Effect of sodium intake on insulin sensitivity

Donovan, Daniel S.; Solomon, Caren G.; Seely, Ellen W.; Williams, Gordon H.; Simonson, Donald C.

doi:10.1152/ajpendo.1993.264.5.e730

Cited by 92 publications

(104 citation statements)

References 3 publications

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“…27 In contrast, increased dietary sodium intake was associated with a decrease in insulin-mediated glucose disposal in young healthy adults. 25 We previously demonstrated that genetically insulin-resistant Wistar fatty rats showed salt sensitivity. 28 Furthermore, salt loading markedly enhanced insulin resistance of Wistar fatty rats.…”

Section: Relationship Between Insulin Sensitivity and Sodium Homeostasismentioning

confidence: 99%

“…Some investigators have indicated that moderate dietary sodium restriction aggravates insulin sensitivity; 11,12 others have suggested that salt loading exacerbates insulin resistance. 25 Dietary salt restriction increases resistance to the vasodilating effects of insulin in young normotensive and hypertensive subjects. 26 Fliser et al 27 reported that 3-day salt restriction decreases insulin sensitivity, but 7-day does not.…”

Section: Relationship Between Insulin Sensitivity and Sodium Homeostasismentioning

confidence: 99%

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Correlation of sodium-related factors with insulin sensitivity in young, lean, male offspring of hypertensive and normotensive subjects

et al. 2001

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Pioneer studies have proposed that multiple metabolic abnormalities, such as insulin resistance, increased Na + -H + exchanger activity and abnormal intracellular calcium homeostasis, are frequently associated with a subset of essential hypertensive patients with low plasma renin activity (PRA). However, it is unclear whether insulin resistance is related to the low renin status in the very early phase of genetical hypertension. Besides, there is controversy on the subject of the in vivo effect of acute hyperinsulinaemia on sodiumrelated factors. We investigated the relationship between sodium-related parameters and insulin sensitivity, and the effects of euglycaemic hyperinsulinaemia on cyclic guanosine monophosphate (cGMP) and atrial natriuretic peptide (ANP) levels in 17 young, lean, normotensive male subjects, who displayed extreme predis-

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Section: Relationship Between Insulin Sensitivity and Sodium Homeostasismentioning

confidence: 99%

Section: Relationship Between Insulin Sensitivity and Sodium Homeostasismentioning

confidence: 99%

Correlation of sodium-related factors with insulin sensitivity in young, lean, male offspring of hypertensive and normotensive subjects

et al. 2001

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“…Evidence is increasing in both humans and experimental animals that besides causing hypertension high sodium (HS) intake leads to insulin resistance [1][2][3][4]. Elevated BP responses to HS intake appear to be heterogeneous in nature [1,2,5,6] with certain animal models and indeed humans displaying insulin resistance in the absence of hypertension [1,2].…”

Section: Introductionmentioning

confidence: 99%

A vascular mechanism for high-sodium-induced insulin resistance in rats

et al. 2014

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Aims/hypothesis High sodium (HS) effects on hypertension are well established. Recent evidence implicates a relationship between HS intake and insulin resistance, even in the absence of hypertension. The aim of the current study was to determine whether loss of the vascular actions of insulin may be the driving factor linking HS intake to insulin resistance. Methods Sprague Dawley rats were fed a control (0.31% wt/wt NaCl) or HS (8.00% wt/wt NaCl) diet for 4 weeks and subjected to euglycaemic-hyperinsulinaemic clamp (10 mU min) or constant-flow pump-perfused hindlimb studies following an overnight fast. A separate group of HS rats was given quinapril during the dietary intervention and subjected to euglycaemichyperinsulinaemic clamp as above. Results HS intake had no effect on body weight or fat mass or on fasting glucose, insulin, endothelin-1 or NEFA concentrations. However, HS impaired whole body and skeletal muscle glucose uptake, in addition to a loss of insulin-stimulated microvascular recruitment. These effects were present despite enhanced insulin signalling (Akt) in both liver and skeletal muscle. Constant-flow pump-perfused hindlimb experiments revealed normal insulin-stimulated myocyte glucose uptake in HS-fed rats. Quinapril treatment restored insulin-mediated microvascular recruitment and muscle glucose uptake in vivo.Conclusions/interpretation HS-induced insulin resistance is driven by impaired microvascular responsiveness to insulin, and is not due to metabolic or signalling defects within myocytes or liver. These results imply that reducing sodium intake may be important not only for management of hypertension but also for insulin resistance, and highlight the vasculature as a potential therapeutic target in the prevention of insulin resistance.

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“…intake was associated with insulin level and that abundant dietary sodium increased insulin resistance, key markers for inflammation and endocrine metabolism. [20][21][22] In line with these findings, although some evidence suggested that the inflammation responses by sodium level may be obesity independent, we still could not dismiss the potential links underlying dietary sodium, obesity, inflammation, and hormone metabolism. Korea has among the highest sodium consumption worldwide.…”

Section: Introductionmentioning

confidence: 82%

The association between dietary sodium intake and adiposity, inflammation, and hormone markers: A preliminary study

Choi

Heo

2017

J Nutr Health

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Purpose: Excess intake of sodium is a major diet-related risk factor for human diseases including hypertension and cancer as well as obesity and inflammation. However, findings are still controversial, and evidence is lacking in Koreans. Therefore, for better understanding of the role of dietary sodium intake in disease etiology, this study investigated the effects of dietary sodium intake on adiposity, inflammation, and hormones in Koreans. Methods: A total of 80 males and females joined the study. The general characteristics and dietary intake data were investigated by trained interviewers using a questionnaire and 24-h dietary recall, respectively. For the markers of adiposity, body weight, body mass index, percent of body fat, visceral fat area, and waist and hip circumference were measured. For the inflammation and hormone markers, leptin, adiponectin, insulin, tumor necrosis factor-α, and interleukin-6 were also analyzed. Results: Multivariate linear regression analyses suggested that dietary sodium intake was not associated with adiposity. However, dietary sodium showed a significant association with insulin level: Plasma insulin concentration increased with sodium intake independent of other dietary intake or percent of body fat (β = 0.296, adjusted r 2 = 0.276, p < 0.01). Other markers for inflammation and hormonal responses were not associated with dietary sodium intake. Conclusion: Findings suggested that dietary sodium intake may be a critical modifying factor in the level of plasma insulin. However, it showed a limited effect on obesity and other inflammation markers and hormone levels. These findings should be confirmed in larger, well-designed investigations.

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Effect of sodium intake on insulin sensitivity

Cited by 92 publications

References 3 publications

Correlation of sodium-related factors with insulin sensitivity in young, lean, male offspring of hypertensive and normotensive subjects

Correlation of sodium-related factors with insulin sensitivity in young, lean, male offspring of hypertensive and normotensive subjects

A vascular mechanism for high-sodium-induced insulin resistance in rats

The association between dietary sodium intake and adiposity, inflammation, and hormone markers: A preliminary study

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