Does valproate therapy in epileptic patients contribute to changing atherosclerosis risk factors? The role of lipids and free fatty acids

2016 ◽  
Vol 68 (6) ◽  
pp. 1339-1344 ◽  
Author(s):  
Elżbieta Płonka-Półtorak ◽  
Paweł Zagrodzki ◽  
Jadwiga Kryczyk-Kozioł ◽  
Tuomas Westermarck ◽  
Pekka Kaipainen ◽  
...  
Keyword(s):  
Risk Factors ◽  
Fatty Acids ◽  
Free Fatty Acids ◽  
Atherosclerosis Risk ◽  
Epileptic Patients ◽  
Atherosclerosis Risk Factors

Alcohol intake impairs glucose counterregulation during acute insulin-induced hypoglycemia in IDDM patients. Evidence for a critical role of free fatty acids

Diabetes ◽  
1993 ◽  
Vol 42 (11) ◽  
pp. 1626-1634 ◽  
Author(s):  
A. Avogaro ◽  
P. Beltramello ◽  
L. Gnudi ◽  
A. Maran ◽  
A. Valerio ◽  
...  
Keyword(s):  
Fatty Acids ◽  
Free Fatty Acids ◽  
Alcohol Intake ◽  
Critical Role

Atherosclerosis risk factors in young patients formerly treated for idiopathic nephrotic syndrome

2008 ◽  
Vol 24 (3) ◽  
pp. 549-554 ◽  
Author(s):  
Maria H. Kniażewska ◽  
Anna K. Obuchowicz ◽  
Tomasz Wielkoszyński ◽  
Joanna Żmudzińska-Kitczak ◽  
Katarzyna Urban ◽  
...  
Keyword(s):  
Risk Factors ◽  
Nephrotic Syndrome ◽  
Idiopathic Nephrotic Syndrome ◽  
Young Patients ◽  
Atherosclerosis Risk ◽  
Atherosclerosis Risk Factors

Wybrane czynniki ryzyka chorób układu sercowo-naczyniowego związane z miażdżycą tętnic jako problem zdrowotny wśród młodzieży ponadgimnazjalnej

2018 ◽  
Vol 21 (1A) ◽  
Author(s):  
Zdzisława Chmiel ◽  
Grażyna Hejda ◽  
Monika Binkowska-Bury
Keyword(s):  
Physical Activity ◽  
Risk Factors ◽  
Risk Factor ◽  
Cardiovascular Diseases ◽  
World Health ◽  
Study Group ◽  
Atherosclerosis Risk ◽  
Atherosclerosis Risk Factors ◽  
Atherosclerosis Risk Factor ◽  
Recommended Physical Activity

Introduction. A World Health Organization (WHO) conference on a “second wave” epidemic of cardiovascular diseases, directly linked to arterial sclerosis (AS), predicts that in 2020 cardiovascular diseases will most likely be the leading cause of death in the world. The development of AS begins in youth and progresses with age. It’s intensity depends on the risk factors involved, such as: smoking, hypertension, obesity and fat and sugar disorders in the body. Aim. The aim of this study was to establish the risk factors of cardiovascular diseases and their existence, among the youth of the upper gymnasium school. Material and methods. The research was conducted using 511 volunteer students from upper and lower gymnasium schools, between 16-19 years of age. Our research methods included: a diagnostic questionnaire, the measurement of blood pressure (BP) and anthropometric measurements. In the statistical study, we used chi-square independence testing, the V-Kramer test and the tau-b Kendall test; the level of changes α = 0.05 – was used. Results. Over a half of the study group (52.5%) was characterised with the lack of recommended physical activity, much more common in girls than boys (p = 0.000), just like smoking (p = 0.009) which was declared by 39.7% of the interviewed youth. In turn, a heightened value of systolic and diastolic pressure occurred more often in boys (19.6%) than in girls (12.1%); (p = 0.000 vs. p = 0.003). Excessive body mass was noted in 15.7% of the respondents, also more often in boys than in girls (p = 0.02), and abdominal obesity occurred in 10.2% of the respondents, with no significant differences between the sexes. 42.3% of the respondents showed one, 29.9% showed two and 18.8% showed three atherosclerosis risk factors. 9.0% of the study group showed 4 and more such risk factors. Accumulation of atherosclerosis risk factors occurred significantly more often in girls than in boys (p = 0.002). Conclusions. In all the respondents at least one atherosclerosis risk factor was found, and in over half of the study group, more frequently in girls than in boys, an accumulation of two or more risk factors was observed. Lack of recommended physical activity was the most frequent atherosclerosis risk factor occurring in the youth.

scholarly journals Free Fatty acids receptors (FFAR2 and FFAR3) control cell proliferation by regulating cellular glucose uptake

2019 ◽  
Author(s):  
Mohammad Aziz ◽  
Saeed Al Mahri ◽  
Amal Alghamdi ◽  
Maaged AlAkiel ◽  
Monira Al Aujan ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Fatty Acids ◽  
Cell Proliferation ◽  
Fatty Acid ◽  
Free Fatty Acid ◽  
Free Fatty Acids ◽  
Glucose Uptake ◽  
Microarray Data ◽  
Free Fatty Acid Receptors

Abstract Background Colorectal cancer is a worldwide problem which has been associated with changes in diet and lifestyle pattern. As a result of colonic fermentation of dietary fibres, short chain free fatty acids are generated which activate Free Fatty Acid Receptors 2 and 3 (FFAR2 and FFAR3). FFAR2 and FFAR3 genes are abundantly expressed in colonic epithelium and play an important role in the metabolic homeostasis of colonic epithelial cells. Earlier studies point to the involvement of FFAR2 in colorectal carcinogenesis. Methods Transcriptome analysis console was used to analyse microarray data from patients and cell lines. We employed shRNA mediated down regulation of FFAR2 and FFAR3 genes which was assessed using qRT-PCR. Assays for glucose uptake and cAMP generation was done along with immunofluorescence studies. For measuring cell proliferation, we employed real time electrical impedance based assay available from xCelligence. Results Microarray data analysis of colorectal cancer patient samples showed a significant down regulation of FFAR2 gene expression. This prompted us to study the FFAR2 in colorectal cancer. Since, FFAR3 shares significant structural and functional homology with FFAR2, we knocked down both these receptors in colorectal cancer cell line HCT 116. These modified cell lines exhibited higher proliferation rate and were found to have increased glucose uptake as well as increased level of GLUT1. Since, FFAR2 and FFAR3 signal through G protein subunit (Gαi), knockdown of these receptors was associated with increased cAMP. Inhibition of PKA did not alter the growth and proliferation of these cells indicating a mechanism independent of cAMP/PKA pathway. Conclusion: Our results suggest role of FFAR2/FFAR3 genes in increased proliferation of colon cancer cells via enhanced glucose uptake and exclude the role of protein kinase A mediated cAMP signalling. Alternate pathways could be involved that would ultimately result in increased cell proliferation as a result of down regulated FFAR2/FFAR3 genes. This study paves the way to understand the mechanism of action of short chain free fatty acid receptors in colorectal cancer.

Abstract 061: Long-chain monounsaturated fatty acids and congestive heart failure incidence: the Atherosclerosis Risk in Communities Study

Circulation ◽  
2012 ◽  
Vol 125 (suppl_10) ◽  
Author(s):  
Fumiaki Imamura ◽  
Rozenn N Lemaitre ◽  
Lyn M Steffen ◽  
Aaron R Folsom ◽  
David S Siscovick ◽  
...  
Keyword(s):  
Risk Factors ◽  
Heart Failure ◽  
Older Adults ◽  
Fatty Acids ◽  
Congestive Heart Failure ◽  
Plasma Phospholipid ◽  
Atherosclerosis Risk In Communities ◽  
Atherosclerosis Risk ◽  
Middle Aged Adults ◽  
Long Chain

Background: Animal experiments in 1970s demonstrated direct cardiotoxicity of long-chain monounsaturated fatty acid (LCMUFA, 22:1 and 24:1 fatty acids) consumption. We recently found plasma phospholipid 22:1 and 24:1 to be associated with 34% and 75% higher risk (quintiles 5 vs. 1), respectively, of congestive heart failure (CHF) among older adults in the Cardiovascular Health Study. We wished to validate these results in a second independent cohort of middle-aged adults. Methods: We evaluated 3,577 adults free of CHF at baseline (age=54.1±5.8) in the Minnesota subcohort of the Atherosclerosis Risk in Communities Study (ARIC) in whom plasma phospholipid LCMUFA were measured. Incident CHF was ascertained from 1988 to 2008 by annual phone contacts, hospitalization discharge codes, and death certificates. Using multivariate Cox models, we evaluated prospective association of each LCMUFA with incident CHF, and potential mediation via CHF risk factors, including ECG left ventricular hypertrophy, and incident coronary heart disease (CHD). As a negative control, we also evaluated incident stroke, given its many shared risk factors for CHF but no link to potentially direct cardiotoxicity. Results: Mean±SD plasma phospholipid levels (% of total fatty acids) of 22:1 and 24:1 were 0.01±0.03 and 0.58±0.17. Over the 64,438 person-years of follow-up, 330 CHF events occurred. After multivariable adjustment, higher levels of 22:1 and 24:1 were associated with higher risk of CHF (Figure). Hazard ratios (95%CI) for quintiles 5 vs. 1 of 22:1 and 24:1 levels were 1.57 (1.11–2.23) and 1.92 (1.22–3.03) (p trend=0.03 and 0.002), respectively. These associations were only partly attenuated by potential mediators, including incident CHD. Neither LCMUFA was associated with incident stroke (not shown). Conclusions: Higher 22:1 and 24:1 LCMUFA levels were associated with CHF risk in middle-aged adults, consistent with our prior findings in older adults. These findings support the possibility of clinical cardiotoxicity of LCMUFA in humans.

Sign in / Sign up

Export Citation Format

Share Document