Association of Changes in Oxidative and Proinflammatory States with Changes in Vascular Function after a Lifestyle Modification Trial Among Obese Children

Kelishadi, Roya; Hashemi, Mohammad; Mohammadifard, Noushin; Asgary, Sedigheh; Khavarian, Noushin

doi:10.1373/clinchem.2007.089953

Cited by 101 publications

(102 citation statements)

References 37 publications

(40 reference statements)

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“…2 Indeed, recent studies showed a positive relationship between obesity, inflammatory C-reactive protein, 3 and oxidized low-density lipoprotein (ox-LDL). 4,5 Moreover, we showed that ox-LDL was associated with the incidence of the metabolic syndrome 6 and with several metabolic syndrome components, especially visceral obesity. 7,8 Stevioside was found to exert antihyperglycemic and insulinotropic effects in a non-obese animal model of type 2 diabetes 9 by acting directly on pancreatic cells.…”

Section: Introductionmentioning

confidence: 93%

Stevioside inhibits atherosclerosis by improving insulin signaling and antioxidant defense in obese insulin-resistant mice

et al. 2009

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Objective: Stevioside is a non-caloric natural sweetener that does not induce a glycemic response, making it attractive as sweetener to diabetics and others on carbohydrate-controlled diets. Obesity is frequently associated with insulin resistance and increased inflammation and oxidative stress. Therefore, we investigated its effects on insulin resistance, inflammation and oxidative stress related to atherosclerosis in obese insulin-resistant mice.Research design: Twelve-week-old mice were treated with stevioside (10 mg kg À1 , n ¼ 14) or placebo (n ¼ 20) for 12 weeks. Results: Stevioside had no effect on weight and triglycerides, but lowered glucose and insulin. Stevioside treatment improved adipose tissue maturation, and increased glucose transport, insulin signaling and antioxidant defense in white visceral adipose tissues. Together, these increases were associated with a twofold increase of adiponectin. In addition, stevioside reduced plaque volume in the aortic arch by decreasing the macrophage, lipid and oxidized low-density lipoprotein (ox-LDL) content of the plaque. The higher smooth muscle cell-to-macrophage ratio was indicative for a more stable plaque phenotype. The decrease in ox-LDL in the plaque was likely due to an increase in the antioxidant defense in the vascular wall, as evidenced by increased Sod1, Sod2 and Sod3. Circulating adiponectin was associated with improved insulin signaling and antioxidant defense in both the adipose tissue and the aorta of stevioside-treated mice. Conclusion: Stevioside treatment was associated with improved insulin signaling and antioxidant defense in both the adipose tissue and the vascular wall, leading to inhibition of atherosclerotic plaque development and inducing plaque stabilization.

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Section: Introductionmentioning

confidence: 93%

Stevioside inhibits atherosclerosis by improving insulin signaling and antioxidant defense in obese insulin-resistant mice

et al. 2009

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“…For example, exercise training lowered sRBP-4 concentrations in adults and overweight children, correlating with improved insulin sensitivity and lower CRP and IL-6 (58 ). Lifestyle modification in obese children reduced CRP and MDA concentrations, correlating with improvements in endothelial function (84 ). Among older adults, 6 months of resistance training improved oxidative stress, assessed by measurement of exercisedinduced lipid hydroperoxides (85 ).…”

Section: Exercisementioning

confidence: 98%

The Perfect Storm: Obesity, Adipocyte Dysfunction, and Metabolic Consequences

2008

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BACKGROUND:As the prevalence of adiposity soars in both developed and developing nations, appreciation of the close links between obesity and disease increases. The strong relationships between excess adipose tissue and poor health outcomes, including cardiovascular disease, diabetes, and cancer, mandate elucidation of the complex cellular, hormonal, and molecular pathophysiology whereby adiposity initiates and maintains adverse health effects.CONTENT: In this report we review adipocyte metabolism and function in the context of energy imbalance and postprandial nutrient excess, including adipocyte hypertrophy and hyperplasia, adipocyte dysfunction, and other systemic consequences. We also discuss implications for laboratory evaluation and clinical care, including the role of lifestyle modifications. Chronic energy imbalance produces adipocyte hypertrophy and hyperplasia, endoplasmic reticulum stress, and mitochondrial dysfunction. These processes lead to increased intracellular and systemic release of adipokines, free fatty acids, and inflammatory mediators that cause adipocyte dysfunction and induce adverse effects in the liver, pancreatic ␤-cells, and skeletal muscle as well as the heart and vascular beds. Several specialized laboratory tests can quantify these processes and predict clinical risk, but translation to the clinical setting is premature. Current and future pharmacologic interventions may target these pathways; modest changes in diet, physical activity, weight, and smoking are likely to have the greatest impact.

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“…Blood samples collected during the study (preingestion and 2-h postingestion) were analyzed for norepinephrine (HPLC), oxidized LDL (ELISA, Mercodia, Uppsala Sweden), glucose (EIA), and insulin (chemiluminescent assay). This was done as these markers, or systems they provide insight into, may be have been influenced by our intervention and can influence endothelium-dependent vasodilation (2,5,26,28). Additionally, we also measured serum total epicatechin to document the effect of cocoa ingestion (preingestion, 1-h postingestion, and 2-h postingestion).…”

Section: Measurementsmentioning

confidence: 99%

Dose-dependent increases in flow-mediated dilation following acute cocoa ingestion in healthy older adults

Monahan

Feehan

Kunselman

et al. 2011

Journal of Applied Physiology

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Monahan KD, Feehan RP, Kunselman AR, Preston AG, Miller DL, Lott ME. Dose-dependent increases in flow-mediated dilation following acute cocoa ingestion in healthy older adults. J Appl Physiol 111: 1568 -1574. First published September 8, 2011 doi:10.1152/japplphysiol.00865.2011.-An inverse relation exists between intake of flavonoid-rich foods, such as cocoa, and cardiovascular-related mortality. Favorable effects of flavonoids on the endothelium may underlie these associations. We performed a randomized, double-blind, placebo-controlled study to test the hypothesis that acute cocoa ingestion dose dependently increases endothelium-dependent vasodilation, as measured by an increase in brachial artery flow-mediated dilation (FMD), in healthy older adults. Measurements were obtained before (preingestion) and after (1-and 2-h postingestion) ingestion of 0 (placebo), 2, 5, 13, and 26 g of cocoa in 23 adults (63 Ϯ 2 yr old, mean Ϯ SE). Changes in brachial artery FMD 1-and 2-h postingestion compared with preingestion were used to determine the effects of cocoa. FMD was unchanged 1 (⌬Ϫ0.3 Ϯ 0.2%)-and 2-h (⌬0.1 Ϯ 0.1%) after placebo (0 g cocoa). In contrast, FMD increased both 1-h postingestion (2 g cocoa ⌬0.0 Ϯ 0.2%, 5 g cocoa ⌬0.8 Ϯ 0.3%, 13 g cocoa ⌬1.0 Ϯ 0.3%, and 26 g cocoa ⌬1.6 Ϯ 0.3%: P Ͻ 0.05 compared with placebo for 5, 13, and 26 g cocoa) and 2-h postingestion (2 g cocoa ⌬0.5 Ϯ 0.3%, 5 g cocoa ⌬1.0 Ϯ 0.3%, 13 g cocoa ⌬1.4 Ϯ 0.2%, and 26 g cocoa ⌬2.5 Ϯ 0.4%: P Ͻ 0.05 compared with placebo for 5, 13, and 26 g cocoa) on the other study days. A serum marker of cocoa ingestion (total epicatechin) correlated with increased FMD 1-and 2-h postingestion (r ϭ 0.44 -0.48; both P Ͻ 0.05). Collectively, these results indicate that acute cocoa ingestion dose dependently increases brachial artery FMD in healthy older humans. These responses may help to explain associations between flavonoid intake and cardiovascular-related mortality in humans.flavonoid; flavanol; chocolate; endothelium; endothelial function THE ENDOTHELIUM CONTRIBUTES critically to cardiovascular homeostasis by influencing factors such as vascular tone, vascular permeability, platelet aggregation, and thrombosis. As abnormal function of the endothelium is a key event in the atherosclerotic process (15), it is not surprising that endothelial dysfunction is a hallmark feature of many cardiovascular disease states (33). Moreover, it is not surprising that aging, which is a primary risk factor for the development of cardiovascular disease and atherosclerosis (29,36), is associated with marked endothelial dysfunction. Specifically, in response to stimulation of the vascular endothelium via pharmacological substances, such as acetylcholine, or physiological stimuli, such as increases in vascular shear stress, a reduced endothelium-dependent vasodilatory response occurs in healthy older adults compared with healthy young adults (7,11,12,41). As low levels of brachial artery flow-mediated dilation (FMD), a commonly used method to assess endothelium-dependent vasodi...

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Association of Changes in Oxidative and Proinflammatory States with Changes in Vascular Function after a Lifestyle Modification Trial Among Obese Children

Cited by 101 publications

References 37 publications

Stevioside inhibits atherosclerosis by improving insulin signaling and antioxidant defense in obese insulin-resistant mice

Stevioside inhibits atherosclerosis by improving insulin signaling and antioxidant defense in obese insulin-resistant mice

The Perfect Storm: Obesity, Adipocyte Dysfunction, and Metabolic Consequences

Dose-dependent increases in flow-mediated dilation following acute cocoa ingestion in healthy older adults

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