Postprandial Dysmetabolism and Oxidative Stress in Type 2 Diabetes: Pathogenetic Mechanisms and Therapeutic Strategies

Sottero, Barbara; Gargiulo, Simona; Russo, Isabella; Barale, Cristina; Poli, Giuseppe; Cavalot, Franco

doi:10.1002/med.21349

Cited by 49 publications

(50 citation statements)

References 502 publications

(890 reference statements)

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“…Although the underlying pathogenic mechanisms are multiple, factors promoting oxidative stress are unanimously considered to contribute significantly to platelet activation. Of particular interest, in T2DM patients a marked oxidative response is induced by the consumption of high-calorie meals, which in these individuals determines an abnormal and sustained elevation of blood glucose and lipid levels, mainly TGs, defined as postprandial dysmetabolism [136]. Since the entry of glucose into platelets does not depend on insulin, intraplatelet glucose concentration mirrors blood glucose levels, and chronic hyperglycemia has been clearly identified as a causal factor leading to platelet hyperreactivity, as indicated by enhanced aggregation, increased fibrinogen binding, and TX production [137].…”

Section: Hyperglycemiamentioning

confidence: 99%

Influence of Cardiometabolic Risk Factors on Platelet Function

Barale

Russo

2020

IJMS

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Platelets are key players in the thrombotic processes. The alterations of platelet function due to the occurrence of metabolic disorders contribute to an increased trend to thrombus formation and arterial occlusion, thus playing a major role in the increased risk of atherothrombotic events in patients with cardiometabolic risk factors. Several lines of evidence strongly correlate metabolic disorders such as obesity, a classical condition of insulin resistance, dyslipidemia, and impaired glucose homeostasis with cardiovascular diseases. The presence of these clinical features together with hypertension and disturbed microhemorrheology are responsible for the prothrombotic tendency due, at least partially, to platelet hyperaggregability and hyperactivation. A number of clinical platelet markers are elevated in obese and type 2 diabetes (T2DM) patients, including the mean platelet volume, circulating levels of platelet microparticles, oxidation products, platelet-derived soluble P-selectin and CD40L, thus contributing to an intersection between obesity, inflammation, and thrombosis. In subjects with insulin resistance and T2DM some defects depend on a reduced sensitivity to mediators-such as nitric oxide and prostacyclin-playing a physiological role in the control of platelet aggregability. Furthermore, other alterations occur only in relation to hyperglycemia. In this review, the main cardiometabolic risk factors, all components of metabolic syndrome involved in the prothrombotic tendency, will be taken into account considering some of the mechanisms involved in the alterations of platelet function resulting in platelet hyperactivation.

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Section: Hyperglycemiamentioning

confidence: 99%

Influence of Cardiometabolic Risk Factors on Platelet Function

Barale

Russo

2020

IJMS

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“…Meal ingestion results in a complex and multifactorial (neuro)endocrine and metabolic response which influences postprandial inflammation via different pathways [22]. Western nutrition, high in calories, fats and refined sugars, results in an exaggerated increase of plasma glucose, triglyceride-rich lipoproteins (VLDLs), chylomicrons and their remnants [23].…”

Section: Three Metabolic Statesmentioning

confidence: 99%

Human Postprandial Nutrient Metabolism and Low-Grade Inflammation: A Narrative Review

et al. 2019

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The importance of the postprandial state has been acknowledged, since hyperglycemia and hyperlipidemia are linked with several chronic systemic low-grade inflammation conditions. Humans spend more than 16 h per day in the postprandial state and the postprandial state is acknowledged as a complex interplay between nutrients, hormones and diet-derived metabolites. The purpose of this review is to provide insight into the physiology of the postprandial inflammatory response, the role of different nutrients, the pro-inflammatory effects of metabolic endotoxemia and the anti-inflammatory effects of bile acids. Moreover, we discuss nutritional strategies that may be linked to the described pathways to modulate the inflammatory component of the postprandial response.

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“…Peptides from the macroalga Palmaria palmata were purified and exhibited dipeptidyl peptidase IV inhibitory effects, suggesting their potential as functional food ingredients in the prevention and management of type 2 diabetes (Harnedy et al, 2015). In particular, due to the close relationship between oxidative stress and diabetes (Sottero et al, 2015), one of the effective strategies in the prevention of diabetes is to control oxidative stress. This prompts researchers to search for bioactive peptides with dual functions: antioxidant and antidiabetic functionssuch as yeast hydrolysates (Jung et al, 2011), milk protein-derived hydrolysates and peptides (Nongonierma & FitzGerald, 2013), and peptides from egg-yolk protein hydrolysates (Zambrowicz et al, 2015).…”

Section: Introductionmentioning

confidence: 99%

Antioxidant and hypoglycaemic effects of tilapia skin collagen peptide in mice

Zhang

Chen

Jiang³

et al. 2016

Int J of Food Sci Tech

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Summary In this study, tilapia collagen peptide (TCP) was prepared by alcalase hydrolysis of tilapia skin, and the antioxidant and hypoglycaemic effects of TCP were investigated. The results showed that TCP possessed DPPH and ABTS+ free radicals‐scavenging activities. In diabetic mice in which diabetes was induced by injection of alloxan (50 mg kg−1 bw), high‐dose TCP (1.7 g kg−1 bw) and the drug metformin (1.0 g kg−1 bw) were found to reduce 31.8% and 30.3% of blood glucose levels in 25 days, respectively. Moreover, in diabetic mice receiving high‐dose TCP, antioxidant enzymes SOD and CAT were increased by 23% and 59.2%, respectively, and MDA was decreased by 39.1%. Comparing the treated high‐dose TCP group with the metformin group, there were similar SOD (61.5 U mg−1 vs. 60.2 U mg−1) and MDA (1.4 nmol mg−1 vs. 1.3 nmol mg−1), but more (~7%) CAT (359.8 U g−1 vs. 336.1 U g−1). Together, the present data, for the first time, demonstrated that TCP possessed hypoglycaemic effects in mice.

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Postprandial Dysmetabolism and Oxidative Stress in Type 2 Diabetes: Pathogenetic Mechanisms and Therapeutic Strategies

Cited by 49 publications

References 502 publications

Influence of Cardiometabolic Risk Factors on Platelet Function

Influence of Cardiometabolic Risk Factors on Platelet Function

Human Postprandial Nutrient Metabolism and Low-Grade Inflammation: A Narrative Review

Antioxidant and hypoglycaemic effects of tilapia skin collagen peptide in mice

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