Insulin resistance and hypertension

Sowers, James R.

doi:10.1152/ajpheart.00026.2004

Cited by 397 publications

(430 citation statements)

References 84 publications

(120 reference statements)

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“…23 Insulin resistance is believed to be a key underlying metabolic abnormality in the syndrome. 24,25 Our hypertensive and age-and sex-matched normotensive subjects differed not just in blood pressure, but also in the other aspects of the metabolic syndrome. We believe that obesity, particularly central obesity, is an early abnormality in the cardiovascular continuum.…”

Section: Discussionmentioning

confidence: 96%

Association of hypertension with single nucleotide polymorphisms in the quantitative trait locus for abdominal obesity-metabolic syndrome on chromosome 17

et al. 2006

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Genome scan in Chinese revealed an association of blood pressure with the microsatellite marker D17S1303, which lies in a quantitative trait locus for the abdominal obesity-metabolic syndrome (AOMS2) at 17p12 on chromosome 17. We previously reported that D17S1303 was associated with hypertension and obesity. Therefore, we studied 10 single nucleotide polymorphisms (SNP) within 3 kb of D17S1303. One hundred and eighty hypertensive subjects (91 men, 89 women, age 53712 years) and 180 normotensive matched controls (91 men, 89 women, age 52711) were genotyped using the Sequenom genotyping platform. Allelic frequencies in these Chinese subjects differed from those reported for Caucasians. Three SNPs (rs11656507, rs1357926, rs852319) were homozygous in our subjects. The genotype frequencies of rs852320, rs852321 and rs852322 did not differ between hypertensive and normotensive subjects. However, there were significant differences for rs1525402 (P ¼ 0.048), rs2692343 (P ¼ 0.022), rs2692344 (P ¼ 0.017) and rs2321313 (P ¼ 0.028). A four-locus haplotype comprising G at rs1525402, C at rs2692343, C at rs2692344 and G at rs2321313 was associated with lower systolic blood pressure (P ¼ 0.023) and normotension (P ¼ 0.048). Our results provide further evidence that there is a gene, as yet unidentified, influencing blood pressure in the vicinity of D17S1303 in a quantitative trait locus for abdominal obesity-metabolic syndrome at 17p12.

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Section: Discussionmentioning

confidence: 96%

Association of hypertension with single nucleotide polymorphisms in the quantitative trait locus for abdominal obesity-metabolic syndrome on chromosome 17

et al. 2006

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“…Delivery of insulin to skeletal muscle cells via blood vessels plays a key role in the regulation of whole-body glucose utilization 46) . Both β2-AR in blood vessels 47) and insulin 48) induce vascular relaxation. Our finding that orexin injection into the VMH enhanced the insulin-induced tyrosine-phosphorylation of IR in skeletal muscle suggests that orexin might promote insulin delivery to muscle cells by inducing the activation of β2-AR in blood vessels.…”

Section: Orexin Increases Glucose Uptake and Insulin Sensitivity In Smentioning

confidence: 99%

Hypothalamic control of glucose and lipid metabolism in skeletal muscle

Minokoshi

2017

JPFSM

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The hypothalamus controls glucose and lipid metabolism in peripheral tissues.Recent studies have revealed that the ventromedial hypothalamus (VMH) and arcuate nucleus (ARC) of the hypothalamus play an important role in the regulation of glucose and lipid metabolism in skeletal muscle and the liver. The fat-derived hormone leptin was thus shown to stimulate glucose uptake and fatty acid oxidation in red-type skeletal muscle by activating VMH neurons -likely mediated in part by augmentation of synaptic plasticity between leptin receptor and proopiomelanocortin (POMC)-expressing neurons in the ARC and melanocortin receptor (MCR)-expressing VMH neurons -and consequent activation of sympathetic nerves innervating the muscle tissue. The VMH -sympathetic nerve axis was also found to be activated by orexin-positive neurons in mediation of hedonic feeding-induced glucose uptake in redtype skeletal muscle. The effects of orexin and leptin on glucose metabolism in skeletal muscle are interconnected with those of insulin, with the action of VMH also being necessary for the beneficial effects of exercise on metabolism. Leptin ameliorates diabetic phenotypes in animals with uncontrolled insulin-deficient diabetes as well as in patients with or animal models of lipodystrophy through the central nervous system (CNS). Finally, a single injection of fibroblast growth factor 1 (FGF1) into the lateral ventricle was shown to induce sustained remission of hyperglycemia in several animal models of type 2 diabetes, at least in part by increasing glucose uptake in skeletal muscle. The CNS thus plays an important role in the control of glucose and lipid metabolism, with the VMH as well as POMC neurons being implicated as key regulators of such metabolism in skeletal muscle.

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“…Ion transport in the renal proximal tubule (RPT) is increased in essential hypertension, which is regulated by numerous hormones and humoral factors, including insulin and dopamine 2, 3. Activation of dopamine receptor inhibits sodium reabsorption, whereas activation of insulin receptor increases sodium reabsorption in RPTs 3, 4. Insulin has various effects.…”

Section: Introductionmentioning

confidence: 99%

Inhibition of D ₄ Dopamine Receptors on Insulin Receptor Expression and Effect in Renal Proximal Tubule Cells

Zhang

Ren

et al. 2016

JAHA

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BackgroundIon transport in the renal proximal tubule (RPT), which is increased in essential hypertension, is regulated by numerous hormones and humoral factors, including insulin and dopamine. Activation of dopamine receptor inhibits sodium reabsorption, whereas activation of insulin receptor increases sodium reabsorption in RPTs, and hyperinsulinemic animals and patients have defective renal dopaminergic system. We presume that there is an inhibition of D4 receptor on insulin receptor expression and effect, and the regulation is lost in spontaneously hypertensive rats (SHRs).Methods and ResultsInsulin receptor expression was determined by immunoblotting, and Na+‐K+‐ATPase activity was detected in both Wistar‐Kyoto (WKY) and SHR RPT cells. Stimulation of D4 receptor with PD168077 decreased expression of insulin receptors, which was blocked in the presence of the calcium‐channel blocker, nicardipine (10−6 mol/L per 24 hours), in cell culture medium without calcium or in the presence of inositol 1,4,5‐trisphosphate (IP3) receptor blocker (2‐aminoethyl diphenylborinate [2‐ADB]; 10−6 mol/L per 24 hours), indicating that extracellular calcium entry and calcium release from the endoplasmic reticulum were involved in the signal pathway. Stimulation of the insulin receptor stimulated Na+‐K+‐ATPase activity, whereas pretreatment with PD168077 for 24 hours decreased the inhibitory effects of insulin receptor on Na+‐K+‐ATPase activity in WKY cells. However, in SHR cells, inhibition of D4 receptor on insulin receptor expression and effect were lost.ConclusionsActivation of D4 receptor inhibits insulin receptor expression in RPT cells from WKY rats. The aberrant inhibition of D4 receptor on insulin receptor expression and effect might be involved in the pathogenesis of essential hypertension.

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Insulin resistance and hypertension

Cited by 397 publications

References 84 publications

Association of hypertension with single nucleotide polymorphisms in the quantitative trait locus for abdominal obesity-metabolic syndrome on chromosome 17

Association of hypertension with single nucleotide polymorphisms in the quantitative trait locus for abdominal obesity-metabolic syndrome on chromosome 17

Hypothalamic control of glucose and lipid metabolism in skeletal muscle

Inhibition of D ₄ Dopamine Receptors on Insulin Receptor Expression and Effect in Renal Proximal Tubule Cells

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Insulin resistance and hypertension

Cited by 397 publications

References 84 publications

Association of hypertension with single nucleotide polymorphisms in the quantitative trait locus for abdominal obesity-metabolic syndrome on chromosome 17

Association of hypertension with single nucleotide polymorphisms in the quantitative trait locus for abdominal obesity-metabolic syndrome on chromosome 17

Hypothalamic control of glucose and lipid metabolism in skeletal muscle

Inhibition of D 4 Dopamine Receptors on Insulin Receptor Expression and Effect in Renal Proximal Tubule Cells

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Inhibition of D ₄ Dopamine Receptors on Insulin Receptor Expression and Effect in Renal Proximal Tubule Cells