Plasma atrial natriuretic peptide and natriuretic peptide receptor gene expression in adipose tissue of normotensive and hypertensive obese patients

Dessı̀-Fulgheri, Paolo; Sarzani, Riccardo; Tamburrini, Paola; Moraca, Alessandra; Espinosa, Emma; Cola, Giovanna; Giantomassi, Laura; Rappelli, A

doi:10.1097/00004872-199715120-00074

Cited by 184 publications

(161 citation statements)

References 24 publications

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“…Patients with T2DM tend to be obese (the median body mass index in LANCET was 35 kg/m 2 ), and obese patients have NT‐proBNP concentrations that are 10% to 30% lower than the nonobese, perhaps because of the hyperinsulinemia and insulin resistance commonly observed in obese patients 26, 27. Some have postulated that this natriuretic “handicap” might partially explain the susceptibility of obese and overweight individuals to salt retention, hypertension, and heart failure 27, 28. We and others have published evidence that elevations in NPs are associated with decreased incidence of diabetes mellitus,15, 29 and Mendelian randomization studies have suggested that these associations may be causal in nature 16.…”

Section: Discussionmentioning

confidence: 99%

Randomized Trial of the Effects of Insulin and Metformin on Myocardial Injury and Stress in Diabetes Mellitus: A Post Hoc Exploratory Analysis

Srivastava

Pradhan

Cook

et al. 2017

JAHA

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BackgroundSubclinical myocardial injury, as measured by high‐sensitivity cardiac troponin T (hsTnT), and myocardial stress, as measured by N‐terminal pro‐B‐type natriuretic peptide (NT‐proBNP), are related to glycemic control in patients with type 2 diabetes mellitus, and are strong predictors of adverse cardiovascular outcomes. We sought to determine whether antihyperglycemic therapy improves measures of myocardial injury and myocardial stress in patients with type 2 diabetes mellitus.Methods and ResultsWe randomized, in a 2×2 factorial fashion, 438 patients with type 2 diabetes mellitus to insulin glargine, metformin, the combination, or placebo and measured changes in NT‐proBNP and hsTnT after 12 weeks of therapy. At baseline, the median (Q1–Q3) plasma concentration was 35.4 (15.7–86.3) ng/L for NT‐proBNP and 6.7 (4.6–10.1) ng/L for hsTnT. The adjusted (95% confidence interval) change in NT‐proBNP concentration was 20.7% (7.9–35.0) in the insulin arm compared with 0.13% (−10.8 to 12.5) in the no‐insulin arm (P=0.03 for comparison). These changes were not related to changes in fasting or postprandial glucose, glycated hemoglobin, weight, blood pressure, or inflammation. In the metformin arm, the adjusted change in NT‐proBNP was 7.8% (−3.7 to 20.7) compared with 13.0% (0.72–26.8) in the no‐metformin arm (P=0.58). No significant changes in hsTnT concentrations were observed for any of the treatment arms.ConclusionsInsulin glargine was associated with a significant 20.7% increase in NT‐proBNP, a marker of myocardial stress, after 12 weeks of therapy. No change in hsTnT, a marker of myocardial injury, was observed. The changes were independent of substantial improvements in glucose control.Clinical Trial Registration URL: http://www.clinicaltrials.gov. Unique identifier: NCT00366301.

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Section: Discussionmentioning

confidence: 99%

Randomized Trial of the Effects of Insulin and Metformin on Myocardial Injury and Stress in Diabetes Mellitus: A Post Hoc Exploratory Analysis

Srivastava

Pradhan

Cook

et al. 2017

JAHA

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“…Increased LV mass/BSA but normal RWT identified eccentric LV hypertrophy, whereas increases in both variables identified concentric LV hypertrophy. 2,27,28 LV internal dimension and wall thickness were measured at end-diastole and end-systole following ASE recommendations 13 on Ն3 cardiac cycles. When optimal orientation of the M-mode cursor could not be obtained, correctly oriented linear dimension measurements were made using 2Dimensional imaging by the leading-edge ASE convention.…”

Section: Echocardiographymentioning

confidence: 99%

“…This is also supported by previous observations that hyperinsulinemic 22 or obese 23 subjects are more sensitive to sodium load because of reduced effect of atrial natriuretic peptide, 24 -26 partly attributable to an increased clearance in adipose tissue. 27,28 This may also relate to Nt-proBNP, but the importance of the natriuretic clearance receptor C for clearance of Nt-proBNP is unknown. 29 Alternatively, BNP or Nt-proBNP may, through lipolytic and lipomobilizing effects, change the metabolic state as demonstrated for atrial natriuretic peptide 30 and reduce the incidence of overweight and obesity.…”

Section: Olsen Et Al Natriuretic Peptides and The Metabolic Syndromementioning

confidence: 99%

N-Terminal Pro Brain Natriuretic Peptide Is Inversely Related to Metabolic Cardiovascular Risk Factors and the Metabolic Syndrome

et al. 2005

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Abstract-We wanted to investigate the relationship of N-terminal pro brain natriuretic peptide (Nt-proBNP) The metabolic syndrome was associated with lower Nt-proBNP (35 pg/mL versus 48 pg/mL; PϽ0.001) and shifted the positive relationship between pulse pressure and Nt-proBNP to the right (ie, higher blood pressure for a given level of Nt-proBNP). The metabolic syndrome was associated with lower Nt-proBNP levels and shifted the positive relationship between Nt-proBNP and pulse pressure to the right, creating a possible link between the metabolic syndrome and hypertension. Key Words: risk factors Ⅲ albuminuria Ⅲ hypertrophy Ⅲ natriuretic peptides Ⅲ obesity B rain natriuretic peptide (BNP) is synthesized in myocardial cells as a response to increased wall stress 1 in relation to heart failure 2 or acute myocardial ischemia 3 as a prohormone that is cleaved into BNP and N-terminal proBNP (Nt-proBNP). High BNP as well as high NtproBNP are new promising cardiovascular (CV) risk markers 4 and have been associated with high blood pressure (BP), 5 left ventricular (LV) hypertrophy, 6 and albuminuria. 7,8 Because Nt-proBNP as well as BP, LV mass, and albuminuria increase with aging, it is unclear whether these associations merely rely on aging. Wang et al 9 demonstrated recently an inverse relationship between serum BNP and body mass index that could be a potential link between obesity and hypertension if obese patients have lower BNP levels at given levels of wall stress. However, others have not found this association, 10 and it has been suggested recently that the inverse relationship between BNP and body mass index may only reflect an increase in BNP and a decrease in body mass index with aging. 11 No studies of the effect of obesity or other elements of the metabolic syndrome on Nt-proBNP are available.Therefore, the aim of the present study was to evaluate the association of Nt-proBNP to metabolic and hemodynamic CV risk factors, including the metabolic syndrome, 24-hour ambulatory BP, LV hypertrophy, pulse wave velocity (PWV), and urine albumin/creatinine ratio (UACR) in 4 different age groups to control for age.

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“…[1][2][3] In several studies, plasma ANP and BNP concentrations have been found to be decreased in obese subjects. [4][5][6][7] Additionally, an increase in natriuretic peptides (NPs) has been reported to parallel an increase in blood pressure. 8 Either by boosting the sympathetic activity, increasing sodium and water reabsorption or upregulating the angiotensinogen type 1 receptors, insulin resistance can lead to the inextricable component of obesity and hypertension.…”

Section: Introductionmentioning

confidence: 99%

The association of brain natriuretic peptide and insulin resistance in obesity-related hypertension

Cikim

2007

J Hum Hypertens

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Hypertension is frequently associated with obesity and natriuretic peptide levels are reported to decrease in obese subjects. Both the lower brain natriuretic peptide (BNP) concentration and insulin resistance are suggested to be associated with hypertension. However, their involvement in obesity-related hypertension has not been clearly defined. Forty-four obese women (21 normotensive and 23 hypertensive) and 25 healthy women matched for age were included in the study. Anthropometrical parameters were determined. Serum BNP, fasting insulin and glucose concentrations, and lipid parameters were evaluated. Insulin resistance was calculated using Homeostasis Model Assessment (HOMA) and Quantative Insulin Sensitivity Check Index (QUICKI) formulations. Within the obese groups, HOMA and QUICKI reflected the increased insulin resistance in hypertensive obese subjects with a significant correlation to blood pressure. The decrease in BNP in the obese groups was in favour of the hypertensive obese subjects (31.4376.43; 26.3674.29; and 17.5173.08 pg/ ml, respectively) with a fractional statistical significance between the hypertensive obese group and the controls (P ¼ 0.047). Only for the obese hypertensive group, fasting glucose, HOMA and QUICKI were significantly correlated with BNP. Moreover, fasting plasma glucose (R 2 ¼ 0.22, P ¼ 0.007) and fasting plasma insulin (R 2 ¼ 0.39, P ¼ 0.03) were independently correlated with BNP only for the obese hypertensive group. It can be concluded that the decrease in BNP concentrations in the obese hypertensive subjects seem to be well correlated with the insulin resistance.

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Plasma atrial natriuretic peptide and natriuretic peptide receptor gene expression in adipose tissue of normotensive and hypertensive obese patients

Cited by 184 publications

References 24 publications

Randomized Trial of the Effects of Insulin and Metformin on Myocardial Injury and Stress in Diabetes Mellitus: A Post Hoc Exploratory Analysis

Randomized Trial of the Effects of Insulin and Metformin on Myocardial Injury and Stress in Diabetes Mellitus: A Post Hoc Exploratory Analysis

N-Terminal Pro Brain Natriuretic Peptide Is Inversely Related to Metabolic Cardiovascular Risk Factors and the Metabolic Syndrome

The association of brain natriuretic peptide and insulin resistance in obesity-related hypertension

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