Influence of Extended-Release Nicotinic Acid on Nonesterified Fatty Acid Flux in the Metabolic Syndrome With Atherogenic Dyslipidemia

2005 ◽  
Vol 95 (11) ◽  
pp. 1309-1313 ◽  
Author(s):  
Gloria Lena Vega ◽  
Nilo B. Cater ◽  
Shinishi Meguro ◽  
Scott M. Grundy
Keyword(s):  
Metabolic Syndrome ◽  
Fatty Acid ◽  
Nicotinic Acid ◽  
Extended Release ◽  
Atherogenic Dyslipidemia ◽  
Nonesterified Fatty Acid ◽  
The Metabolic Syndrome

scholarly journals Increased Levels of Adipocyte and Epidermal Fatty Acid-Binding Proteins in Acute Lymphoblastic Leukemia Survivors

2021 ◽  
Vol 10 (8) ◽  
pp. 1567
Author(s):  
Katarzyna Konończuk ◽  
Eryk Latoch ◽  
Beata Żelazowska-Rutkowska ◽  
Maryna Krawczuk-Rybak ◽  
Katarzyna Muszyńska-Rosłan
Keyword(s):  
Metabolic Syndrome ◽  
Fatty Acid ◽  
Acute Lymphoblastic Leukemia ◽  
Binding Proteins ◽  
Lymphoblastic Leukemia ◽  
Fatty Acid Binding Proteins ◽  
Fatty Acid Binding ◽  
The Metabolic Syndrome ◽  
Increased Risk ◽  
Significant Difference

Childhood cancer survivors are highly exposed to the development of side effects after many years of cessation of anticancer treatment, including altered lipid metabolism that may result in an increased risk of overweight and metabolic syndrome. Adipocyte (A-FABP) and epidermal (E-FABP) fatty acid-binding proteins are expressed in adipocytes and are assumed to play an important role in the development of lipid disturbances leading to the onset of metabolic syndrome. The aim of this study was to investigate the association between serum A-FABP and E-FABP levels, overweight, and components of the metabolic syndrome in acute lymphoblastic leukemia survivors. Sixty-two acute lymphoblastic leukemia (ALL) survivors (34 females) were included in the study. The mean age at the time of the study was 12.41 ± 4.98 years (range 4.71–23.43). Serum levels of A-FABP and E-FABP were analyzed using a commercially available ELISA kit. The ALL survivors presented statistically higher A-FABP levels in comparison with the healthy controls (25.57 ± 14.46 vs. 15.13 ± 7.61 ng/mL, p < 0.001). The subjects with body mass index (BMI) above the normal range (18 overweight, 10 obese) had a greater level of A-FABP compared to the ALL group with normal BMI (32.02 ± 17.10 vs. 20.33 ± 9.24 ng/mL, p = 0.006). Of all participants, 53.23% had at least one risk factor of metabolic syndrome; in this group, only the A-FABP level showed a statistically significant difference compared to the healthy control group (30.63 ± 15.91 vs. 15.13 ± 7.61 ng/mL, p < 0.001). The subjects with two or more metabolic risk factors (16.13%) presented higher levels of both A-FABP (33.62 ± 17.16 vs. 15.13 ± 7.61 ng/mL, p = 0.001) and E-FABP (13.37 ± 3.62 vs. 10.12 ± 3.21 ng/mL, p = 0.021) compared to the controls. Univariable regression models showed significant associations between BMI and systolic blood pressure with the A-FABP level (coeff. 1.02 and 13.74, respectively; p < 0.05). In contrast, the E-FABP level was only affected by BMI (coeff. 0.48; p < 0.01). The findings reported herein suggest that the increased levels of A-FABP and E-FABP may be involved in the pathogenesis of overweight and the onset of metabolic syndrome in acute lymphoblastic leukemia. However, further longitudinal, prospective studies of fatty acid-binding proteins and their potential role in the pathogenesis of obesity and metabolic syndrome in ALL survivors remain to be performed.

Dietary lipids and gene expression

2004 ◽  
Vol 32 (6) ◽  
pp. 999-1002 ◽  
Author(s):  
H.M. Roche
Keyword(s):  
Insulin Resistance ◽  
Metabolic Syndrome ◽  
Transcription Factors ◽  
Fatty Acid ◽  
Regulatory Element ◽  
Nuclear Factor Κb ◽  
Dietary Lipids ◽  
Dietary Fatty Acids ◽  
Dietary Fatty Acid ◽  
The Metabolic Syndrome

Nutrition is a key environmental factor that is particularly involved in the pathogenesis and progression of several polygenic, diet-related diseases. Nutrigenomics refers to the interaction between nutrition and the human genome. Dietary fatty acids interact with multiple nutrient-sensitive transcription factors. This explains the molecular basis of some of the health effects associated with altered dietary fatty acid composition. The metabolic syndrome is a very common condition, characterized by insulin resistance, abdominal obesity, dyslipidaemia and hypertension. It often precedes Type 2 diabetes mellitus, and is associated with a greater risk of cardiovascular disease. Several lines of evidence suggest that the interaction between nutrient-derived metabolic stressors and pro-inflammatory signals play an important role in the aetiology of insulin resistance and the development of the metabolic syndrome. This paper will address the interaction between several nutrient-sensitive transcription factors, including SREBP (sterol-regulatory-element-binding protein) and NFκB (nuclear factor κB), demonstrating how this interaction may be altered with dietary fatty acid interventions.

Abstract 1186: Overexpression Of Endothelial Lipase In The Liver Promotes The Clearance Of Plasma Lipids But Accelerates Liver Steatosis In A Mouse Model Of Metabolic Syndrome

Circulation ◽  
2007 ◽  
Vol 116 (suppl_16) ◽  
Author(s):  
Tomoyuki Yasuda ◽  
Tatsuro Ishida ◽  
Yoko Kojima ◽  
Hanayo Tanaka ◽  
Takeaki Okada ◽  
...  
Keyword(s):  
Metabolic Syndrome ◽  
Fatty Acid ◽  
Mouse Model ◽  
Fatty Acid Synthase ◽  
Plasma Lipids ◽  
Recombinant Adenovirus ◽  
Mrna Level ◽  
Liver Steatosis ◽  
Endothelial Lipase ◽  
The Metabolic Syndrome

The metabolic syndrome includes high triglyceride (TG) and low HDL-cholesterol (HDL-C) levels in the plasma, and often accompanies steatosis in the liver. Endothelial lipase (EL) is a phospholipase that regulates HDL metabolism. EL is expressed by hepatocytes, while the function of EL in the liver has not been identified. Here, we examined the role of EL in the liver using a mouse model of metabolic syndrome. The EL expression in the liver was analyzed by real-time PCR. It revealed that liver EL expression was significantly increased in obese and diabetic db/db mice compared to that of control mice. To examine the significance of the EL upregulation in the liver, we injected the recombinant adenovirus encoding human EL into mice. The EL overexpression in the liver resulted in a significant decrease in plasma HDL-C, TG, and free fatty acid levels. Interestingly, the EL overexpression in the liver increased liver weight and liver TG content both in wild-type and db/db mice. In db/db mice, particularly, EL overexression accelerated the formation of steatosis by increasing the mRNA level of fatty acid synthase. These findings indicate that EL expression is increased in the liver in the metabolic syndrome. The upregulation of EL promotes the uptake of plasma lipids by hepatocytes, and accelerates the progression of steatosis in db/db mice. Thus EL may play a role in the genesis of steatosis as well as dyslipidemia in the metabolic syndrome.

Abstract 1319: Plasma Levels of Fatty Acid Binding Proteins 4 and 5 are Markers of Adiposity and the Metabolic Syndrome but are not Independent Predictors of Subclinical Atherosclerosis in Type 2 Diabetes

Circulation ◽  
2007 ◽  
Vol 116 (suppl_16) ◽  
Author(s):  
Roshanak Bagheri ◽  
Michael Lehrke ◽  
Shiv Kapoor ◽  
Megan Wolfe ◽  
Karen Terembula ◽  
...  
Keyword(s):  
Risk Factors ◽  
Metabolic Syndrome ◽  
Fatty Acid ◽  
Subclinical Atherosclerosis ◽  
Fatty Acid Binding Proteins ◽  
Tobit Regression ◽  
Fatty Acid Binding ◽  
The Metabolic Syndrome ◽  
Type 2 Dm

Objectives: Adipocyte-fatty acid binding protein (aP2) or FABP4 is expressed predominantly in adipose and macrophages. Its less abundant family member, FABP5 (Mal1), is more diffusely expressed but also found in adipocytes and macrophages. Gene deletion studies in rodents suggest that FABP4, to a greater extent than FABP5, modulates obesity and atherosclerosis. Preliminary clinical studies support a relationship of circulating FABP4 with obesity and the metabolic syndrome (MetSyn). However, there are no studies of circulating FABPs and atherosclerosis in humans. Methods: We evaluated the association of FABP4 and 5 (ELISA, Biovender) with cardiovascular risk factors, NCEP-defined MetSyn and Coronary Artery Calcification (CAC) in 846 asymptomatic, type 2 DM subjects (62.5% Caucasian, 32.5% African-American; 60% male; aged 58.6±9.2) recruited to the Penn Diabetes Heart Study. Findings : Levels [(median (IQ range)] of FABP4 [37.1 (23.0–55.2) vs 20.9 (14.0–31.0) ng/mL; p<0.001] and FABP5 [1.5 (1.2–1.9) vs 1.4 (1.1–1.8) ng/mL; p<0.01] were higher in women than men. FABP4 was significantly correlated with waist circumference (r=0.4, p<0.001), levels of leptin (r=0.5, p<0.001), insulin (r=0.21, p<0.001), hsCRP (r=0.23, p<0.001), triglycerides (r=0.25, p<0.001) and inversely with HDL cholesterol (women r=−0.23, p<0.001; men r=−0.11, p<0.05). Plasma FABP5 had similar, but weaker biomarker correlations. Both were strongly associated with MetSyn (FABP4 χ 2 =29.8, p<0.0001; FABP5 χ 2 =36.2, p<0.0001). Notably, FABP4 [22.7 (15.0–35.9) vs 34.4 (22.9–55.0), p<0.001], but not FABP5 (p<0.89), levels were lower in subjects on thiazolidinedione therapy. In tobit regression, FABP4, but not FABP5, levels above the median were associated with CAC scores after adjustment for age, gender and ethnicity [1.68 (1.05–2.66), Ratio (CI), p<0.03] but this was attenuated after further adjusting for BMI and established risk factors [1.52 (0.49–2.48), Ratio (CI), p<0.09]. Conclusion: Both FABP 4 and 5 are biomarkers of adiposity and MetSyn. In the first study of its kind, plasma FABP4, but not FABP5, was associated with CAC in type 2 DM, but neither were independent predictors of this subclinical atherosclerosis measure.

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