The effect of low and high NaCl diets on oral glucose tolerance

Iwaoka, Taisuke; Umeda, Teruhisa; Ohno, Miho; Inoue, Junnosuke; Naomi, Shojiro; Satô, Tatsuo; Kawakami, Ikuo

doi:10.1007/bf01726415

Cited by 46 publications

(33 citation statements)

References 18 publications

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“…A similar effect was observed by Iwaoka et al 14 In the Indiana cohort, levels of C peptide fell after saline infusion, indicating that saline lowers insulin levels by suppressing insulin secretion (data not shown).…”

supporting

confidence: 84%

Salt loads raise plasma fatty acids and lower insulin.

et al. 1991

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Some fatty acids are potent inhibitors of angiotensin binding and aldosterone production in adrenal glomerulosa cells and thereby may be involved in regulating salt and water balance. To study the possible regulation of fatty acids by salt, we measured the levels of unesterified fatty acids in plasma from patients subjected to extremes of dietary salt intake and saline infusion. Insulin and catecholamines, two known regulators of plasma fatty acids, also were measured. Infusion of 2 1 saline over 4 hours caused the levels of most unesterified fatty acids to rise. Total unesterified fatty acids rose 60-100%. A high salt diet caused a smaller rise in total unesterified fatty acids (approximately 33%). In both instances, oleic and palmitoleic acids showed the greatest proportionate increases, whereas stearic acid was relatively unaffected. When salt loads were administered by either intravenous or dietary routes, plasma insulin levels fell by approximately 50%. Plasma norepinephrine increased after saline infusion but not during a high salt diet Postsaline levels of fatty acids correlated inversely with postsaline levels of aldosterone, supporting a possible role for fatty acids as physiological regulators of the adrenal glomerulosa. A rise in plasma fatty acids and fall in insulin in response to salt loads could act in concert to increase sodium excretion, constituting a physiological mechanism contributing to salt and water balance. (Hypertension 1991;17:958-964) W hile studying the interaction of angiotensin with adrenal glomerulosa cells, we found that some fatty acids are potent inhibitors of angiotensin receptors and aldosterone secretion. 1 Among naturally occurring fatty acids, the most potent inhibitors are several unsaturated, long-chain congeners, including oleic (18:1), linoleic(18:2), and arachidonic (20:4) acids. These fatty acids inhibit aldosterone secretion in vitro at concentrations in the micromolar range. We also obtained evidence that bovine, rat, and rabbit adrenal glomerulosa cells are under tonic inhibition by endogenous fatty acids, inhibition that can be reversed by washing the cells

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supporting

confidence: 84%

Salt loads raise plasma fatty acids and lower insulin.

et al. 1991

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“…Further support for this notion comes from recent reports of some [6,12], but not all, laboratories [13]. A correlation between salt sensitivity and changes in glucose tolerance has been found by Sharma et al [14].…”

Section: Discussionmentioning

confidence: 79%

The effect of dietary salt on insulin sensitivity

Fliser¹,

Fode²,

Arnold³

et al. 1995

Eur J Clin Investigation

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Abstract. Acute reduction of salt intake causes an increase in serum lipid and insulin levels in healthy volunteers and patients with essential hypertension, suggesting induction of insulin resistance by salt restriction. Direct measurements of insulin sensitivity using the euglycaemic clamp showed no significant change after 7 days of salt restriction. Our previous study showed a time dependent course of dyslipidaemia after institution of a low salt diet. We therefore assessed insulin sensitivity (M-value) under euglycaemic conditions (clamp technique) at discrete time points using a parallel group design. Two groups of healthy males were examined on high (200 mmol d-I) and low (20 mmol d-l) salt intake. One group (n = 7, 25 f 3 years, BMI 22.4 f 2-1 kgm-2) received high and low salt diet in random order each for 7 days.

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“…However, a severe restriction of sodium chloride intake has shown adverse effects on glucose and lipid metabolism (Iwaoka et al 1988, Sharma et al 1990, Egan et al 1991, Ruppert et al 1991, Catanozi et al 2001. In previous reports, chronic salt restriction in Wistar rats induced increases in body weight and adiposity (Prada et al 2000, Xavier et al 2003, Okamoto et al 2004) which were associated with a decrease in whole body glucose uptake evaluated with the euglycemic hyperinsulinemic clamp (Prada et al 2000).…”

Section: Introductionmentioning

confidence: 99%

Low salt intake modulates insulin signaling, JNK activity and IRS-1ser307 phosphorylation in rat tissues

Prada

Coêlho²,

Zecchin³

et al. 2005

Journal of Endocrinology

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A severe restriction of sodium chloride intake has been associated with insulin resistance and obesity. The molecular mechanisms by which the low salt diet (LS) can induce insulin resistance have not yet been established. The c-jun N-terminal kinase (JNK) activity has been involved in the pathophysiology of obesity and induces insulin resistance by increasing inhibitory IRS-1 ser307 phosphorylation. In this study we have evaluated the regulation of insulin signaling, JNK activation and IRS-1 ser307 phophorylation in liver, muscle and adipose tissue by immunoprecipitation and immunoblotting in rats fed with LS or normal salt diet (NS) during 9 weeks. LS increased body weight, visceral adiposity, blood glucose and plasma insulin levels, induced insulin resistance and did not change blood pressure. In LS rats a decrease in PI3-K/Akt was observed in liver and muscle and an increase in this pathway was seen in adipose tissue. JNK activity and IRS-1 ser307 phosphorylation were higher in insulin-resistant tissues. In summary, the insulin resistance, induced by LS, is tissue-specific and is accompanied by activation of JNK and IRS-1 ser307 phosphorylation. The impairment of the insulin signaling in these tissues, but not in adipose tissue, may lead to increased adiposity and insulin resistance in LS rats.

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The effect of low and high NaCl diets on oral glucose tolerance

Cited by 46 publications

References 18 publications

Salt loads raise plasma fatty acids and lower insulin.

Salt loads raise plasma fatty acids and lower insulin.

The effect of dietary salt on insulin sensitivity

Low salt intake modulates insulin signaling, JNK activity and IRS-1ser307 phosphorylation in rat tissues

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