Effects of black raspberry on lipid profiles, vascular endothelial function and circulating endothelial progenitor cells in patients with metabolic syndrome

Underlying mechanisms of endothelial dysfunction in obesity are not fully understood. Circulating Endothelial Progenitor Cells (EPCs) are known to promote endothelial repair. Our aim was to assess the number/function of EPCs in morbid obese individuals and its correlation with endothelial function and inflammatory markers. EPCs were isolated from 33 morbid obese patients (age 47±1.8 y; men=34%; BMI=49±2.1 kg/m 2 , metabolic syndrome=84%) and 20 lean controls. Peripheral blood EPC number was significantly reduced in obese patients both with flow cytometry (KDR + /CD34 + ; 0.041±0.04 vs 0.074±0.05 %events, p<0.001) and fluorescence analysis after short-term culture (49±4 vs 28±2 cells/field, p<0.001). The plasma number of primitive CD 133 + cells, and concentrations of VEGF (Elisa) and nitrogen oxides (which potentially recruit EPCs), were similar to control, suggesting that reduction of EPCs occurs distally to early cell differentiation. Importantly, C-Reactive Protein (CRP), robustly increased in obese patients (0.15±0.04 vs 1.3±0.3; p=0.003), was a strong predictor of reduced EPC number at multivariate analysis (r=0.623; p < 0.001). Likewise, the migratory response of EPCs to VEGF in vitro was significantly impaired in obese vs controls, despite similar VEGF receptor numbers. Multivariate analysis suggested potential roles of metabolic syndrome and leptin in such effect. Endothelial function at flow-mediated brachial artery reactivity was markedly reduced (by 60%) in obese patients, and had a significant inverse correlation with EPC number (r= 0.678; p< 0.001). Carotid intimal thickness was also increased in obese patients (0.68±0.02 vs 0.58±0.08; p=0.001). On the other hand, the number of circulating endothelial cells (CD31 + /CD106 + ) was similar in both groups, suggesting that apoptosis was not enhanced in the obese. These results suggest for the first time that reduced number and migratory capacity of EPCs correlate with endothelial dysfunction or increased CRP and may be a key underlying mechanism of vascular complications and atherosclerosis in obesity.

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Downregulated GTCPH I/BH4 Pathway and Decreased Function of Circulating Endothelial Progenitor Cells and Their Relationship with Endothelial Dysfunction in Overweight Postmenopausal Women

Stem Cells International ◽

10.1155/2018/4756263 ◽

2018 ◽

Vol 2018 ◽

pp. 1-11 ◽

Cited By ~ 5

Author(s):

Ying Luo ◽

Zhenhua Huang ◽

Jinli Liao ◽

Zhihao Liu ◽

Xiaopeng Li ◽

...

Keyword(s):

Endothelial Function ◽

Postmenopausal Women ◽

Progenitor Cells ◽

Endothelial Progenitor Cells ◽

Premenopausal Women ◽

Endothelial Damage ◽

Normal Weight ◽

Vascular Endothelial ◽

Vascular Endothelial Function ◽

Endothelial Progenitor

Endothelial progenitor cells (EPCs) have endogenous endothelium-reparative potential, but obesity impairs EPCs. Overweight premenopausal women have a normal number of circulating EPCs with functional activity, but whether EPCs in overweight postmenopausal women can repair obesity-related endothelial damage requires further investigation. For this purpose, we examined the function and number of circulating EPCs, evaluated vascular endothelial function, and explored the underlying mechanism. Compared with normal weight or overweight age-matched men, postmenopausal women (overweight or normal weight) had a diminished number of circulating EPCs and impaired vascular endothelial function, as detected by flow-mediated dilatation. Moreover, GTCPH I expression and the nitric oxide level in overweight postmenopausal women and men were significantly decreased. Together, our findings demonstrate that the number or function of circulating EPCs and endothelial function, which is partially regulated by the GTCPH I/BH4 signaling pathway, is not preserved in overweight postmenopausal women. The GTCPH I/BH4 pathway in circulating EPCs may be a potential therapeutic target for endothelial injury in overweight postmenopausal women.

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Effects of Black Raspberry on Lipid Profiles and Vascular Endothelial Function in Patients with Metabolic Syndrome

Phytotherapy Research ◽

10.1002/ptr.5154 ◽

2014 ◽

Vol 28 (10) ◽

pp. 1492-1498 ◽

Cited By ~ 26

Author(s):

Han Saem Jeong ◽

Soon Jun Hong ◽

Tae-Bum Lee ◽

Ji-Wung Kwon ◽

Jong Tae Jeong ◽

...

Keyword(s):

Metabolic Syndrome ◽

Endothelial Function ◽

Lipid Profiles ◽

Vascular Endothelial ◽

Black Raspberry ◽

Vascular Endothelial Function

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Abstract 1749: Endothelial Progenitor Cells and Vascular Endothelial Function Follow a Parallel Circadian Pattern

Circulation ◽

10.1161/circ.118.suppl_18.s_382-a ◽

2008 ◽

Vol 118 (suppl_18) ◽

Author(s):

Ibhar Al Mheid ◽

Konstantinos Aznaouridis ◽

Riyaz Patel ◽

Farheen Shirazi ◽

Diane J Sutcliffe ◽

...

Keyword(s):

Endothelial Function ◽

Progenitor Cells ◽

Endothelial Progenitor Cells ◽

Circadian Variation ◽

List Type ◽

Vascular Endothelial ◽

Vascular Endothelial Function ◽

Endothelial Progenitor ◽

Cell Counts ◽

Flow Mediated Vasodilation

Background: Endothelial Progenitor Cells (EPCs) are mobilized in response to endothelial injury and their counts correlate with endothelial function and cardiovascular risk burden. This rare cell population can be characterized by either flow cytometric analysis or mononuclear cell culture and colony counting, however, the 24-hour circadian variation and inter-relation of EPC measures with endothelial function remain unknown. We hypothesized that EPC levels and endothelial function will have a similar circadian variation. Methods: In 12 healthy subjects (8 men, 42 ± 18 yrs), we investigated the circadian variation of: 1-circulating cells positive for: CD34, CD133 andCD34, the number of colonies formed by culturing mononuclear cells utilizing a 7-day assay and flow-mediated vasodilation utilizing brachial artery reactivity at 8am, noon, 4pm, 8pm, midnight, 4am and 8am. Results: ANOVA for repeated measures over 24 hours indicated significant changes in the number of colony counts (p < .001, highest at midnight). Similarly, flow-mediated vasodilation was highest at midnight (p < .001). In contrast, CD34+ and dual positive CD34+ /CD133+ cell counts peaked a little earlier at 8 pm (8 pm vs.8 am p = .07 and .01 for paired t-tests, respectively). (Figure ) Conclusion: Endothelial function and EPCs estimated as colony forming units peak at midnight and are lower at other times of the day. The highest counts of circulating progenitors are seen at 8pm. There is a parallel change in circulating EPCs and vascular endothelial function during a 24-hour period, with lower levels in the morning hours.

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