Changes in the IGF-1 and TNF-α synthesis pathways before and after three-month reduction diet with low glicemic index in women with PCOS

Objectives: An increase in IGF-I and TNF-α may be a cardioprotective effect. To examine the relationships between IGF-I and TNF-α and test the anthropometric and biochemical parameters before and after a low-glycemic index reduction diet using a correlation matrix. Material and methods: Twenty-two women diagnosed with PCOS according to Rotterdam’s criteria were eligible for this study, which analysed the results before and after a three months dietary intervention. Body composition measurements were determined by bioimpedance and performed twice, along with the labelling of lipid, carbohydrate and hormonal profiles. IGF-I and TNF-α were also determined in the serum. Results: Before dietary intervention, a significant correlation was observed. A correlation was also noted between the increase in TNF-α and DHEA-SO4, FSH, glucose level and total cholesterol. The increase in IGF-I was not related to anth­ropometric measurements: however, its concentration was observed to be related to the level of SHBG and HDL. After dietary intervention, the correlation between TNF-α and muscle mass percentage was confirmed, as was the correlation between WHR and fasting blood glucose levels. A significant negative correlation was observed between extracellular water, provided in litres, and SHBG level. Conclusions: One important role of IGF-I in PCOS pathogenesis is the stimulation of increased synthesis of SHBG and HDL. The increased level of IGF-I after the reduction diet had a cardioprotective effect. TNF-α inhibits FSH synthesis, preventing the growth of numerous follicles. Its synthesis is also related to DHEA-SO4. After three-month reduction diet does not significantly reduce TNF-α

Analysis for genotyping Duffy blood group in inhabitants of Sudan, the Fourth Cataract of the Nile

<p>Abstract</p> <p>Background</p> <p>Genetic polymophisms of the Duffy antigen receptor for the chemokines (DARC) gene successfully protected against blood stage infection by <it>Plasmodium vivax </it>infection. The Fy (a-, b-) phenotype is predominant among African populations, particularly those originating from West Africa, and it is rare among non-African populations. The aim of this study was to analyse the frequency of four Duffy blood groups based on SNPs (T-33C, G125A, G298A and C5411T) in two local tribes of Sudanese Arabs, the <it>Shagia </it>and <it>Manasir</it>, which are both from the region of the Fourth Nile cataract in Sudan.</p> <p>Methods</p> <p>An analysis of polymorphisms was performed on 217 individuals (126 representatives of the <it>Shagia </it>tribe and 91 of the <it>Manasir)</it>. Real-time PCR and TaqMan Genotyping Assays were used to study the prevalence of alleles and genotypes.</p> <p>Results</p> <p>The analysis of allelic and genotype frequency in the T-33C polymorphisms demonstrated a significant dominance of the <it>C </it>allele and <it>CC </it>genotype (OR = 0.53 [0.32-0.88]; p = 0.02) in both tribes. The G125A polymorphism is associated with phenotype Fy(a-, b-) and was identified in 83% of <it>Shagia </it>and 77% of <it>Manasir</it>. With regard to G298A polymorphisms, the genotype frequencies were different between the tribes (p = 0,002) and no single <it>AA </it>homozygote was found. Based on four SNPs examined, 20 combinations of genotypes for the <it>Shagia </it>and <it>Manasir </it>tribes were determined. The genotype <it>CC/AA/GG/CT </it>occurred most often in <it>Shagia </it>tribe (45.9%) but was rare in the <it>Manasir </it>tribe (6.6%) (p < 0.001 <it>Shagia </it>versus <it>Manasir</it>). The <it>FY*A^ES</it>allele was identified in both analysed tribes. The presence of individuals with the <it>FY*A/FY*A </it>genotype was demonstrated only in the <it>Shagia </it>tribe.</p> <p>Conclusion</p> <p>This is probably the first report showing genotypically Duffy-negative people who carry both <it>FY*B^ES</it>and <it>FY*A^ES</it>. The identification of the <it>FY*A^ES</it>allele in both tribes may be due to admixture of the non-African genetic background. Taken as a whole, allele and genotype frequencies between the <it>Shagia </it>and the <it>Manasir </it>were statistically different. However, the presence of individuals with the <it>FY*A/FY*A </it>genotype was demonstrated only in the <it>Shagia </it>tribe.</p

Smoking Affects the Post-Stroke Inflammatory Response of Lipid Mediators in a Gender-Related Manner

The main goal of our study was to determine the effect of cigarette smoking on selected derivatives of arachidonic acid, linoleic acid, DHA, and EPA, which may be markers of post-stroke inflammation. The eicosanoid profile was compared in both smoking and non-smoking patients, without division and with division into gender. In the group of non-smokers, we observed higher levels of the linolenic acid derivative (LA) 9S HODE (p ≤ 0.05) than in smokers. However, after dividing the results by sex, it turned out that the level of this derivative was higher in non-smoking women compared to smoking women (p ≤ 0.01) and did not differentiate the group of men. Similarly, the level of the arachidonic acid metabolite LTX A4 (p ≤ 0.05) differed only in the group of women. In this group, we also observed a decreased level of 15S HETE in smoking women, but it was statistically insignificant (p ≤ 0.08). On the other hand, the level of this derivative was statistically significantly higher in the group of non-smoking women compared to male non-smokers. The group of men was differentiated by two compounds: TXB2 and NPD1. Male smokers had an almost two-fold elevation of TXB2 (p ≤ 0.01) compared with non-smokers, and in this group, we also observed an increased level of NPD1 compared with male non-smokers. On the other hand, when comparing female non-smokers and male non-smokers, in addition to the difference in 15S HETE levels, we also observed elevated levels of TXB2 in the group of non-smokers. We also analyzed a number of statistically significant correlations between the analyzed groups. Generally, men and women smokers showed a much smaller amount of statistically significant correlations than non-smokers. We believe that this is related to the varying degrees of inflammation associated with acute ischemic stroke and post-stroke response. On the one hand, tobacco smoke inhibits the activity of enzymes responsible for the conversion of fatty acids, but on the other hand, it can cause the failure of the inflammatory system, which is also the body’s defense mechanism. Smoking cigarettes is a factor that increases oxidative stress even before the occurrence of a stroke incident, and at the same time accelerates it and inhibits post-stroke repair mechanisms. This study highlights the effect of smoking on inflammation in both genders mediated by lipid mediators, which makes smoking cessation undeniable

The Role of Thromboxane in the Course and Treatment of Ischemic Stroke: Review

Cardiovascular diseases are currently among the leading causes of morbidity and mortality in many developed countries. They are distinguished by chronic and latent development, a course with stages of worsening of symptoms and a period of improvement, and a constant potential threat to life. One of the most important disorders in cardiovascular disease is ischemic stroke. The causes of ischemic stroke can be divided into non-modifiable and modifiable causes. One treatment modality from a neurological point of view is acetylsalicylic acid (ASA), which blocks cyclooxygenase and, thus, thromboxane synthesis. The legitimacy of its administration does not raise any doubts in the case of the acute phase of stroke in patients in whom thrombolytic treatment cannot be initiated. The measurement of thromboxane B2 (TxB2) in serum (a stable metabolic product of TxA2) is the only test that measures the effect of aspirin on the activity of COX-1 in platelets. Measurement of thromboxane B2 may be a potential biomarker of vascular disease risk in patients treated with aspirin. The aim of this study is to present the role of thromboxane B2 in ischemic stroke and to present effective therapies for the treatment of ischemic stroke. Scientific articles from the PubMed database were used for the work, which were selected on the basis of a search for “thromboxane and stroke”. Subsequently, a restriction was introduced for works older than 10 years, those concerning animals, and those without full text access. Ultimately, 58 articles were selected. It was shown that a high concentration of TXB2 may be a risk factor for ischemic stroke or ischemic heart disease. However, there is insufficient evidence to suggest that thromboxane could be used in clinical practice as a marker of ischemic stroke. The inclusion of ASA in the prevention of stroke has a beneficial effect that is associated with the effect on thromboxane. However, its insufficient power in 25% or even 50% of the population should be taken into account. An alternative and/or additional therapy could be a selective antagonist of the thromboxane receptor. Thromboxane A2 production is inhibited by estrogen; therefore, the risk of CVD after the menopause and among men is higher. More research is needed in this area

High Levels of Thromboxane (TX) Are Associated with the Sex-Dependent Non-Dipping Phenomenon in Ischemic Stroke Patients

Background: Inflammation and high blood pressure (nondipping profile) during the rest/sleep period have been associated with an effect on the incidence of cardiovascular disorders and a more severe course in the ischemic cerebrovascular event. There are no available data on the relationship between dipping status and the pro-inflammatory metabolites of arachidonic acid (AA); therefore, we undertook a study to investigate the influence of thromboxane on the incidence of nondipping among patients after stroke. Methods: Sixty-two patients with ischemic stroke (including 34 women and 28 men) were tested for the involvement of thromboxane in the nondipping phenomenon. Subjects were analyzed for the presence of the physiological phenomenon of dipping (DIP group) versus its absence&mdash;nondipping (NDIP group). Thromboxane (TX) measurements were performed using liquid chromatography, and blood pressure was measured 24 h a day in all subjects. Results: The analysis of the thromboxane level in the plasma of patients after ischemic stroke showed significant differences in terms of sex (p = 0.0004). Among women in both groups, the concentration of TX was high, while similar levels were observed in the group of men from the NDIP group. However, when comparing men in the DIP and NDIP groups, a lower TX level was noticeable in the DIP group. Conclusions: A higher level of TX may be associated with a disturbance of the physiological phenomenon of DIP in men and women. However, in our opinion, TX is not the main determinant of the DIP phenomenon and, at the same time, other pro-inflammatory factors may also be involved in the occurrence of this singularity

Decrease in the level of nervonic acid and increased gamma linolenic acid in the plasma of women with polycystic ovary syndrome after a three-month low-glycaemic index and caloric reduction diet

The aetiology of polycystic ovary syndrome (PCOS) remains uncertain and thus dedicated studies are still of much importance. Patients in this group are at high risk for metabolic syndrome, diabetes and ischemic heart disease. Our goal was to use a dietary intervention, facilitating the regression of the disease, through the observation of lipid and hormonal profiles, carbohydrate metabolic parameters and metabolomics of plasma fatty acids. There were 39 Caucasian women with PCOS aged 26.76 ±5.08 that qualified for this study. Fatty acid profiles were investigated using gas chromatography. The results of plasma fatty acids were compared with the initial results and the control group. A three-month caloric reduction diet with low glycemic index (GI) reduces the level of nervonic acid and is a great alternative in PCOS therapy. The introduction of rapeseed oil and olive oil to the lowered GI reduction diet caused the increase in the ratio of average length chain fatty acids (C10:0, C14:0) and the enhancement of synthesis pathways for pentadecanoic acid (C15:0) and gamma-linolenic acid (GLA, C18:3n-6), but did not inhibit the synthesis of the derivatives of arachidic acid (C20:0). Additionally, a decrease in the level of nervonic acid (C24:1) was observed. Biochemical analysis of blood showed the improvement of plasma lipid fractions, but a significant reduction of androgen levels was not observed

Fatty Acid Levels and Their Inflammatory Metabolites Are Associated with the Nondipping Status and Risk of Obstructive Sleep Apnea Syndrome in Stroke Patients

Background: This paper discusses the role of inflammation in the pathogenesis of nondipping blood pressure and its role in the pathogenesis of obstructive sleep apnea syndrome. The aim of the study was to assess the impact of free fatty acids (FAs) and their inflammatory metabolites on the nondipping phenomenon and the risk of sleep apnea in stroke patients. Methods: Sixty-four ischemic stroke patients were included in the prospective study. Group I consisted of 33 patients with a preserved physiological dipping effect (DIP), while group II included 31 patients with the nondipping phenomenon (NDIP). All subjects had FA gas chromatography and inflammatory metabolite measurements performed with the use of liquid chromatography, their 24 h blood pressure was recorded, and they were assessed with the Epworth sleepiness scale (ESS). Results: In the nondipping group a higher level of C16:0 palmitic acid was observed, while lower levels were observed in regard to C20:0 arachidic acid, C22:0 behenic acid and C24:1 nervonic acid. A decreased leukotriene B4 level was recorded in the nondipping group. None of the FAs and derivatives correlated with the ESS scale in the group of patients after stroke. Correlations were observed after dividing into the DIP and NDIP groups. In the DIP group, a higher score of ESS was correlated with numerous FAs and derivatives. Inflammation of a lower degree and a higher level of anti-inflammatory mediators from EPA and DHA acids favored the occurrence of the DIP. A high level of C18: 3n6 gamma linoleic acid indicating advanced inflammation, intensified the NDIP effect. Conclusions: We demonstrated potential novel associations between the FA levels and eicosanoids in the pathogenesis of the nondipping phenomenon. There are common connections between fatty acids, their metabolites, inflammation, obstructive sleep apnea syndrome and nondipping in stroke patients

Involvement of Proinflammatory Arachidonic Acid (ARA) Derivatives in Crohn&rsquo;s Disease (CD) and Ulcerative Colitis (UC)

Recently, an increase in the incidence of inflammatory bowel disease (IBD) has been observed, especially among children and adolescents. Currently, few studies focus on the differentiation of inflammation in IBD subunits, i.e., Crohn&rsquo;s Disease (CD) and Ulcerative Colitis (UC). The aim of this study was to compare the concentrations of proinflammatory mediators of arachidonic acid (ARA) and linoleic acid (LA) in patients with CD (n = 34) and UC (n = 30), in order to identify differences in inflammation in both diseases and within the same entity, according to disease activity. Sixty-four adolescents with a mean age of 13.76 &plusmn; 2.69 and 14.15 &plusmn; 3.31, for CD and UC, respectively, were enrolled in the study. Biochemical analysis of ARA and LA derivatives was performed using a liquid chromatography. A trend was observed in the concentration of 15S-HETE (hydroxyeicosatetraenoic acids) in CD relative to UC. The active phase of both diseases showed a higher 15S-HETE concentration in active CD relative to active UC. Comparing patients with CD with active and inactive disease showed a trend of increased levels of thromboxane B2, leukotriene B4 and 9S-HODE (hydroxyoctadecadienoic acid) in the active versus the inactive disease. We also observed statistically significantly higher levels of 12S-HETE in inactive CD relative to active CD. In the UC group, on the other hand, statistically significantly higher levels of prostaglandin E2 and 16RS-HETE were observed in active UC relative to inactive UC. Moreover, significantly higher concentrations of LTX A4 5S, 6R were observed in inactive UC relative to the active phase. In conclusion, the present study indicated the activity of the 15-LOX pathway in CD. Further studies involving lipid mediators in patients with IBD may contribute to the development of new therapies for the treatment of IBD. The identification of differences in the course of inflammation may help to target therapy in CD and UC, and perhaps allow the introduction of an additional diagnostic marker between the two main IBD subtypes

Involvement of Proinflammatory Arachidonic Acid (ARA) Derivatives in Crohn’s Disease (CD) and Ulcerative Colitis (UC)

Recently, an increase in the incidence of inflammatory bowel disease (IBD) has been observed, especially among children and adolescents. Currently, few studies focus on the differentiation of inflammation in IBD subunits, i.e., Crohn’s Disease (CD) and Ulcerative Colitis (UC). The aim of this study was to compare the concentrations of proinflammatory mediators of arachidonic acid (ARA) and linoleic acid (LA) in patients with CD (n = 34) and UC (n = 30), in order to identify differences in inflammation in both diseases and within the same entity, according to disease activity. Sixty-four adolescents with a mean age of 13.76 ± 2.69 and 14.15 ± 3.31, for CD and UC, respectively, were enrolled in the study. Biochemical analysis of ARA and LA derivatives was performed using a liquid chromatography. A trend was observed in the concentration of 15S-HETE (hydroxyeicosatetraenoic acids) in CD relative to UC. The active phase of both diseases showed a higher 15S-HETE concentration in active CD relative to active UC. Comparing patients with CD with active and inactive disease showed a trend of increased levels of thromboxane B2, leukotriene B4 and 9S-HODE (hydroxyoctadecadienoic acid) in the active versus the inactive disease. We also observed statistically significantly higher levels of 12S-HETE in inactive CD relative to active CD. In the UC group, on the other hand, statistically significantly higher levels of prostaglandin E2 and 16RS-HETE were observed in active UC relative to inactive UC. Moreover, significantly higher concentrations of LTX A4 5S, 6R were observed in inactive UC relative to the active phase. In conclusion, the present study indicated the activity of the 15-LOX pathway in CD. Further studies involving lipid mediators in patients with IBD may contribute to the development of new therapies for the treatment of IBD. The identification of differences in the course of inflammation may help to target therapy in CD and UC, and perhaps allow the introduction of an additional diagnostic marker between the two main IBD subtypes