , and a matching placebo during the other . Insulin resistance , serum insulin , lipids , and blood pressure were measured in the fasting state at the end of each study week . Urinary sodium excretion ( 185 + /- 46 v 52 + /- 25 mmol/day , P < .001 ) , serum sodium ( 141.2 + /- 1.2 v 140.1 + /- 1.3 mmol/L , P < .001 ) and body weight ( 75.4 + /- 9.1 v 75.0 + /- 9.3 kg , P < .05 ) were higher during the high salt than the low salt period . Serum creatinine was higher during the low salt period ( 100 + /- 8 v 90 + /- 9 mumols/L , P < .01 ) . There was no difference in blood pressure , insulin resistance , serum insulin , C-peptide , total cholesterol , low density lipoprotein cholesterol , high density lipoprotein cholesterol or its subfractions , triglycerides , apolipoprotein A1 , or apolipoprotein B between the high salt and low salt periods . We conclude that short-term , moderate dietary salt restriction does not adversely affect insulin sensitivity or levels of atherogenic lipids in normotensive nonobese men A case-control design involving only cases may be used when brief exposure causes a transient change in risk of a rare acute-onset disease . The design resembles a retrospective nonr and omized crossover study but differs in having only a sample of the base population -time . The average incidence rate ratio for a hypothesized effect period following the exposure is estimable using the Mantel-Haenszel estimator . The duration of the effect period is assumed to be that which maximizes the rate ratio estimate . Self-matching of cases eliminates the threat of control- selection bias and increases efficiency . Pilot data from a study of myocardial infa rct ion onset illustrate the control of within-individual confounding due to temporal association of exposures Insulin resistance was demonstrated in hypertensive patients and in salt-sensitive subjects . It was recently reported that the salt-sensitive state was related to a reduced fall in blood pressure during the night in essential hypertension . In the present study , the relationship among insulin sensitivity , blood pressure response to salt intake , and nocturnal fall in blood pressure was examined in 20 subjects with nondiabetic and nonobese essential hypertension during a low-salt and a high-salt diet .  The subjects were maintained on a low-salt diet ( 50 mmol/d ) and a high-salt diet ( 255 mmol/d ) for 1 week each , in r and om order . On the sixth day of each diet , blood pressure was measured every hour for 24 hours with an automatic device . Insulin sensitivity was measured according to the steady-state plasma glucose ( SSPG ) method on the seventh day of each diet . Salt-induced increase in blood pressure , which we defined as the change in 24-hour mean arterial pressure between the low and the high dietary salt intakes , was significantly correlated with SSPG ( r=0.60 , P<0.01 ) during the high-salt period . There was a significant negative correlation ( r=-0.61 , P<0.01 ) between SSPG and a nocturnal fall in mean arterial pressure during the high-salt period . Salt-induced increase in blood pressure was inversely correlated with a nocturnal fall in mean arterial pressure ( r=-0.52 , P<0.02 ) with the high-salt diet . These results suggest that insulin resistance , salt sensitivity , and failed nocturnal fall in blood pressure are associated with each other in subjects with essential hypertension Evidence suggests that dietary salt reduction similar to diuretic therapy may adversely affect lipid and glucose metabolism . We studied 147 non-obese normotensive subjects ( 60 females and 87 males ) aged 19 - 78 years who entered a single-blind crossover trial and were r and omly assigned to a low salt diet of 20 mmol or a high salt diet of 300 mmol sodium per day , for 7 days each . Sodium restriction lowered mean arterial blood pressure ( MAP ) by a mean of 7.5 mmHg in 17 % ( salt-sensitive ) , had no hemodynamic effect in 67 % ( salt-resistant ) and raised MAP by a mean of 6 mmHg in 16 % of the subjects ( reverse reactors ) . With dietary salt restriction serum total- and LDL-cholesterol as well as serum insulin and uric acid concentrations increased significantly in all three groups . The largest increases in total ( 10 % ) and LDL- ( 12 % ) cholesterol occurred in the reverse reactors . Salt-sensitives had significant higher lipoprotein(a ) values than the other two groups . Salt-restriction had no significant effect on this parameter . Plasma renin activity , as well as plasma aldosterone and noradrenaline concentrations rose in all three groups during the low salt diet , the largest increases being observed in the reverse reactors . Short-term sodium restriction in normotensive adults has unfavourable effects on lipid and glucose metabolism , especially in subjects who do not derive hemodynamic benefit . Further studies are necessary to examine the effects of more moderate salt reduction for longer periods on the risk factor profile for cardiovascular disease before a low salt diet can be regarded as a safe public health measure for the general population We have previously reported that modest dietary sodium restriction , as advocated in management guidelines for diabetes , 
    Output:
    
Results differed little when the analyses were restricted to studies with a low risk of bias and duration of ≥7 d. CONCLUSIONS This meta- analysis revealed no evidence that , in trials with a short intervention and large reductions in sodium , circulating glucose concentrations differed between groups .