Relationship between autonomic dysfunction, insulin resistance and hypertension, in diabetes

Frontoni, Simona; Bracaglia, Daniela; Gigli, Fabrizio

doi:10.1016/j.numecd.2005.06.010

Cited by 65 publications

(45 citation statements)

References 49 publications

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“…24 -26 An increased incidence of insulin resistance has been reported in hypertensive patients, as well as animal models of hypertension, such as the SHR. 7,8,27,28 In this study, we observed a significant increase in plasma insulin levels in both WKY rats and SHRs fed a high-fat diet compared with those fed a normal diet. However, euglycemic hyperinsulinemic clamp experiments did not indicate a reduction in peripheral insulin sensitivity as a result of 10 weeks of a high-fat diet.…”

Section: Discussionsupporting

confidence: 50%

Endothelial Dysfunction and the Development of Renal Injury in Spontaneously Hypertensive Rats Fed a High-Fat Diet

et al. 2008

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Abstract-Obesity and hypertension have been identified as cardiovascular risk factors that contribute to the progression of end-stage renal disease. To examine the mechanisms by which a high-fat diet and hypertension contribute to endothelial dysfunction and renal injury, 8-week-old male spontaneously hypertensive rats and Wistar rats were fed a high-fat (36% fat) or a normal-fat (7% fat) diet for 10 weeks. The high-fat diet increased body weight in Wistar and hypertensive rats by 25 and 31 g, respectively. Systolic blood pressure was higher in the hypertensive rats compared with Wistar rats; however, blood pressure was unaltered by the high-fat diet. Afferent arteriole response to acetylcholine was impaired in the high-fat groups after just 3 weeks. Renal macrophage infiltration was increased in the hypertensive high-fat group compared with others, and monocyte chemoattractant protein-1 excretion was increased in both of the high-fat-fed groups. Renal PCR arrays displayed significant increases in 2 inflammatory genes in hypertensive rats fed a normal diet, 1 gene was increased in high-fat-fed Wistar rats, whereas 12 genes were increased in high-fat-fed hypertensive rats. Urinary albumin excretion was increased in the hypertensive rats compared with the Wistar rats, which was further exacerbated by the high-fat diet. Glomerular nephrin expression was reduced and desmin was increased by the high-fat diet in the hypertensive rats. Our results indicate that endothelial dysfunction precedes renal injury in normotensive and spontaneously hypertensive rats fed a high-fat diet, and hypertension with obesity induces a powerful inflammatory response and disruption of the renal filtration barrier. Key Words: obesity Ⅲ inflammation Ⅲ hypertension Ⅲ renal disease O besity and hypertension are comorbid pathological conditions that have been identified as independent risk factors for the development of endothelial dysfunction and renal disease. 1 These risk factors are increasing in prevalence at an alarming rate, with Ͼ30% of the US population classified as obese, and 1 in 3 adult Americans currently suffering from hypertension. Blood pressure is strongly correlated with body mass index, and in the Framingham Offspring Study, Յ78% of male hypertensive cases were attributable to obesity. 2 Independently obesity increases the risk for chronic kidney disease 4-fold, 3 hypertensive patients account for 25% of all chronic kidney disease patients, and obese patients with hypertension are at the greatest risk for developing chronic renal disease. 4 -6 Independently, hypertension and obesity have been linked with the development of insulin resistance, endothelial dysfunction, inflammation, and renal injury. 7,8 However, these conditions are commonly found in combination, and it is now becoming apparent that the ensuing renal injury and vascular dysfunction are results of the combination of the 2 risk factors. 9 Animal models of obesity and hypertension, such as the obese Zucker rat, have been shown to develop albuminuria, progress...

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Section: Discussionsupporting

confidence: 50%

Endothelial Dysfunction and the Development of Renal Injury in Spontaneously Hypertensive Rats Fed a High-Fat Diet

et al. 2008

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“…Another pathogenic mechanism of hypertension onset may be attributed to the role of arterial stiffening which precedes the hypertension occurrence [20]. In this regard, it was suggested that low-grade inflammation may contribute to arterial stiffness, since the impairments in pulse wave velocity, a measure of large vessels distension ability, were correlated with the increases in circulating levels of IL-6 and tumor necrosis factor (TNF)-α [21,22]. Furthermore, there are assumptions that pro-inflammatory cytokines may exert a direct pathogenic influence on vascular tone regulation leading to the hypertension development [23].…”

Section: Resultsmentioning

confidence: 99%

Body mass index and insulin resistance as independent predictors of hypertension in postmenopausal women

Klisić¹,

Stanišić²,

Jovanović³

et al. 2017

Tim Med Glas

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Sažetak:Cilj: Premda su ranije studije potvrdile vezu između gojaznosti i hipertenzije, patofiziološki mehanizam ove povezanosti još uvek nije rasvetljen, naročito što postoje oprečni rezultati kada je u pitanju nezavisna uloga gojaznosti i/ili insulinske rezistencije u nastanku hipertenzije. Stoga je cilj studije bio da se ispita da li je gojaznost [merena indeksom telesne mase (ITM)] prediktor za nastanak hipertenzije, nezavisno od insulinske rezistencije [merene HOMA indeksom (HOMA-IR)] u kohorti žena u postmenopauzi. Metode: Ukupno 150 žena u postmenopauzi koje nisu na terapiji (među njima 44,7% sa hipertenzijom) su uključene u studiju preseka. Antropometrijski i biohemijski parametri, kao i krvni pritisak su mereni. HOMA-IR je računat. Rezultati: Multivarijantna logistička regresiona analiza je pokazala da su i ITM (OR=1,240; p=0,035) i HOMA-IR (OR=2,419; p=0,008)nezavisni prediktori krvnog pritiska kod žena u postmenopauzi. Povećanje ITMza1 kg/m2 povećava verovatnoću za pojavu hipertenzije za 24%. Takođe, porast HOMA-IR za 1 jedinicu povećava verovatnoću za pojavu hipertenzije za skoro 2,5 puta. Čak 47% varijacije u vrednosti krvnog pritiska može biti objašnjeno ovim modelom. Takođe, ovaj model je ispravno klasifikovao 76% žena u postmenopauzi koje imaju hipertenziju. Zaključak: I gojaznost, i insulinska rezistencija su nezavisni prediktori krvnog pritiska kod žena u postmenopauzi. Ključne reči: hipertenzija, insulinska rezistencija, gojaznost, žene u postmenopauzi Abstract:Aim: Although previous studies confirmed the association between obesity and hypertension, the underlying pathophysiological mechanism is not well elucidated, specially considering the fact that discordant results exist when examining the independent role of obesity and/or insulin resistance on risk for hypertension onset. Therefore, we aimed to examine if obesity [as measured with body mass index (BMI)] is a predictor for hypertension, independently of insulin resistance [as measured with Homeostasis model assessment of insulin resistance (HOMA-IR)] in the cohort of postmenopausal women. Methods: A total of 150 postmenopausal women non-treated with medications(among them 44.7% hypertensive)were included in cross-sectional study. Anthropometric and biochemical parameters, so as blood pressure were obtained. HOMA-IR was calculated. Results: Multivariate logistic regression analysisrevealed that both, BMI and HOMA-IR were the independent predictors of blood pressure in postmenopausal women (OR=1.240, p=0.035 and OR=2.419, p=0.008, respectively). Rise in BMI for 1 kg/m2 enhanced the probability for higher blood pressure by 24%. Also, elevation in HOMA-IR for 1 unit, rose the probability for higher blood pressure almost 2.5 times. Even 47% of variation in blood pressure could be explained with this Model. Also, this Model correctly classified 76% of postmenopausal women having hypertension. Conclusions: Both, obesity and insulin resistance are the independent predictors of blood pressure in postmenopausal women.

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“…Reasonable amount of data provide evidences for prediction hypertension or diabetes onset due autonomic imbalance evaluated by HRV parameters in time or frequency domain [9][10][11][12][13][14]. Autonomic imbalance causes, at first, increased insulin sensitivity and reduced energy dissipation [15]. Concomitantly, insulin resistance impairs the overall mean levels of cardiac autonomic modulation among persons with T2D [30].…”

Section: Historical Aspects Of Autonomic Dysfunctionmentioning

confidence: 99%

“…In addition to genetic background and environment, AI (autonomic imbalance) could be a common root of HTN (hypertension) or HTN plus T2D (type 2 diabetes) comorbidity development. T2D comorbidity can be added to HTN by decreased energy dissipation, gaining weight and then insulin resistance [15]. It is known that a chronic increase in sympathetic outflow has been reported to decrease β-adrenergic responsiveness itself, by a down-regulation of β-adrenergic receptors, which are known to mediate energy expenditure either at rest or after food intake [16].…”

Section: Introductionmentioning

confidence: 99%

Relationship of Autonomic Imbalance and Circadian Disruption With Obesity and Type 2 Diabetes in Resistant Hypertensive Patients

Boer-Martins¹,

Figueiredo²,

Martins³

et al. 2011

Journal of Hypertension

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Background: Hypertension, diabetes and obesity are not isolated findings, but a series of interacting interactive physiologic derangements. Taking into account genetic background and lifestyle behavior, AI (autonomic imbalance) could be a common root for RHTN (resistant hypertension) or RHTN plus type 2 diabetes (T2D) comorbidity development. Moreover, circadian disruption can lead to metabolic and vasomotor impairments such as obesity, insulin resistance and resistant hypertension. In order to better understand the triggered emergence of obesity and T2D comorbidity in resistant hypertension, we investigated the pattern of autonomic activity in the circadian rhythm in RHTN with and without type 2 diabetes (T2D), and its relationship with serum adiponectin concentration.

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Relationship between autonomic dysfunction, insulin resistance and hypertension, in diabetes

Cited by 65 publications

References 49 publications

Endothelial Dysfunction and the Development of Renal Injury in Spontaneously Hypertensive Rats Fed a High-Fat Diet

Endothelial Dysfunction and the Development of Renal Injury in Spontaneously Hypertensive Rats Fed a High-Fat Diet

Body mass index and insulin resistance as independent predictors of hypertension in postmenopausal women

Relationship of Autonomic Imbalance and Circadian Disruption With Obesity and Type 2 Diabetes in Resistant Hypertensive Patients

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