High- or Low-Salt Diet From Weaning to Adulthood

Prada, Patrícia de Oliveira; Okamoto, M M; Furukawa, Luzia Naôko Shinohara; Machado, Ubiratan Fabres; Heimann, Joel Cláudio; Dolnikoff, Miriam Sterman

doi:10.1161/01.hyp.35.1.424

Cited by 62 publications

(28 citation statements)

References 38 publications

(31 reference statements)

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“…Hyperinsulinemic-euglycemic clamp. After 5 h of fasting, six animals from each group were anesthetized intraperitoneally with sodium pentobarbital (50 mg/kg body wt), and catheters were then inserted into the left jugular vein (for glucose and insulin infusion) and carotid artery (for blood sampling), as previously described (29). Blood pressure measurement.…”

Section: L-[mentioning

confidence: 99%

Defective Insulin and Acetylcholine Induction of Endothelial Cell–Nitric Oxide Synthase Through Insulin Receptor Substrate/Akt Signaling Pathway in Aorta of Obese Rats

et al. 2007

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The actions of acetylcholine (ACh) on endothelium mainly are mediated through muscarinic receptors, which are members of the G protein-coupled receptor family. In the present study, we show that ACh induces rapid tyrosine phosphorylation and activation of Janus kinase 2 (JAK2) in rat aorta. Upon JAK2 activation, tyrosine phosphorylation of insulin receptor substrate (IRS)-1 is detected. In addition, ACh induces JAK2/IRS-1 and IRS-1/phosphatidylinositol (PI) 3-kinase associations, downstream activation of Akt/protein kinase B, endothelial cell-nitric oxide synthase (eNOS), and extracellular signal-regulated kinase (ERK)-1/2. The pharmacological blockade of JAK2 or PI 3-kinase reduced ACh-stimulated eNOS phosphorylation, NOS activity, and aorta relaxation. These data indicate a new signal transduction pathway for IRS-1/PI 3-kinase/Akt/ eNOS activation and ERK1/2 by means of JAK2 tyrosine phosphorylation stimulated by ACh in vessels. Moreover, we demonstrate that in aorta of obese rats (high-fat diet), there is an impairment in the insulin-and ACh-stimulated IRS-1/PI 3-kinase pathway, leading to reduced activation with lower protein levels of eNOS associated with a hyperactivated ERK/mitogen-activated protein kinase pathway. These results suggest that in aorta of obese rats, there not only is insulin resistance but also ACh resistance, probably mediated by a common signaling pathway that controls the activity and the protein levels of eNOS. Diabetes 56: 1014 -1024, 2007 U nder physiological conditions, insulin regulates many vascular functions (1,2), including the release of nitric oxide (NO) (3) and the regulation of mRNA expression of matrix proteins (4,5) and constitutive endothelial cell-nitric oxide synthase (eNOS) (6,7). At the molecular level, binding of insulin to its cognate receptor (insulin receptor) results in activation of the insulin receptor's tyrosine kinase activity, which, in turn, phosphorylates tyrosine residues of insulin receptor substrates (IRSs). IRSs are adaptor proteins that transduce signals from the insulin receptor to downstream signaling cascades, including the phosphatidylinositol (PI) 3-kinase/Akt pathway (8,9). In the vasculature, the activation of PI 3-kinase increases serine phosphorylation of Akt, which, in turn, directly phosphorylates eNOS on ser1177 and activates the enzyme, leading to increased NO production (10,11). In addition, a second postreceptor insulin signaling pathway involves the activation of Ras, Raf, mitogen-activated protein and extracellular signalregulated kinase kinase (MEK), and mitogen-activated protein kinase (MAPK) (extracellular signal-regulated kinase [ERK]-1/2), which is related to cellular growth (12,13). Recent findings (14,15) suggest that impaired IRS-1/PI 3-kinase/Akt/eNOS signal transduction may play a mechanistic role in endothelial dysfunction and in the development of cardiovascular diseases in situations of insulin resistance.Although insulin is well known in inducing vascular relaxation, the physiological significance of circulating insulin ...

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Section: L-[mentioning

confidence: 99%

Defective Insulin and Acetylcholine Induction of Endothelial Cell–Nitric Oxide Synthase Through Insulin Receptor Substrate/Akt Signaling Pathway in Aorta of Obese Rats

et al. 2007

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“…), and catheters were placed into the left jugular vein (for tracer infusions) and the carotid artery (for blood sampling), as previously described (Prada et al 2000). Each animal was monitored for food intake and weight gain for 5 days after surgery to ensure complete recovery.…”

Section: Hyperinsulinemic-euglycemic Clamp Proceduresmentioning

confidence: 99%

Intracerebroventricular injection of citrate inhibits hypothalamic AMPK and modulates feeding behavior and peripheral insulin signaling

Stoppa¹,

Cesquini²,

Roman³

et al. 2008

Journal of Endocrinology

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We hypothesized that citrate might modulate the AMP-activated protein kinase/acetyl-CoA carboxylase (AMPK)/(ACC) pathway and participate in neuronal feeding control and glucose homeostasis. To address this issue, we injected citrate into the lateral ventricle of rats. Intracerebroventricular (ICV) injection of citrate diminished the phosphorylation of hypothalamic AMPK/ACC, increased the expression of anorexigenic neuropeptide (pro-opiomelanocortin and corticotropinreleasing hormone), elevated the level of malonyl-CoA in the hypothalamus, and reduced food intake. No change was observed in the concentration of blood insulin after the injection of citrate. With a euglycemic-hyperinsulinemic clamp, the glucose infusion rate was higher in the citrate group than in the control group (28 . 6G0 . 8 vs 19 . 3G0 . 2 mU/kg body weight/min respectively), and so was glucose uptake in skeletal muscle and the epididymal fat pad. Concordantly, insulin receptor (IR), IR substrate type 1 (IRS1), IRS2, and protein kinase B (AKT) phosphorylation in adipose tissue and skeletal muscle was improved by citrate ICV treatment. Moreover, the treatment with citrate for 7 days promoted body weight loss and decreased the adipose tissue. Our results suggest that citrate and glucose may serve as signals of energy and nutrient availability to hypothalamic cells.

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“…Some previous studies have shown increased insulin sensitivity when salt overload is performed. Chronic HSD has been associated with higher insulin sensitivity in young (16,17) and old Wistar rats (18). One week of salt overload in healthy humans was also associated with higher insulin sensitivity when compared to salt restriction (19).…”

mentioning

confidence: 99%

Salt and insulin sensitivity after short and prolonged high salt intake in elderly subjects

Lima

Tozetto

Lima

et al. 2009

Braz J Med Biol Res

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Salt sensitivity and insulin resistance are correlated with higher cardiovascular risk. There is no information about changes in salt sensitivity (SS) and insulin sensitivity (IS) after a chronic salt overload in humans. The aim of this study was to evaluate these parameters in the elderly. Seventeen volunteers aged 70.5 ± 5.9 years followed a low-salt diet (LSD) for 1 week and a high-salt diet (HSD) for 13 weeks. We evaluated SS after one week (HSD1) and after 13 weeks (HSD13), and subjects’ IS and lipids on their usual diet (UD) at HSD1, and at HSD13. Blood pressure (BP) was measured at each visit and ambulatory blood pressure monitoring (ABPM) was performed twice. SS was the same at HSD1 and HSD13. Systolic BP was lower on LSD than on UD (P = 0.01), HSD1 (P < 0.01) and HSD13 (P < 0.01). When systolic and diastolic BP were evaluated by ABPM, they were higher at HSD13 during the 24-h period (P = 0.03 and P < 0.01) and during the wakefulness period (P = 0.02 and P < 0.01) compared to the UD. Total cholesterol was higher (P = 0.04) at HSD13 than at HSD1. Glucose and homeostasis model assessment (HOMA) were lower at HSD1 (P = 0.02 and P = 0.01) than at HSD13. Concluding, the extension of HSD did not change the SS in an elderly group. The higher IS found at HSD1 did not persist after a longer HSD. A chronic HSD increased BP as assessed by ABPM

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High- or Low-Salt Diet From Weaning to Adulthood

Cited by 62 publications

References 38 publications

Defective Insulin and Acetylcholine Induction of Endothelial Cell–Nitric Oxide Synthase Through Insulin Receptor Substrate/Akt Signaling Pathway in Aorta of Obese Rats

Defective Insulin and Acetylcholine Induction of Endothelial Cell–Nitric Oxide Synthase Through Insulin Receptor Substrate/Akt Signaling Pathway in Aorta of Obese Rats

Intracerebroventricular injection of citrate inhibits hypothalamic AMPK and modulates feeding behavior and peripheral insulin signaling

Salt and insulin sensitivity after short and prolonged high salt intake in elderly subjects

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