Glucose-dependent leukocyte activation in patients with type 2 diabetes mellitus, familial combined hyperlipidemia and healthy controls

Vries, Marijke A. de; Alipour, Arash; Klop, Boudewijn; Geijn, Gert‐Jan M. van de; Janssen, Hans W.; Njo, Tjin L.; Meulen, N. van der; Rietveld, A.P.; Liem, Anho; Westerman, Elsbeth M; Herder, Wouter W. de; Cabezas, Manuel Castro

doi:10.1016/j.metabol.2014.10.011

Cited by 38 publications

(34 citation statements)

References 19 publications

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“…96 Recent data also demonstrate that postprandial hyperglycemia is involved in increased leucocyte activation in patients with type 2 diabetes and familial combined hyperlipidemia. 97 Concerning the coagulation system, there are data demonstrating that postprandial hyperglycemia constitutes a significant predictor of platelet activation, as this was shown by measurement of urinary 11-dehydro-thromboxane (TX)B(2), a marker of in vivo platelet activation, in subjects with type 2 early diabetes. 98 It has also been found that induction of acute short-term hyperglycemia in type 2 diabetic patients results in increased platelet activation markers, such as shear-induced platelet activation, P-selectin and LIMP expression on platelets, urinary 11-dehydroTxB2 excretion and plasma vWF.…”

Section: Pathophysiology Of Postprandial Dysmetabolism Induced Cardiomentioning

confidence: 99%

Postprandial dysmetabolism: Too early or too late?

Pappas¹,

Kandaraki²,

Tsirona³

et al. 2016

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postprandial dysmetabolism is a postprandial state characterized by abnormal metabolism of glucose and lipids and, more specifically, of elevated levels of glucose and triglyceride (Tg) containing lipoproteins. Since there is evidence that postprandial dysmetabolism is associated with increased cardiovascular mortality and morbidity, due to macro-and microvascular complications, as well as with conditions such as polycystic ovary syndrome (pCOS) and nonalcoholic fatty liver disease (NaFlD), it is recommended that clinicians be alert for early detection and management of this condition. management consists of a holistic approach including dietary modification, exercise and use of hypoglycemic and hypolipidemic medication aiming to decrease the postprandial values of circulating glucose and triglycerides. This review aims to explain glucose and lipid homeostasis and the impact of postprandial dysmetabolism on the cardiovascular system as well as to offer suggestions with regard to the therapeutic approach for this entity. however, more trials are required to prevent or reverse early and not too late the actual tissue damage due to postprandial dysmetabolism.

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Section: Pathophysiology Of Postprandial Dysmetabolism Induced Cardiomentioning

confidence: 99%

Postprandial dysmetabolism: Too early or too late?

Pappas¹,

Kandaraki²,

Tsirona³

et al. 2016

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“…The baseline characteristics of these subjects are presented in Table . Data on the healthy controls have been published in part before .…”

Section: Resultsmentioning

confidence: 99%

“…Previous studies have shown that the postprandial phase is a pro‐inflammatory state in which leucocyte activation increases, especially in patients with insulin resistant conditions . CD11b and CD66b are involved in degranulation of neutrophils and the adhesion of leucocytes to the endothelium of the vessel wall . These markers have been linked directly to the development of atherosclerosis.…”

Section: Discussionmentioning

confidence: 99%

“…A recent study by de Vries et al . showed that post‐OGTT hyperglycaemia in patients with familial combined hyperlipidaemia is associated with increased leucocyte activation. However, it is currently unknown whether there is an effect, and to what degree, of postprandial hyperglycaemia on leucocyte activation in patients with FH.…”

Section: Introductionmentioning

confidence: 99%

“…Patients with familial combined hyperlipidaemia and familial hypercholesterolemia (FH) have higher levels of leucocyte activation in comparison with healthy controls [13,14]. A recent study by de Vries et al [5] showed that post-OGTT hyperglycaemia in patients with familial combined hyperlipidaemia is associated with increased leucocyte activation. However, it is currently unknown whether there is an effect, and to what degree, of postprandial hyperglycaemia on leucocyte activation in patients with FH.…”

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

Glucose‐dependent leucocyte activation in familial hypercholesterolemia

Koks

Vries

Birnie

et al. 2017

Eur J Clin Investigation

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Molecular mechanisms, prevalence, and molecular methods for familial combined hyperlipidemia disease: A review

Taghizadeh

Mardani

Rostami

et al. 2018

J of Cellular Biochemistry

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Familial combined hyperlipidemia (FCHL) is the most common genetic dyslipidemia disorder which is accompanied by increasing of triglyceride and cholesterol. This disorder is a complex genetic disease although it also has monogenic forms. The familial form has several criteria for diagnosis that can be distinguished of nonfamilial position. It has been shown that a variety of internal and external risk factors are involved in the pathogenesis of FCHL. Environmental factors and the genetic background also play an important role in the FCHL pathogenesis. Many mechanisms and pathways are involved in lipid metabolism (ie, dysfunctional adipose tissue, hepatic fat and very low-density lipoprotein overproduction, triglyceride-rich lipoproteins, and clearance of low-density lipoprotein particles) that could lead to FCHL. Individuals with a positive family history like those who have a positive family history of cardiovascular diseases are more predispositions for this disorder. To date several methods have been used to identify the genetic background of the FCHL. In the current review, we summarized the prevalence and the molecular mechanisms involved in the FCHL disease. Moreover, we highlighted the used molecular methods for determining the genes involved in the FCHL. K E Y W O R D S dyslipidemia, familial combined hyperlipidemia, molecular aspects J Cell Biochem. 2019;120:8891-8898.wileyonlinelibrary.com/journal/jcb

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Glucose-dependent leukocyte activation in patients with type 2 diabetes mellitus, familial combined hyperlipidemia and healthy controls

Cited by 38 publications

References 19 publications

Postprandial dysmetabolism: Too early or too late?

Postprandial dysmetabolism: Too early or too late?

Glucose‐dependent leucocyte activation in familial hypercholesterolemia

Molecular mechanisms, prevalence, and molecular methods for familial combined hyperlipidemia disease: A review

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