scholarly journals Recent Topic of Saturated Fatty Acid (SFA) for Atherosclerotic Diseases

2021 ◽  
Vol 2 (1) ◽  
pp. 13-16
Author(s):  
Bando M ◽  
Bando H

Whether saturated fatty acid (SFA) has a clinical influence on atherosclerotic cardiovascular disease (ASCVD) or not has been disputed. Prospective Urban Rural Epidemiology (PURE) study was recently summarized from 21 countries with about 150 thousand data. Dairy intake was negatively correlated with the prevalence of metabolic syndrome and the incidence of diabetes and hypertension. To increase the intake of dairy products would be easy and inexpensive to continue for treatment. Polyunsaturated fatty acid (PUFA) and monounsaturated fatty acid (MUFA) may reduce atherosclerotic diseases with beneficial effects. Clinical evidence of SFA will be hopefully accumulated for practice and research in the future.

Nutrients ◽  
2020 ◽  
Vol 12 (7) ◽  
pp. 1913
Author(s):  
Sanjay Basak ◽  
Asim K. Duttaroy

Conjugated linoleic acid (CLA) is a dietary polyunsaturated fatty acid found in animal fats such as red meat and dairy products [...]


Circulation ◽  
2008 ◽  
Vol 118 (suppl_18) ◽  
Author(s):  
Yumiko Oishi ◽  
Ichiro Manabe ◽  
Kazuyuki Tobe ◽  
Takashi Kadowaki ◽  
Ryozo Nagai

Metabolic syndrome is increasingly recognized as a major risk factor for cardiovascular disease. We have previously shown that a zinc finger transcription factor, Krüppel-like factor 5 (KLF5), plays an important role in cardiovascular diseases, such as atherosclerosis and cardiac hypertrophy. Interestingly, KLF5 is also expressed in metabolic tissues, such as adipose tissue, skeletal muscle and pancreatic β-cells. Moreover, we found that KLF5 is crucial for adipocyte differentiation. Therefore, it is very likely that KLF5 plays multiple roles in development and progression of metabolic syndrome and its cardiovascular and metabolic consequences including atherosclerotic cardiovascular disease. Indeed, KLF5 heterozygous knockout ( KLF5 +/− ) mice were resistant to high-fat-induced obesity and metabolic syndrome, despite consuming more food than wild-type mice. This appears to in part reflect their enhanced energy expenditure. Expression of the genes involved in lipid oxidation and energy uncoupling, including uncoupling protein (UCP) and carnitine-palmitoyl transferase 1b (CPT1b) was upregulated in the soleus muscles of KLF5 +/− mice. KLF5 could be reversibly modified by small ubiquitin-like modifier 1 (SUMO1), after which SUMOylated KLF5 strongly inhibited CPT1b , UCP3 and UCP2 promoter activity. Results of chromatin immunoprecipitation, two-hybrid, and reporter assays showed that under basal conditions SUMOylated KLF5 associated with transcriptionally repressive regulatory complexes containing unliganded PPARδ and corepressors. However, upon agonist stimulation of PPARδ, the deSUMOylating enzyme was recruited and KLF5 was deSUMOylated. The unSUMOylated KLF5 now formed transactivating complexes with liganded PPARδ and CBP. Thus, SUMOylation appears to be a molecular switch affecting function of KLF5 and the transcriptional regulatory programs governing lipid metabolism. Moreover, KLF5 is essential for the PPARδ agonist-dependent transcriptional control. Results of the present study have established KLF5 as a novel key molecule in lipid metabolism and suggest that the posttranscriptional modification of KLF5 is an attractive novel therapeutic target for both metabolic and cardiovascular diseases.


2020 ◽  
Vol 19 (1) ◽  
Author(s):  
João Pedro Ferreira ◽  
Subodh Verma ◽  
David Fitchett ◽  
Anne Pernille Ofstad ◽  
Sabine Lauer ◽  
...  

Abstract Background Patients with type 2 diabetes (T2D) and metabolic syndrome (MetS) are at greater cardiovascular risk than those with T2D without MetS. In the current report we aim to study the characteristics, cardio-renal outcomes and the effect of empagliflozin in patients with MetS enrolled in the EMPA-REG OUTCOME trial. Methods A total of 7020 patients with T2D and atherosclerotic cardiovascular disease were treated with empagliflozin (10 mg or 25 mg) or placebo for a median of 3.1 years. The World Health Organization MetS criteria could be determined for 6985 (99.5%) patients. We assessed the association between baseline MetS and multiple cardio-renal endpoints using Cox regression models, and we studied the change in the individual component over time of the MetS using mixed effect models. Results MetS at baseline was present in 5740 (82%) patients; these were more often white and had more often albuminuria and heart failure, had lower eGFR and HDL-cholesterol, and higher blood pressure, body mass index, waist circumference, and triglycerides. In the placebo group, patients with MetS had a higher risk of all outcomes including cardiovascular death: HR = 1.73 (95% CI 1.01–2.98), heart failure hospitalization: HR = 2.64 (95% CI 1.22, 5.72), and new or worsening nephropathy: HR = 3.11 (95% CI 2.17–4.46). The beneficial effect of empagliflozin was consistent on all cardio-renal outcomes regardless of presence of MetS. Conclusions A large proportion of the EMPA-REG OUTCOME population fulfills the criteria for MetS. Those with MetS had increased risk of adverse cardio-renal outcomes. Compared with placebo, empagliflozin improved cardio-renal outcomes in patients with and without MetS. Trial registration Clinical Trial Registration: URL: https://www.clinicaltrials.gov. Unique identifier: NCT 01131676


2011 ◽  
Vol 93 (5) ◽  
pp. 1136-1141 ◽  
Author(s):  
Pablo Perez-Martinez ◽  
Javier Delgado-Lista ◽  
Antonio Garcia-Rios ◽  
Jane F Ferguson ◽  
Hanne L Gulseth ◽  
...  

2014 ◽  
Vol 2014 ◽  
pp. 1-17 ◽  
Author(s):  
Cidália Dionísio Pereira ◽  
Milton Severo ◽  
João Ricardo Araújo ◽  
João Tiago Guimarães ◽  
Diogo Pestana ◽  
...  

The Metabolic Syndrome increases the risk for atherosclerotic cardiovascular disease and type 2 Diabetes Mellitus. Increased fructose consumption and/or mineral deficiency have been associated with Metabolic Syndrome development. This study aimed to investigate the effects of 8 weeks consumption of a hypersaline sodium-rich naturally sparkling mineral water on 10% fructose-fed Sprague-Dawley rats (Metabolic Syndrome animal model). The ingestion of the mineral water (rich in sodium bicarbonate and with higher potassium, calcium, and magnesium content than the tap water used as control) reduced/prevented not only the fructose-induced increase of heart rate, plasma triacylglycerols, insulin and leptin levels, hepatic catalase activity, and organ weight to body weight ratios (for liver and both kidneys) but also the decrease of hepatic glutathione peroxidase activity and oxidized glutathione content. This mineral-rich water seems to have potential to prevent Metabolic Syndrome induction by fructose. We hypothesize that its regular intake in the context of modern diets, which have a general acidic character interfering with mineral homeostasis and are poor in micronutrients, namely potassium, calcium, and magnesium, could add surplus value and attenuate imbalances, thus contributing to metabolic and redox health and, consequently, decreasing the risk for atherosclerotic cardiovascular disease.


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