Association of adipokines and inflammatory markers with lipid control in type 2 diabetes

Kapłon‐Cieślicka, Agnieszka; Postuła, Marek; Rosiak, Marek; Peller, Michał; Kondracka, Agnieszka; Serafin, Agnieszka; Trzepla, Ewa; Opolski, Grzegorz; Filipiak‬, Krzysztof J.

doi:10.20452/pamw.2880

Cited by 22 publications

(21 citation statements)

References 7 publications

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“…Our findings are consistent with the published data obtained from the studies on larger population. Similar results were also noted in the study in patients with type 2 diabetes [5]. However the analysis performed by Borges MC et al [6] indicates the limited clinical benefits of this correlation.…”

Section: Discussionsupporting

confidence: 84%

Cardioprotective properties of leptin in patients with excessive body mass

et al. 2020

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Background Adipose tissue is producing adipokines that play different roles in the pathophysiology of cardiovascular disease. Aims The study aimed to assess the role of selected biomarkers in hypertensive patients with overweight and obesity compared with those with normal body-mass index (BMI). Methods A total of 62 patients with BMI < 25 kg/m 2 (median age 54 (46-58) yrs., 57% males) and 51 with BMI ≥ 25 kg/m 2 (median age 53 (48-59) yrs., 37% males) were enrolled. Biochemical parameters, leptin, adiponectin, and resistin; asymmetric dimethylarginine; interleukin 6; and N-terminal propeptide of type III procollagen, were assessed in plasma. The evaluation of hemodynamic parameters was performed using SphygmoCor 9.0 tonometer. Echocardiography was performed using AlokaAlpha 10 Premier device. Results Overweight and obese patients had significantly higher concentration of leptin (34 vs 18 ng/ml; p = 0.03), ADMA (0.43 vs 0.38 μmol/l, p = 0.04), and lower concentration of adiponectin (5.3 vs 7 μg/ml, p = 0.01). The only significant difference in tonometry analysis was higher aortic pulse pressure (mmHg) in patients with BMI ≥ 25 kg/m 2 group (34 vs 30; p = 0.03). These patients had also significantly lower peak systolic velocity and early diastolic velocity in tissue Doppler imaging of the right ventricle free wall at the level of the tricuspid annulus compared with controls (p = 0.02 and p = 0.001, respectively). The level of leptin is correlated negatively with the left ventricular mass index (LVMI) (R Spearman = − 0.5; p = 0.002) and PWV (R = − 0.4; p = 0.01) and ADMA with total and LDL cholesterol (R = − 0.42; p = 0.008), and adiponectin is correlated positively with HDL cholesterol (R = 0.67; p = 0.0001). Conclusions Leptin concentrations were inversely proportional to LVMI and PWV in patients with BMI < 25 kg/m 2 . Trial registration Clinicaltrials.gov study ID: NCT04175080.

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Section: Discussionsupporting

confidence: 84%

Cardioprotective properties of leptin in patients with excessive body mass

et al. 2020

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“…A few adipokines have been suggested to participate in the development of systemic low-grade inflammation, IR and metabolic syndrome [9]. Moreover, disturbances in adipokine profiles have also been associated with inadequate lipid control [10]. Since dysregulation of adipokine secretion plays an important role in the pathogenesis of DM2 and its macrovascular complications, the amelioration of adipokine pattern may improve prognosis in patients with DM2.…”

Section: Introductionmentioning

confidence: 99%

Treatment with high-dose n-3 PUFAs has no effect on platelet function, coagulation, metabolic status or inflammation in patients with atherosclerosis and type 2 diabetes

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Siniarski

et al. 2017

Cardiovasc Diabetol

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BackgroundDespite numerous studies on cardioprotective effects of omega-3 polyunsaturated fatty acids (n-3 PUFAs), there is limited evidence for n-3 PUFA-mediated effects, especially at its higher dose, on cardiovascular risk in patients with type 2 diabetes (DM2) and established atherosclerosis.PurposeTo investigate the effect of daily treatment with a higher dose (2 g) of n-3 PUFAs on platelet function, coagulation parameters, fibrin clot properties, markers of systemic inflammation and metabolic status, in patients with atherosclerotic vascular disease and DM2 who receive optimal medical therapy.MethodsWe conducted a prospective, double-blind, placebo-controlled, randomized, double-center study, in which thrombin generation (plasma thrombogenic potential from automated thrombogram), fibrin clot properties (plasma fibrin clot permeability; lysis time), platelet aggregation (light transmission aggregometry with adenosine diphosphate and arachidonic acid used as agonists), HbA1c, insulin level, lipid profiles, leptin and adiponectin levels, as well as markers of systemic inflammation (i.e., hsCRP, IL-6, TNF-α, ICAM-1, VCAM-1, and myeloperoxidase) were determined at baseline and at 3 months after treatment with 2 g/day of n-3 PUFAs (n = 36) or placebo (n = 38). Moreover, we assessed serum fatty acids of the phospholipid fraction by gas chromatography both at baseline and at the end of the study.ResultsMajority of patients were treated with optimal medical therapy and achieved recommended treatment targets. Despite higher serum levels of eicosapentaenoic acid (EPA) (by 204%; p < 0.001) and docosahexaenoic acid (DHA) (by 62%; p < 0.0001) in n-3 PUFA group at the end of treatment no changes in platelet aggregation, thrombin generation, fibrin clot properties or markers of systemic inflammation were observed. No intergroup differences in the insulin, HbA1c and lipid levels were found at the end of the study. There was no change in adiponectin and leptin in interventional group, however leptin increased in control group (p = 0.01), therefore after study period leptin levels were lower in the interventional group (p = 0.01). Additionally, resolvin D1 did not differ between interventional and control group.ConclusionsIn conclusion, our study demonstrated that in patients with long-standing, well-controlled DM2 and atherosclerotic disease the treatment with a high dose of n-3 PUFAs (namely, 1 g/day of EPA and 1 g/day of DHA for 3 months) does not improve coagulation, metabolic, and inflammatory status when measured with the specified tests.The study was registered in ClinicalTrials.gov; identifier: NCT02178501. Registration date: April 12, 2014Electronic supplementary materialThe online version of this article (doi:10.1186/s12933-017-0523-9) contains supplementary material, which is available to authorized users.

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“…14 These macrophages secrete cytokines such as tumor necrosis factor α (TNF -α), which augments the impairment of the endocrine and paracrine function of adipocytes (eg, secretion of visfatin, leptin, resistin, and others). [15][16][17] This enhances the intensity of inflammatory response, which accelerates the progression of atherosclerosis. The extent of this response (concentration of inflammatory markers such as C -reactive protein or procalcitonin) is a result of interaction between environmental and genetic factors.…”

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confidence: 99%