High serum high-sensitivity C-reactive protein concentrations are associated with relative cardiac sympathetic overactivity during the early morning period in type 2 diabetic patients with metabolic syndrome

Aso, Yoshimasa; Wakabayashi, Shigeo; Nakano, Takashi; Yamamoto, Ruriko; Takebayashi, Kohzo; Iwamoto, Toshihiko

doi:10.1016/j.metabol.2006.03.011

Cited by 38 publications

(29 citation statements)

References 48 publications

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“…Chiodini et al [28••] ↑ Urine free cortisol, dexamethasone-suppressed cortisol, and noon cortisol in diabetes Godoy-Matos ↑ Adrenal gland volume in diabetic women [29] and correlation with visceral fat in entire population of diabetic and nondiabetic women Association of SNS function with depressed mood Heart rate variability Udupa et al [34] ↑ Low/high frequency ratio and ↑ basal heart rate among untreated depressed Carroll et al [35•] ↓ Heart rate and blood pressure response to stress task among higher depression scores Association of SNS function with diabetes and metabolic risk factors Heart rate variability Stein et al [37•] ↓ Heart rate variability among diabetes or impaired fasting glucose Aso et al [38] ↑ Low/high frequency ratio in diabetic subjects with metabolic syndrome Skrapari et al [39] ↑ Low/high frequency in obese vs nonobese Serum/urine catecholamines Tentolouris et al [40] ↑ Serum and urine catecholamines in obesity and hypertension Grassi et al [41] ↑ Plasma norepinephrine in glucose intolerant subjects Association of inflammatory markers with depressed mood…”

Section: Hpa Axis Hyperactivity Catecholaminesmentioning

confidence: 99%

“…↑ CRP, IL-6, and fibrinogen associated with incident diabetes Anagnostis et al [52] ↑ CRP, IL-6 in metabolic syndrome Aso et al [38] ↑ CRP, IL-6, and plasminogen activator inhibitor-1 among diabetes subjects Valle Gotlieb et al [53] ↑ hs-CRP, IL-6, oxidized LDL, and oxidized LDL autoantibodies in metabolic syndrome Rytter et al [54•] Positive correlation between waist circumference and hs-CRP Chou et al [55] ↑ CRP associated with higher fasting glucose, waist circumference, and insulin resistance Pou et al [56] ↑ CRP, IL-6 associated with visceral adipose tissue Zeugmann et al. [57] ↑ IL-6 and adiponectin associated with metabolic syndrome diurnal cortisol pattern [9].…”

Section: Association Of Inflammatory Markers With Diabetes and Metabomentioning

confidence: 99%

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Biological Basis of Depression in Adults with Diabetes

et al. 2010

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Diabetes and depression are common comorbid conditions. Although certain health behaviors and risk factors partially explain the association of depression and diabetes, other potential mechanisms have yet to be elucidated. Certain neuroendocrine alterations such as activation of the hypothalamic-pituitary-adrenal (HPA) axis and sympathetic nervous system (SNS) may contribute to the association. Additionally, presence of a proinflammatory state shown in recent literature in both diabetes and depression may contribute to this as well. The objectives of this review are to summarize and review the recent evidence showing alterations of these three biological systems-HPA axis, SNS, and inflammatory cascade--in depression, diabetes, and diabetes-related risk factors.

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Section: Hpa Axis Hyperactivity Catecholaminesmentioning

confidence: 99%

Section: Association Of Inflammatory Markers With Diabetes and Metabomentioning

confidence: 99%

Biological Basis of Depression in Adults with Diabetes

et al. 2010

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“…[8][9][10] The role of brainstem TRH in disturbed autonomic balance has been previously evidenced in the impaired insulin response to hyperglycemia in GK rats. 25 Peripheral inflammation, oxidative stress, dyslipidemia and altered renin-angiotensin system function have important roles in the pathology of obesity, T2D and hypertension, and are all associated with overactivation of adrenal-sympathetic functions.…”

Section: Discussionmentioning

confidence: 99%

“…This autonomic dysregulation contributes to increased blood pressure (BP), cardiac arrhythmias and atrial fibrillation, and the resulting progression to heart failure. [8][9][10][11][12][13] Although autonomic imbalance in T2D has been extensively documented, the neural mechanisms underlying the sympathetic hyperactivity involved in high cardiac morbidity and mortality in T2D patients remains elusive.…”

Section: Introductionmentioning

confidence: 99%

Role of brainstem thyrotropin-releasing hormone-triggered sympathetic overactivation in cardiovascular mortality in type 2 diabetic Goto–Kakizaki rats

Yang

Nyby

et al. 2011

Hypertens Res

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Sympathetic hyperactivity has an important role in cardiovascular mortality in patients with type 2 diabetes (T2D). Thyrotropinreleasing hormone (TRH)-containing fibers innervate autonomic motor and premotor nuclei of the brainstem and spinal cord that regulate cardiovascular functions. We compared cardiovascular responses to application of TRH-analog in the brainstem of Wistar and T2D Goto-Kakizaki (GK) rats. GK rats exhibited basal systolic hypertension (152±2 mm Hg) and had a significantly potentiated, dose-related hypertensive response to intracisternal (i.c.) injection of the TRH-analog RX77368 (10-60 ng). In GK rats only, i.c. RX77368 (30-60 ng) markedly increased heart rate (HR; +88 b.p.m.) and induced acute cardiac mortality (100%), concurrent with extreme hyperglycemia (426 mmol l À1 ), increased plasma H 2 O 2 and 8-isoprostane, and enhanced heart expression of NADPH oxidase 4 and vascular cell adhesion molecule-1 mRNAs. GK rats also had elevated basal plasma epinephrine, higher adrenal gene expression of tyrosine hydroxylase and dopamine b-hydroxylase (DbH), and greater plasma catecholamine and adrenal DbH responses to i.c. TRH-analog, compared with Wistar rats. In GK rats, hexamethonium blocked i.c. RX77368-induced hypertensive and tachycardic responses, and reduced mortality by 86%, whereas phentolamine abolished the hypertensive response but enhanced tachycardia (+160 b.p.m.), and reduced mortality by 50%. The angiotensin II type 1 receptor antagonist irbesartan prevented i.c. RX77368-induced increases in blood pressure, HR and mortality. In conclusion, sympathetic overactivation triggered by brainstem TRH contributes to the mechanism of cardiovascular morbidity and mortality in T2D, which involves heightened cardiac inflammation and peripheral oxidative stress responses to sympathetic drive, and a mediating role of the renin-angiotensin system.

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“…Some of the mechanisms by which SAS may increase blood pressure include the reninangiotensin-aldosterone system [24,25], sympathetic nerve activation [26], endothelial dysfunction [27], endothelin [28], and oxidative stress [29]. These parameters also have been reported to be correlated with hsCRP levels [30][31][32][33]. It has been reported that hsCRP is increased with the severity of SAS independently of BMI [16], and that treatment with nasal continuous positive airway pressure lowers hsCRP in association with reduction of AHI [34].…”

Section: Discussionmentioning

confidence: 99%

Increased low-grade inflammation and plasminogen-activator inhibitor-1 level in nondippers with sleep apnea syndrome

Ishikawa¹,

Hoshide²,

Eguchi³

et al. 2008

Journal of Hypertension

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Objective-Patients with sleep apnea syndrome (SAS) have an increased risk of cardiovascular events and frequently show a non-dipper pattern (blunted nocturnal decline <10%) of systolic blood pressure (BP). We investigated neurohumoral activation and risk factors in relation to nocturnal BP dipping pattern and SAS.Methods-We conducted sleep polysomnography and ambulatory BP monitoring, and measured high-sensitivity C-reactive protein (hsCRP), tissue-type plasminogen activator inhibitor-1 (PAI-1), and neurohumoral factors in 121 outpatients with suspected SAS, who were classified in 4 groups depending on the presence or absence of dipping/non-dipping and SAS.Results-Non-dippers with SAS had higher hsCRP (overall P<0.001), PAI-1 (overall P=0.004), and aldosterone levels (overall P=0.010) than any of the other 3 groups. After adjustment for significant covariates such as age, sex, body mass index, waist circumference, smoking, alcohol drinking, aspirin use, presence of DM, and insulin, non-dippers with SAS still had a higher hsCRP level than non-dippers without SAS (geometric mean: 1.47 vs. 0.37 mg/L, P=0.001). In multiple linear regression analysis controlling for confounding factors that related with SAS, hsCRP was significantly correlated with 3% oxygen desaturation index (P=0.047). PAI-1 was also highest in the non-dippers with SAS, but this was not independent of obesity. PAI-1 was correlated with insulin (r=0.32, P=0.002) and hsCRP levels (r=0.26, P=0.005).Conclusion-Non-dipper status was associated with an increased hsCRP in patients who also had SAS, but not in those who did not, and hsCRP was closely affected by the desaturation level. PAI-1 is also increased in non-dippers with SAS, and is related to insulin and hsCRP.

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High serum high-sensitivity C-reactive protein concentrations are associated with relative cardiac sympathetic overactivity during the early morning period in type 2 diabetic patients with metabolic syndrome

Cited by 38 publications

References 48 publications

Biological Basis of Depression in Adults with Diabetes

Biological Basis of Depression in Adults with Diabetes

Role of brainstem thyrotropin-releasing hormone-triggered sympathetic overactivation in cardiovascular mortality in type 2 diabetic Goto–Kakizaki rats

Increased low-grade inflammation and plasminogen-activator inhibitor-1 level in nondippers with sleep apnea syndrome

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