Relationship of autonomic imbalance and circadian disruption with obesity and type 2 diabetes in resistant hypertensive patients

Boer-Martins, Leandro; Figueiredo, Valéria Maria Chaves de; Demacq, Caroline; Martins, Luíz Cláudio; Consolim‐Colombo, Fernanda Marciano; Figueiredo, Márcio Jansen de Oliveira; Cannavan, Fernando P. S.; Moreno, Heitor

doi:10.1186/1475-2840-10-24

Cited by 57 publications

(70 citation statements)

References 54 publications

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“…Additionally, the decreased number of intracardiac neurons may result in the defects of balance between parasympathetic and sympathetic tone on the heart. Autonomic imbalance characterized by the impairment of parasympathetic function and a relative increase of sympathetic function is one of serious complications that appear early in DM [35,50]. Thus, further studies are essential to find measures preventing negative effect of DM on intracardiac ganglia.…”

Section: Discussionmentioning

confidence: 99%

Remodelling of the intracardiac ganglia in diabetic Goto-Kakizaki rats: an anatomical study

Batulevičius

Frese²,

Peschke

et al. 2013

Cardiovasc Diabetol

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BackgroundAlthough cardiac autonomic neuropathy is one of major complications of diabetes mellitus (DM), anatomical data on cardiac innervation of diabetic animal models is scant and controversial. We performed this study to check whether long-term diabetic state impacts the anatomy of intracardiac ganglia in Goto-Kakizaki (GK) rats, a genetic model of type 2 DM.MethodsTwelve GK rats (276 ± 17 days of age; mean ± standard error) and 13 metabolically healthy Wistar rats (262 ± 5 days of age) as controls were used for this study. Blood glucose was determined using test strips, plasma insulin by radioimmunoassay. Intrinsic ganglia and nerves were visualized by acetylcholinesterase histochemistry on whole hearts. Ganglion area was measured, and the neuronal number was assessed according to ganglion area.ResultsThe GK rats had significantly elevated blood glucose level compared to controls (11.0 ± 0.6 vs. 5.9 ± 0.1 mmol/l, p < 0.001), but concentration of plasma insulin did not differ significantly between the two groups (84.0 ± 9.8 vs. 67.4 ± 10.9 pmol/l, p = 0.17). The GK rats contained significantly fewer intracardiac ganglia, decreased total area of intracardiac ganglia (1.4 ± 0.1 vs. 2.2 ± 0.1 mm2, p < 0.001) and smaller somata of ganglionic neurons. Mean total number of intracardiac neurons in GK rats was 1461 ± 62, while this number in control rats was higher by 39% and reached 2395 ± 110 (p < 0.001).ConclusionsResults of our study demonstrate the decreased number of intracardiac neurons in GK rats compared to metabolically healthy Wistar rats of similar age. It is likely that the observed structural remodelling of intracardiac ganglia in GK rats is caused by a long-term diabetic state.

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Section: Discussionmentioning

confidence: 99%

Remodelling of the intracardiac ganglia in diabetic Goto-Kakizaki rats: an anatomical study

Batulevičius

Frese²,

Peschke

et al. 2013

Cardiovasc Diabetol

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“…Significant disturbance of the 24 h sleep/wake rhythm, whether or not the consequence of a sleep disorder, that typically occurs with bedroom ALAN exposure induces modification of the A and/or Φ of the core body temperature circadian rhythm that in turn alters the A and/or Φ of the central plasma blood volume, melatonin and autonomic nervous system circadian rhythms. Furthermore, aging, renal disease, metabolic disorders and salt sensitivity commonly give rise to perturbation of the A, mean level and sometimes Φ of the renal H 2 O and Na + handling circadian rhythms in association with CD of the RAAS, ANP, AVP and calcitonin gene-related peptide systems (Asplund, 1995;Boer-Martins et al, 2011;Bonny & Firsov, 2013;Doi, 2012;Ishigaki, 2016;Isobe et al, 2015;Natsume, 2006;Ouslander et al, 1998;Portaluppi et al, 1992;Smolensky et al, 2016;Trasforini et al, 1991). Such CTS alterations favor sleep-time nondipping and rising BP 24 h patterns -nocturnal hypertension (Smolensky et al, 2016).…”

Section: Non-dipper and Riser Bp 24 H Patterning (Sleeptime Hypertensmentioning

confidence: 99%

Circadian disruption: New clinical perspective of disease pathology and basis for chronotherapeutic intervention

Smolensky

Hermida

Reinberg

et al. 2016

Chronobiology International

151

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Biological processes are organized in time as innate rhythms defined by the period (τ), phase (peak [Φ] and trough time), amplitude (A, peak-trough difference) and mean level. The human time structure in its entirety is comprised of ultradian (τ < 20 h), circadian (20 h > τ < 28 h) and infradian (τ > 28 h) bioperiodicities. The circadian time structure (CTS) of human beings, which is more complicated than in lower animals, is orchestrated and staged by a brain central multioscillator system that includes a prominent pacemaker - the suprachiasmatic nuclei of the hypothalamus. Additional pacemaker activities are provided by the pineal hormone melatonin, which circulates during the nighttime, and the left and right cerebral cortices. Under ordinary circumstances this system coordinates the τ and Φ of rhythms driven by subservient peripheral cell, tissue and organ clock networks. Cyclic environmental, feeding and social time cues synchronize the endogenous 24 h clocks and rhythms. Accordingly, processes and functions of the internal environment are integrated in time for maximum biological efficiency, and they are also organized and synchronized in time to the external environment to ensure optimal performance and response to challenge. Artificial light at night (ALAN) exposure can alter the CTS as can night work, which, like rapid transmeridian displacement by air travel, necessitates realignment of the Φ of the multitude of 24 h rhythms. In 2001, Stevens and Rea coined the phrase "circadian disruption" (CD) to label the CTS misalignment induced by ALAN and shift work (SW) as a potential pathologic mechanism of the increased risk for cancer and other medical conditions. Current concerns relating to the effects of ALAN exposure on the CTS motivated us to renew our long-standing interest in the possible role of CD in the etiopathology of common human diseases and patient care. A surprisingly large number of medical conditions involve CD: adrenal insufficiency; nocturia; sleep-time non-dipping and rising blood pressure 24 h patterns (nocturnal hypertension); delayed sleep phase syndrome, non-24 h sleep/wake disorder; recurrent hypersomnia; SW intolerance; delirium; peptic ulcer disease; kidney failure; depression; mania; bipolar disorder; Parkinson's disease; Smith-Magenis syndrome; fatal familial insomnia syndrome; autism spectrum disorder; asthma; byssinosis; cancers; hand, foot and mouth disease; post-operative state; and ICU outcome. Poorly conceived medical interventions, for example nighttime dosing of synthetic corticosteroids and certain β-antagonists and cyclic nocturnal enteral or parenteral nutrition, plus lifestyle habits, including atypical eating times and chronic alcohol consumption, also can be causal of CD. Just as surprisingly are the many proven chronotherapeutic strategies available today to manage the CD of several of these medical conditions. In clinical medicine, CD seems to be a common, yet mostly unrecognized, pathologic mechanism of human disease as are the many effective chronotherapeutic int...

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“…Concentration of adiponectin decreases in patients with the phenotypes of the metabolic syndrome [2], including obesity [3], type-2 diabetes [4], insulin resistance [5], hypertension [6]. Lower plasma concentrations of adiponectin are also associated with coronary artery disease (CAD) [7,8].…”

Section: Introductionmentioning

confidence: 99%

Common variants in adiponectin gene are associated with coronary artery disease and angiographical severity of coronary atherosclerosis in type 2 diabetes

Tong

Wang

Leng

et al. 2013

Cardiovasc Diabetol

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BackgroundAdiponectin, an adipokine facilitating insulin action, has antiatherogenic effects. This study investigated whether common single nucleotide polymorphisms (SNPs) in the adiponectin gene influenced plasma adiponectin level and whether they were associated with the risk of coronary artery disease (CAD) and its angiographical severity in type 2 diabetes in Chinese population.Methods11 tagging SNPs were genotyped in 1110 subjects with or without CAD in type 2 diabetes. Variants of adiponectin gene were determined by Taqman polymerase chain reaction method. The plasma adiponectin concentrations were measured by sandwich enzyme-linked immunosorbent assay. The severity and extent of coronary atherosclerosis were assessed using the angiographic Gensini score and Sullivan Extent score.ResultsAmong the 11 SNPs, the minor G allele of SNP rs266729 was significantly associated with higher odds of CAD (odds ratio (95% CI) = 1.49 (1.10 - 2.16), P = 0.022) after adjusting for covariates. In stepwise multivariate logistic regression, SNP rs266729 was a significant independent factor of CAD. Multivariate linear regression analysis revealed that rs266729 (β = −0.101, P < 0.0001), rs182052 (β = −0.044, P = 0.0035), and rs1501299 (β = 0.073, P < 0.0001) were significantly associated with adiponectin level, and also indicated that the minor G allele of SNP rs266729 had higher Gensini score (β = 0.139, P < 0.001) and Sullivan Extent score (β = 0.107, P < 0.001). Haplotypes analysis revealed different haplotype distributions in case and control subjects (P = 0.0003), with two common haplotypes GGG and GAG of the rs266729, rs182052, and rs1501299 being associated in heterozygotes with a greater than threefold increase in cardiovascular risk (odds ratio (95% CI)=3.39 (1.83 - 6.30), P = 0.0001).ConclusionsIn our population, genetic variants in the adiponectin gene influence plasma adiponectin levels, and one of them is a strong determinant of CAD susceptibility and its angiographical severity in type 2 diabetes. This study has provided further evidence for a role of adiponectin in the development of CAD.

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Relationship of autonomic imbalance and circadian disruption with obesity and type 2 diabetes in resistant hypertensive patients

Cited by 57 publications

References 54 publications

Remodelling of the intracardiac ganglia in diabetic Goto-Kakizaki rats: an anatomical study

Remodelling of the intracardiac ganglia in diabetic Goto-Kakizaki rats: an anatomical study

Circadian disruption: New clinical perspective of disease pathology and basis for chronotherapeutic intervention

Common variants in adiponectin gene are associated with coronary artery disease and angiographical severity of coronary atherosclerosis in type 2 diabetes

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