Oral glucose loading attenuates endothelial function in normal individual

Watanabe, Kentaro; Oba, Koji; Suzuki, Tatsuya; Ouchi, Motoshi; Suzuki, Kazunari; Futami-Suda, Shoko; Sekimizu, Ken-ichi; Yamamoto, Naofumi; Nakano, Hiroshi

doi:10.1111/j.1365-2362.2010.02424.x

Cited by 32 publications

(26 citation statements)

References 45 publications

(91 reference statements)

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“…The subjects of the OG and control groups had previously been included in our study of postprandial attenuation of FMD [12]. The test meal for the TM group (Table2) was a commercial energy-supplement food (CalorieMate®, Otsuka Pharmaceutical Co., Ltd., Tokyo, Japan).…”

Section: Methodsmentioning

confidence: 99%

“…Attenuation of brachial artery FMD is induced by postprandial hyperglycemia in subjects with normal glucose tolerance and in prediabetic or diabetic patients, and FMD is negatively correlated with plasma glucose (PG) levels after oral glucose loading [8-11]. We have previously reported that postprandial hyperinsulinemia also induces attenuation of FMD in persons with normal glucose tolerance [12]. Several studies have evaluated differences in FMD attenuation after meals with different carbohydrate contents [13-17].…”

Section: Introductionmentioning

confidence: 99%

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The effects of postprandial glucose and insulin levels on postprandial endothelial function in subjects with normal glucose tolerance

Suzuki

Watanabe

Futami-Suda

et al. 2012

Cardiovasc Diabetol

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BackgroundPrevious studies have demonstrated that postprandial hyperglycemia attenuates brachial artery flow-mediated dilation (FMD) in prediabetic patients, in diabetic patients, and even in normal subjects. We have previously reported that postprandial hyperinsulinemia also attenuates FMD. In the present study we evaluated the relationship between different degrees of postprandial attenuation of FMD induced by postprandial hyperglycemia and hyperinsulinemia and differences in ingested carbohydrate content in non-diabetic individuals.MethodsThirty-seven healthy subjects with no family history of diabetes were divided into 3 groups: a 75-g oral glucose loading group (OG group) (n = 14), a test meal group (TM group) (n = 12; 400 kcal, carbohydrate content 40.7 g), and a control group (n = 11). The FMD was measured at preload (FMD0) and at 60 minutes (FMD60) and 120 (FMD120) minutes after loading. Plasma glucose (PG) and immunoreactive insulin (IRI) levels were determined at preload (PG0, IRI0) and at 30 (PG30, IRI30), 60 (PG60, IRI60), and 120 (PG120, IRI120) minutes after loading.ResultPercentage decreases from FMD0 to FMD60 were significantly greater in the TM group (−21.19% ± 17.90%; P < 0.001) and the OG group (−17.59% ± 26.64%) than in the control group (6.46% ± 9.17%; P < 0.01), whereas no significant difference was observed between the TM and OG groups. In contrast, the percentage decrease from FMD0 to FMD120 was significantly greater in the OG group (−18.91% ± 16.58%) than in the control group (6.78% ± 11.43%; P < 0.001) or the TM group (5.22% ± 37.22%; P < 0.05), but no significant difference was observed between the control and TM groups. The FMD60 was significantly correlated with HOMA-IR (r = −0.389; P < 0.05). In contrast, FMD120 was significantly correlated with IRI60 (r = −0.462; P < 0.05) and the AUC of IRI (r = −0.468; P < 0.05). Furthermore, the percentage change from FMD0 to FMD120 was significantly correlated with the CV of PG (r = 0.404; P < 0.05), IRI60 (r = 0.401; p < 0.05) and the AUC of IRI (r = 0.427; P < 0.05). No significant correlation was observed between any other FMDs and glucose metabolic variables.ConclusionDifferences in the attenuation of postprandial FMD induced by different postprandial insulin levels may occur a long time postprandially but not shortly after a meal.

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Section: Methodsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

The effects of postprandial glucose and insulin levels on postprandial endothelial function in subjects with normal glucose tolerance

Suzuki

Watanabe

Futami-Suda

et al. 2012

Cardiovasc Diabetol

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“…Similar observations regarding increased endothelial activation markers were also made following OGTT (42,43) . Recently, Watanabe et al (44) and many others observed that an OGTT significantly decreased endothelial function assessed by ultrasonography that was correlated with postprandial hyperglycaemia (r 20·61; P,0·05) and insulin release (r 2 0·55; P, 0·05). Importantly, some groups have observed no demonstrable increases in postprandial oxidative stress (malondialdehyde (MDA), nitrate/ nitrite and H 2 O 2 levels) or decreases in plasma antioxidant capacity (i.e.…”

Section: Pathophysiology Of Oxidative Stressmentioning

confidence: 99%

The role of oxidative stress in postprandial endothelial dysfunction

et al. 2012

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Endothelial dysfunction is a turning point in the initiation and development of atherosclerosis and its complications and is predictive of future cardiovascular events. Ingestion of high-carbohydrate or high-fat meals often results in postprandial hyperglycaemia and/or hypertriacylglycerolaemia that may lead to a transient impairment in endothelial function. The present review will discuss human studies evaluating the impact of high-carbohydrate and high-fat challenges on postprandial endothelial function as well as the potential role of oxidative stress in such postprandial metabolic alterations. Moreover, the present review will differentiate the postprandial endothelial and oxidative impact of meals rich in varying fatty acid types.

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“…However, Major-Pedersen et al (2008) reported that oral glucose load does not cause endothelial dysfunction in healthy individuals when the mean glucose level is at 5.6 mmol/L and insulin is at 27.2 mmol/L, at 2 hours after glucose [11]. Nevertheless, a recent study has shown that oral glucose load attenuated flow-mediated dilation in brachial artery of healthy individuals [12]. …”

Section: Introductionmentioning

confidence: 99%

Effects of Glucose Load and Nateglinide Intervention on Endothelial Function and Oxidative Stress

Wang

Guo²,

Zhang³

et al. 2013

Journal of Diabetes Research

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We analysed endothelial function and oxidative stress in patients with abnormal glucose metabolism, the effect of glucose load, and the impact of nateglinide. 109 participants were grouped into newly diagnosed diabetes, prediabetes, and control. Fasting plasma glucose (FPG), postprandial plasma glucose (PPG), glycosylated haemoglobin (HbA1c), and glycated albumin (GA) varied significantly among the study groups (P < 0.01). Nitric oxide (NO) and insulin resistance index (HOMA-IRI) levels were markedly different between the newly diagnosed diabetes and the control (P < 0.01). Glucose loading lowered flow-mediated endothelium-dependent dilation (FMEDD), NO, and superoxide dismutase (SOD) (P < 0.01). Fasting and glucose loading FMEDD, FPG, PPG, HbA1c, and GA were negatively correlated (r = −0.4573, −0.4602, −0.3895, −0.3897, and r = −0.4594, −0.4803, −0.4494, −0.3885; P < 0.01), whereas NO, SOD, and HOMA-β were positively correlated (r = 0.2983, 0.3211, 0.311, and r = 0.1954, 0.361, 0.2569; P < 0.05). After the treatment with nateglinide, significant decreases in FPG, PPG, GA, HbA1C, endothelin-1(ET-1), malondialdehyde (MDA), and HOMA-IRI were observed, whereas FMEDD, NO, and SOD increased (P < 0.01). Thus, the study demonstrated the adverse effect of glucose load on endothelial function and oxidative stress. Nateglinide lowers blood glucose, reduces insulin resistance and oxidative stress, and improves endothelial function in newly diagnosed diabetes.

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Oral glucose loading attenuates endothelial function in normal individual

Abstract: Our study showed that oral glucose loading attenuates FMD and shortens elapsed time at the maximum after-hyperaemia diameter, and the effect of glucose fluctuation on atherosclerosis in individuals with normal glucose tolerance remains despite only the attenuation of endothelial function.

Cited by 32 publications

References 45 publications

The effects of postprandial glucose and insulin levels on postprandial endothelial function in subjects with normal glucose tolerance

The effects of postprandial glucose and insulin levels on postprandial endothelial function in subjects with normal glucose tolerance

The role of oxidative stress in postprandial endothelial dysfunction

Effects of Glucose Load and Nateglinide Intervention on Endothelial Function and Oxidative Stress

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