Serum resistin in acute myocardial infarction patients with and without diabetes mellitus

Korah, Tarek E.; Ibrahim, Hussein; Badr, Eman; El-Shafie, Maathir Kamel

doi:10.1136/pgmj.2010.113571

Cited by 26 publications

(19 citation statements)

References 35 publications

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“…The up-regulation and production of resistin represent an intrinsic response against myocardial injury. Our results were consistent with recent findings showing that resistin levels were increased in patients with acute MI [29]. Given the large infarction size in the present study, either sustained cytokine up-regulation or a second wave of cytokine up-regulation .…”

Section: Discussionsupporting

confidence: 94%

Sitagliptin decreases ventricular arrhythmias by attenuated glucose-dependent insulinotropic polypeptide (GIP)-dependent resistin signalling in infarcted rats

2016

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SynopsisMyocardial infarction (MI) was associated with insulin resistance, in which resistin acts as a critical mediator. We aimed to determine whether sitagliptin, a dipeptidyl peptidase-4 (DPP-4) inhibitor, can attenuate arrhythmias by regulating resistin-dependent nerve growth factor (NGF) expression in postinfarcted rats. Normoglycaemic male Wistar rats after ligating coronary artery were randomized to either vehicle or sitagliptin for 4 weeks starting 24 h after operation. Post-infarction was associated with increased myocardial noradrenaline [norepinephrine (NE)] levels and sympathetic hyperinnervation. Compared with vehicle, sympathetic innervation was blunted after administering sitagliptin, as assessed by immunofluorescent analysis of tyrosine hydroxylase, growth-associated factor 43 and neurofilament and western blotting and real-time quantitative RT-PCR of NGF. Arrhythmic scores in the sitagliptintreated infarcted rats were significantly lower than those in vehicle. Furthermore, sitagliptin was associated with reduced resistin expression and increased Akt activity. Ex vivo studies showed that glucose-dependent insulinotropic polypeptide (GIP) infusion, but not glucagon-like peptide-1 (GLP-1), produced similar reduction in resistin levels to sitagliptin in postinfarcted rats. Furthermore, the attenuated effects of sitagliptin on NGF levels can be reversed by wortmannin (a phosphatidylinositol 3-kinase antagonist) and exogenous resistin infusion. Sitagliptin protects ventricular arrhythmias by attenuating sympathetic innervation in the non-diabetic infarcted rats. Sitagliptin attenuated resistin expression via the GIP-dependent pathway, which inhibited sympathetic innervation through a signalling pathway involving phosphatidylinositol 3-kinase (PI3K) and Akt protein.

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Section: Discussionsupporting

confidence: 94%

Sitagliptin decreases ventricular arrhythmias by attenuated glucose-dependent insulinotropic polypeptide (GIP)-dependent resistin signalling in infarcted rats

2016

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“…Significantly elevated serum resistin levels in patients with type 2 diabetes during acute STEMI (acute ST segment elevation myocardial infarction) has been described compared to patients with acute STEMI but without type 2 diabetes, or to a control group [101]. This suggests that resistin may be involved in the pathogenesis of metabolic syndrome.…”

Section: Resistinmentioning

confidence: 84%

Biochemical markers of psoriasis as a metabolic disease

Gerkowicz

Pietrzak

Szepietowski

et al. 2012

Folia Histochem Cytobiol.

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Psoriasis is a chronic immune mediated inflammatory skin disease with a population prevalence of 2-3%. In recent years, psoriasis has been recognized as a systemic disease associated with metabolic syndrome or its components such as: obesity, insulin resistance, hypertension and atherogenic dyslipidemia. Many bioactive substances have appeared to be related to metabolic syndrome. Based on current literature, we here discuss the possible role of adiponectin, leptin, ghrelin, resistin, inflammatory cytokines, plasminogen activator inhibitor 1, uric acid, C-reactive protein and lipid abnormalities in psoriasis and in metabolic syndrome.

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“…Moreover, markedly different populations have been used in different studies. For example, the present study is based on a sample of the general population, whereas other studies have focused on patients with metabolic syndrome 35) or myocardial infarction 36) . Some experimental studies have documented an increase in the serum resistin concentration during the postprandial period 37) , a phenomenon that may be explained by the increase in triglycerides following food intake, consistent with the positive association between resistin and triglycerides observed in this study.…”

Section: Resultsmentioning

confidence: 99%

Relationships between Serum Resistin and Fat Intake, Serum Lipid Concentrations and Adiposity in the General Population

León

González

Hernández

et al. 2014

J Atheroscler Thromb

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Aims:The serum resistin level is associated with the incidence of ischemic heart disease in the general population. We analyzed the associations between serum resistin and fat intake, serum lipid concentrations and adiposity in the general population. Methods: A cross-sectional study of 6,637 randomly recruited adults was conducted. The resistin levels were measured in thawed aliquots of serum using an enzyme immunoanalysis technique. Conclusions:In the general population, the serum resistin level is associated with fat intake: positively with saturated fat intake and inversely with monounsaturated fat intake. As a consequence, the resistin level is also inversely associated with adherence to the Mediterranean diet. In addition, the resistin level is inversely associated with the serum cholesterol level and adiposity.

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Serum resistin in acute myocardial infarction patients with and without diabetes mellitus

Cited by 26 publications

References 35 publications

Sitagliptin decreases ventricular arrhythmias by attenuated glucose-dependent insulinotropic polypeptide (GIP)-dependent resistin signalling in infarcted rats

Sitagliptin decreases ventricular arrhythmias by attenuated glucose-dependent insulinotropic polypeptide (GIP)-dependent resistin signalling in infarcted rats

Biochemical markers of psoriasis as a metabolic disease

Relationships between Serum Resistin and Fat Intake, Serum Lipid Concentrations and Adiposity in the General Population

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