Clinical Endocrinology

2018

DOI: 10.1111/cen.13540

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Adiponectin concentration data improve the estimation of atherosclerotic risk in normal and in overweight subjects

Adriana Bertolami

¹

,

José Carlos de Lima-Júnior

²

,

Riobaldo M.R. Cintra

³

et al.

Abstract: Combining plasma adiponectin measurements and BMI improves estimation of cIMT as compared to anthropometric parameters.

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Subclinical Atherosclerosis Sample1

Rt Associated Effects On Adipokines and Hormones (Paper V)1

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Cited by 5 publications

(3 citation statements)

References 42 publications

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“…Carotid Doppler ultrasound was performed using high-resolution Vivid 7 ultrasound (GE, USA) and high-frequency linear transducer (9 MHz) with automatic border recognizer detection as described previously in Bertolami et al [9]. Briefly, the cIMT was obtained by means of image processing of B-mode ultrasonograms of the right and left automatic measurement.…”

Section: Methodsmentioning

confidence: 99%

Excess weight mediates changes in HDL pool that reduce cholesterol efflux capacity and increase antioxidant activity

¹

,

²

,

³

et al. 2019

Preprint

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Objective: Obesity-related decline in high-density lipoprotein (HDL) functions such as cholesterol efflux capacity (CEC) has supported the notion that this lipoprotein dysfunction may contribute for atherogenesis among obese patients. Besides, potentially other HDL protective actions may be affected with weight gain and these changes may occur even before the obesity range. Methods: Lipid profile, body mass index (BMI), biochemical measurements, and carotid intima-media thickness (cIMT) were obtained in this cross-sectional study with 899 asymptomatic individuals. HDL functions were measured in a subgroup (n=101). Results: Individuals with increased HDL-C had an attenuated increase in cIMT with elevation of BMI. CEC, HDL-C, HDL size and HDL-antioxidant activity were negatively associated with cIMT. BMI was inversely associated with HDL-mediated inhibition of platelet aggregation and CEC, but surprisingly it was directly associated with the antioxidant activity. Thus, even in non-obese, non-diabetic individuals, increased BMI is associated with a wide change in protective functions of HDL, reducing CEC and increasing antioxidant activity. In these subjects, decreased HDL concentration, size or function are related to increased atherosclerotic burden. Conclusion: Our findings demonstrate that in non-obese, non-diabetic individuals, the increasing values of BMI are associated with impaired protective functions of HDL and concomitant increase in atherosclerotic burden.

“…Carotid Doppler ultrasound was performed using high-resolution Vivid 7 ultrasound (GE, USA) and high-frequency linear transducer (9 MHz) with automatic border recognizer detection as described previously in Bertolami et al [9]. Briefly, the cIMT was obtained by means of image processing of B-mode ultrasonograms of the right and left automatic measurement.…”

Section: Methodsmentioning

confidence: 99%

Excess weight mediates changes in HDL pool that reduce cholesterol efflux capacity and increase antioxidant activity

¹

,

²

,

³

et al. 2019

Preprint

Self Cite

View full text Add to dashboard Cite

Objective: Obesity-related decline in high-density lipoprotein (HDL) functions such as cholesterol efflux capacity (CEC) has supported the notion that this lipoprotein dysfunction may contribute for atherogenesis among obese patients. Besides, potentially other HDL protective actions may be affected with weight gain and these changes may occur even before the obesity range. Methods: Lipid profile, body mass index (BMI), biochemical measurements, and carotid intima-media thickness (cIMT) were obtained in this cross-sectional study with 899 asymptomatic individuals. HDL functions were measured in a subgroup (n=101). Results: Individuals with increased HDL-C had an attenuated increase in cIMT with elevation of BMI. CEC, HDL-C, HDL size and HDL-antioxidant activity were negatively associated with cIMT. BMI was inversely associated with HDL-mediated inhibition of platelet aggregation and CEC, but surprisingly it was directly associated with the antioxidant activity. Thus, even in non-obese, non-diabetic individuals, increased BMI is associated with a wide change in protective functions of HDL, reducing CEC and increasing antioxidant activity. In these subjects, decreased HDL concentration, size or function are related to increased atherosclerotic burden. Conclusion: Our findings demonstrate that in non-obese, non-diabetic individuals, the increasing values of BMI are associated with impaired protective functions of HDL and concomitant increase in atherosclerotic burden.

“…The clinical outcome of the SA patients was according to protocols presented by Bertolami et al 23 . Carotid Doppler ultrasound (CDU) and Coronary tomography with calcium score (CAC) were used to detect SA.…”

Section: Subclinical Atherosclerosis Samplementioning

confidence: 99%

TREML4 polymorphisms increase the mRNA in blood leukocytes in the progression of atherosclerosis

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,

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³

et al. 2022

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TREML4 and other members of the triggering receptor expressed in the myeloid cell family are associated with a risk of atherosclerosis and progression in coronary artery disease, acute coronary syndrome, and coronary artery calcification. Herein, the relationship between TREML4 expression and its polymorphisms (rs2803495 and rs280396) was evaluated in patients with subclinical atherosclerosis (n = 340) and heart failure post-acute myocardial infarction (MI) (n = 68) for the first time. TREML4 variants rs2803495 (A > G) and rs2803496 (T > C) and leukocyte mRNA expression was analyzed by qRT–PCR. The rs2803495 G allele was associated with TREML4 expression (OR 8.01, CI 3.78–16.99, p < 0.001). Patients carrying the rs2803496 C minor allele (TC/CC genotypes) were more likely to express TREML4 than those without the C allele (OR 10.42, CI 4.76–22.78, p < 0.001), as well as having higher levels of TREML4 expression (OR 4.88, CI 2.35–10.12, p < 0.001). Thus, we report for the first time that TREML4 is not associated with the early stages of atherosclerotic plaque formation and later stages after MI. In conclusion, TREML4 mRNA expression in blood leukocytes is influenced by minor alleles (G and C) and may regulate differently during the atherosclerosis progression stages, but not in asymptomatic atherosclerosis disease and post-MI.

“…Adipokines are cytokines secreted from adipose tissue and can be measured systemically and locally, by blood sampling or adipose tissue culturing, respectively. 141,142 Adipokines can be proinflammatory or anti-inflammatory, with adiponectin being anti-inflammatory, and lipocalin-2 and resistin being proinflammatory.…”

Section: Rt Associated Effects On Adipokines and Hormones (Paper V)mentioning

confidence: 99%

Sex differences in atherosclerosis and exercise effects

¹

2019

Linköping University Medical Dissertations

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i Cardiovascular disease (CVD) is the leading cause of death globally, with atherosclerosis being the main cause of cardiovascular diseases. Atherosclerosis is an inflammatory disease of the blood vessel wall, which over time will cause thickening and hardening of the vessel wall. Atherosclerosis can result in catastrophic vascular events, such as myocardial infarction and stroke. There are distinct sex differences in CVD mortality at different ages, before menopause women have a lower mortality of CVD in comparison to men, which equalises after menopause. In addition to sex differences in the incidence of CVD, there are also distinct sex differences in the phenotype of atherosclerotic plaques, with men generally developing more severe and vulnerable plaques that are at risk of rupture.This thesis aimed to investigate the sex differences in atherosclerosis, in particular how the proteome and pathophysiology differs. In addition, we sought to investigate the potential benefit of an exercise programme, in reducing CVD risks, using a randomised controlled trial including postmenopausal women.Sex differences in atherosclerosis were first investigated via proteomic analysis of human carotid endarterectomy samples. Initially, five intraplaque biopsies were taken from distinct atheroma regions, including; internal control, fatty streak, plaque shoulder, plaque centre, and fibrous cap. Protein extracts from these biopsies were subjected to analysis by mass spectrometry. The novel sampling method was successful in reducing the effect of plaque heterogeneity, a limitation in previous proteomic studies of atherosclerosis, and a number of previously unreported proteins were identified in human carotid atheroma. In addition to this, with the inclusion of multivariate statistical modelling, it was found that 43 proteins significantly discriminated the carotid atheroma between men and women. These proteins were grouped by function, and it was found that atheroma from men was associated with the increased abundance of inflammatory response proteins, including phospholipase-A2 membrane associated and lysozyme C, and atheroma from women was associated with increased abundance of blood coagulation, complement activation, and transport proteins, notably including; antithrombin-III, coagulation factor XII, and afamin. In addition, differences were also ii observed in the abundance of iron metabolism related proteins. These sex differences were further expanded upon from a pathophysiological perspective.Immunohistochemistry stainings of ferritin and transferrin receptor 1 were found significantly increased in the atheroma from men. Moreover, the levels of plasma haemoglobin were also significantly increased in men and were associated with the development of more vulnerable and severe plaque types. The more vulnerable and severe plaque types were also associated with significantly greater macrophage infiltration. In summary, these results are indicative of men developing atheroma with greater inflammation that are more vulnerable, due ...

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