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Postprandial endothelial dysfunction in subjects with new-onset type 2 diabetes: an acarbose and nateglinide comparative study
Toru Kato, Teruo Inoue, Koichi Node
Cardiovascular Diabetology , 2010, DOI: 10.1186/1475-2840-9-12
Abstract: We recruited a total of 30 patients with newly diagnosed type 2 diabetes (19 men and 11 women, age 67.8 ± 7.3 years). Patients were randomly assigned to 3 groups receiving either 300 mg/day acarbose, 270 mg/day nateglinide, or no medication. A cookie test (consisting of 75 g carbohydrate, 25 g butter fat, and 7 g protein for a total of 553 kcal) was performed as dietary tolerance testing. During the cookie test, glucose and insulin levels were determined at 0, 30, 60, and 120 min after load. In addition, endothelial function was assessed by % flow-mediated dilation (FMD) of the brachial artery at 0 and 120 min after cookie load.Postprandial glucose and insulin levels were similar in the 3 groups. Postprandial endothelial dysfunction was similar in the 3 groups before treatment. After 12 weeks of intervention, postprandial FMD was significantly improved in the acarbose group compared with the control group (6.8 ± 1.3% vs 5.2 ± 1.1%, p = 0.0022). Area under the curve (AUC) for insulin response was significantly increased in the nateglinide and control groups; however, no significant change was observed in the acarbose group.Our results suggest that acarbose improves postprandial endothelial function by improvement of postprandial hyperglycemia, independent of postprandial hyperinsulinemia. Acarbose may thus have more beneficial effects on postprandial endothelial function in patients with type 2 diabetes than nateglinide.Epidemiological studies have revealed that postprandial hyperglycemia is a more powerful predictor of future cardiovascular events than fasting hyperglycemia [1,2]. Endothelial dysfunction is not only an early marker of atherosclerosis but is also strongly associated with risk of future cardiovascular events [3]. Endothelial dysfunction is associated with cardiovascular risk factors such as smoking [4], dyslipidemia [5,6], hypertension [7,8], obesity [9], type 2 diabetes [10], and postprandial hyperglycemia [11]. Postprandial endothelial dysfunction,
Suppressive response of confections containing the extractive from leaves of Morus Alba on postprandial blood glucose and insulin in healthy human subjects
Mariko Nakamura, Sadako Nakamura, Tsuneyuki Oku
Nutrition & Metabolism , 2009, DOI: 10.1186/1743-7075-6-29
Abstract: Ten healthy females (22.3 years, BMI 21.4 kg/m2) participated in this within-subject, repeated measures study. For the first aim of this study, the test solutions containing 30 g of sucrose and 1.2 or 3.0 g of ELM were repeatedly and randomly given to each subject. To identify the practically suppressive effects on postprandial blood glucose and insulin, some confections with added ELM were prepared as follows: Mizu-yokan, 30 g of sucrose with the addition of 1.5 or 3.0 g ELM; Daifuku-mochi, 9.0 g of starch in addition to 30 g of sucrose and 1.5 or 3.0 g ELM; Chiffon-cake, 24 g of sucrose, starch, and 3.0 or 6.0 g of ELM, and were ingested by each subject. Blood and end-expiration were collected at selected periods after test food ingestion.When 30 g of sucrose with 1.2 or 3.0 g of ELM were ingested by subjects, the elevations of postprandial blood glucose and insulin were effectively suppressed (p < 0.01), and the most effective ratio of ELM to sucrose was evaluated to be 1:10. AUC (area under the curve) of breath hydrogen excretion for 6 h after the ingestion of an added 3 g of ELM significantly increased (p < 0.01). When AUCs-3h of incremental blood glucose of confections without ELM was 100, that of Mizu-yokan and Daifuku-mochi with the ratio (1:10) of ELM to sucrose was decreased to 53.4 and 58.2, respectively. Chiffon-cake added one-fourth ELM was 29.0.ELM-containing confections for which the ratio of ELM and sucrose is one-tenth effectively suppress the postprandial blood glucose and insulin by inhibiting the intestinal sucrase, thus creating a prebiotic effect. The development of confections with ELM can therefore contribute to the prevention and the quality of life for prediabetic and diabetic patients.It has recently become important for not only adults but also children to prevent metabolic syndrome, particularly when prevention of hyperglycemia and hyperlipidemia is also an issue [1-3]. In order to decrease the incidence and prevalence of life-style rela
Postprandial glycemia and cardiovascular disease in diabetes mellitus
Wajchenberg, Bernardo Léo;
Arquivos Brasileiros de Endocrinologia & Metabologia , 2007, DOI: 10.1590/S0004-27302007000200010
Abstract: this article reviews the role of fasting and postprandial glycemia to the overall glycemic control of patients with type 2 diabetes and glucose intolerance, as well as their causal relationship upon micro and macrovascular complications. recent studies have suggested that a third component of the glucose triad, the postprandial glucose excursions, might have a role in the overall glycemic load and might also reflect glycemic control. epidemiological and intervention studies are presented in the article, supporting the conclusion that postprandial hyperglycemia in impaired glucose tolerance and diabetic subjects is a more powerful marker of cardiovascular disease risk than fasting hyperglycemia, then the treatment directed at specifically lowering postprandial glucose is crucial, as underlined by the american diabetes association.
Type 2 diabetes: postprandial hyperglycemia and increased cardiovascular risk
Ajikumar V Aryangat, John E Gerich
Vascular Health and Risk Management , 2010, DOI: http://dx.doi.org/10.2147/VHRM.S8216
Abstract: iabetes: postprandial hyperglycemia and increased cardiovascular risk Review (8181) Total Article Views Authors: Ajikumar V Aryangat, John E Gerich Published Date March 2010 Volume 2010:6 Pages 145 - 155 DOI: http://dx.doi.org/10.2147/VHRM.S8216 Ajikumar V Aryangat, John E Gerich University of Rochester, Rochester, New York, USA Abstract: Hyperglycemia is a major risk factor for both the microvascular and macrovascular complications in patients with type 2 diabetes. This review summarizes the cardiovascular results of large outcomes trials in diabetes and presents new evidence on the role of hyperglycemia, with particular emphasis on postprandial hyperglycemia, in adverse cardiovascular outcomes in patients with type 2 diabetes. Treatment options, including the new dipeptidyl peptidase-4 inhibitors and glucagon-like peptide-1 mimetics that primarily target postprandial hyperglycemia, are also discussed. Hyperglycemia increases cardiovascular mortality, and reducing hyperglycemia lowers cardiovascular risk parameters. Control of both fasting and postprandial hyperglycemia is necessary to achieve optimal glycated hemoglobin control. Therefore, antihyperglycemic agents that preferentially target postprandial hyperglycemia, along with those that preferentially target fasting hyperglycemia, are strongly suggested to optimize individual diabetes treatment strategies and reduce complications.
Type 2 diabetes: postprandial hyperglycemia and increased cardiovascular risk  [cached]
Ajikumar V Aryangat,John E Gerich
Vascular Health and Risk Management , 2010,
Abstract: Ajikumar V Aryangat, John E GerichUniversity of Rochester, Rochester, New York, USAAbstract: Hyperglycemia is a major risk factor for both the microvascular and macrovascular complications in patients with type 2 diabetes. This review summarizes the cardiovascular results of large outcomes trials in diabetes and presents new evidence on the role of hyperglycemia, with particular emphasis on postprandial hyperglycemia, in adverse cardiovascular outcomes in patients with type 2 diabetes. Treatment options, including the new dipeptidyl peptidase-4 inhibitors and glucagon-like peptide-1 mimetics that primarily target postprandial hyperglycemia, are also discussed. Hyperglycemia increases cardiovascular mortality, and reducing hyperglycemia lowers cardiovascular risk parameters. Control of both fasting and postprandial hyperglycemia is necessary to achieve optimal glycated hemoglobin control. Therefore, antihyperglycemic agents that preferentially target postprandial hyperglycemia, along with those that preferentially target fasting hyperglycemia, are strongly suggested to optimize individual diabetes treatment strategies and reduce complications.Keywords: postprandial hyperglycemia, diabetes mellitus, drugs, cardiovascular risk
SILIBININ DIHEMISUCCINATE DAMPENS POSTPRANDIAL HYPERGLYCEMIA IN NORMAL RATS CHALLENGED WITH CARBOHYDRATES LOAD: COMPARATIVE STUDY WITH ACARBOSE  [PDF]
Bushra Hassan Marouf
International Research Journal of Pharmacy , 2012,
Abstract: Postprandial hyperglycemia is a major risk factor for diabetic complications leading to disabilities and mortality in diabetics. Silibinin (SDH), a flavonoid, has been tried in traditional medicine for treating many disorders including diabetes. The present study was designed to evaluate the potential of SDH to damp postprandial blood glucose level after maltose and glucose loading in normal rats. Normal, non-diabetic male Albino Wistar rats were treated with 100mg/kg SDH orally to evaluate the effect on postprandial hyperglycemia after carbohydrate loading, using acarbose as comparator. The results clearly showed ameliorated postprandial hyperglycemia due to the use of SDH, it significantly dampened the postprandial hyperglycemia both in maltose and glucose loaded normal rats, greater than control and comparable to acarbose. In conclusion, SDH effectively suppresses postprandial hyperglycemia in normal rats loaded with maltose, which may be attributed to α-glucosidase inhibition, or glucose due to unexplored mechanism.
Platelet function in the postprandial period  [cached]
Sinzinger Helmut,Berent Robert
Thrombosis Journal , 2012, DOI: 10.1186/1477-9560-10-19
Abstract: Background Postprandial hyperlipidemia and hyperglycemia have been related to cardiovascular events. Among different underlying mechanisms platelet activation seems to be responsible too. No comparable data between various tests in normo- vs. hyperlipidemics before and at different time intervals are available after a fat meal. We aimed to compare 9 of them within the same patients at several time points in postprandial hyperlipidemia. Results For some tests baseline values between the groups were significantly different (TXB2, platelet sensitivity, sedimentation and WU-test). However, hyperlipidemia revealed a variable influence on the tests examined. Some of the available tests apparently sensitive to show platelet activation reflect the increase in triglycerides (TG), such as the sedimentation index. ADP-induced platelet aggregatory activity in count adjusted washed isolated platelet samples during postprandial hyperlipidemia indicates mildly enhanced platelet activity, but does not seem to induce significant changes in aggregation. In patients with severe hypertriglyceridemia (> 400 mg/dl fasting) changes in platelet function are more pronounced due to delayed decay and may last up to 16 hours paralleling TG reaching the prevalue. The overwhelming majority of platelet function tests do not significantly respond to postprandial hyperlipidemia. The correlation between the tests applied is poor. For standardization purpose, platelet aggregation tests, aimed to examine proaggregatory capacity in atherosclerosis, should only be performed at the same time of the day after a fasting period > 6 hours. The great variation in preanalytical work-up on comparison of various tests, large number of platelet tests available and their respective potential value are discussed. Conclusions At present, the suspicion that platelet function is significantly activated in the postprandial period cannot be supported by any of the tests used. The information provided is valuable to know for which test and group of patients a fasting period of which duration is recommendable.
Effect of quercetin on postprandial glucose excursion after mono- and disaccharides challenge in normal and diabetic rats  [PDF]
Saad Abdulrahman Hussain, Zheen Aorahman Ahmed, Taha Othman Mahwi, Tavga Ahmed Aziz
Journal of Diabetes Mellitus (JDM) , 2012, DOI: 10.4236/jdm.2012.21013
Abstract: Postprandial hyperglycemia is a major risk factor for diabetic complications leading to disabilities and mortality in diabetics. Quercetin, a flavonoid, has been tried in traditional medicine for treating diabetes. The present study was designed to evaluate the potential of quercetin to control postprandial blood glucose level after maltose and glucose loading in normal and STZ-induced diabetic rats. Normal male Albino wistar rats and STZ-induced diabetic rats were treated with 300 and 600 mg/kg quercetin orally to evaluate the effect on postprandial hyperglycemia after carbohydrate loading, using acarbose as comparator. The results clearly showed ameliorated postprandial hyperglycemia due to the use of quercetin (300 and 600 mg/kg), it significantly dampened the postprandial hyperglycemia by 32.0% and 64.0% respectively, in maltose loaded diabetic rats, and 30.3% after 300 mg/kg dose in normal rats, compared to control; while acarbose produced 51% and 54% decrease in this respect in the two models respecttively. Quercetin in 600 mg/kg dose produces significantly more reduction in postprandial hyperglycemia compared to acarbose, while in rats that received glucose and quercetin, postprandial hyperglycemia was not significantly affected. In conclusion, quercetin effectively suppresses postprandial hyperglycemia in STZ-induced diabetic rats loaded with maltose, which may be attributed to α-glucosidase inhibition. Quercetin could be used as a potential supplement for treating postprandial hyperglycemia.
Mechanism of the mitogenic influence of hyperinsulinemia
Boris Draznin
Diabetology & Metabolic Syndrome , 2011, DOI: 10.1186/1758-5996-3-10
Abstract: Insulin is a major anabolic hormone that governs carbohydrate metabolism and contributes greatly to the metabolism of lipids and proteins. Clinically, its primary role is to promote glucose utilization and regulate hepatic glucose production. At the same time, insulin is an important, albeit mild growth factor. It promotes cell growth, cell division, migration, and inhibits apoptosis. These aspects of insulin action are collectively known as the "mitogenic actions" of insulin [1] and because they are so critical to cellular physiology, insulin is always present in cell culture medium for the propagation and maintenance of cells in culture. Although insulin is a much weaker mitogen [2] than insulin-like growth factors (IGFs), platelet-derived growth factor (PDGF), vascular endothelial growth factor (VEGF) and epidermal growth factor (EGF), insulin has a very specific mitogenic action that in fact modulates cellular responsiveness to all other growth factors, potentiating other growth factors' action [3,4].Let us now briefly review the molecular mechanisms by which insulin and hyperinsulinemia, particularly when it occurs in the setting of insulin resistance, can augment proliferative events. In order for all growth factors to stimulate mitogenesis, they must activate the Ras-Raf-Map kinase signalling pathway (Figure 1). Ras proteins are activated by binding guanosine triphosphate (GTP), a process promoted by the guanine nucleotide exchange factor, Sos. This activation can occur only if Ras proteins are anchored at the plasma membrane (Figure 1) [5].Isoprenylation of Ras is the first step that commits Ras to the process of translocation to the plasma membrane (Figure 1) [reviewed in [6]]. Because isoprenylation of Ras involves an attachment of a farnesyl moiety (a 15-carbon intermediary in the cholesterol synthesis pathway), the process is also known as farnesylation and is activated by the enzyme farnesyltransferase (FTase). Farnesylated Ras is then destined to ancho
Atherogenic Factors and Their Epigenetic Relationships  [PDF]
Ana Z. Fernandez,Andrew L. Siebel,Assam El-Osta
International Journal of Vascular Medicine , 2010, DOI: 10.1155/2010/437809
Abstract: Hypercholesterolemia, homocysteine, oxidative stress, and hyperglycemia have been recognized as the major risk factors for atherogenesis. Their impact on the physiology and biochemistry of vascular cells has been widely demonstrated for the last century. However, the recent discovery of the role of epigenetics in human disease has opened up a new field in the study of atherogenic factors. Thus, epigenetic tags in endothelial, smooth muscle, and immune cells seem to be differentially affected by similar atherogenic stimuli. This paper summarizes some recent works on expression of histone-modifying enzymes and DNA methylation directly linked to the presence of risk factors that could lead to the development or prevention of the atherosclerotic process. 1. Introduction Cardiovascular-related diseases are the most serious threat to human health that authorities will have to manage worldwide. All of these pathological outcomes, like stroke, thrombosis, or infarction, are pathological events resulting from the long-lasting and silent process, known as atherosclerosis [1]. Atherosclerosis is considered to be a multifactorial pathology where preferential zones within the arteries, such as branches and curvatures, are prone to differential expression of genes with a proatherosclerotic profile, serving as potential substratum for lesions when risk factors are introduced [2, 3]. In this sense epigenetics, defined as the structural adaptation of chromosomal regions so as to register, signal, or perpetuate altered gene activity states [4] might play a significant role in the pathogenicity of cardiovascular risk factors, which could explain the specificity in the establishment and further development of the atherosclerotic lesion. 2. Atherosclerosis Overview Atherosclerosis is a progressive disease characterized by the accumulation of lipids and fibrous elements in susceptible zones in the large and medium arteries [5]. Normal arteries are characterized by one internal or luminal surface of nonadherent endothelial cells (ECs) over a layer of extracellular matrix (ECM), mainly formed by collagen and proteoglycans, followed by a media layer of smooth muscle cells (SMC) and an external adventitia layer. Diverse stimuli, such as hypercholesterolemia, smoking, or hypertension, lead to a pathological activation of EC, attracting blood monocytes into the intima layer, where they differentiate into macrophages in order to remove cholesterol accumulated in this layer. Monocyte chemoattractant protein-1 (MCP-1) appears responsible for the direct migration of monocytes into the
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