Metabolic syndrome affects fatty acid composition of plasma lipids in obese prepubertal children.
ABSTRACT The aim of the present study was to assess the plasma fatty acid composition of the total plasma lipids and lipid fractions in obese prepubertal children with and without metabolic syndrome (MS). Thirty-four obese prepubertal children were recruited: 17 who met MS criteria and 17 who did not; and twenty prepubertal children of normal weight. MS characteristics, insulin resistance (by homeostasis model assessment [HOMA-IR]), and plasma adiponectin (by radioimmunoassay) were recorded. Separation of lipid fractions was performed by liquid chromatography and the concentration of fatty acids in total plasma lipids and fractions was determined by gas-liquid chromatography. Concentrations of 16:1n-7, 16:1n-9, 18:3n-3, 22:6n-3, and n-3 PUFA in total plasma lipids (P < 0.05) and of 16:0, 16:1n-7, 18:1n-9, 18:2n-6, and n-6 PUFA in triacylglycerols (TG) (P < 0.05) were significantly higher in obese MS versus normal-weight children. Increased risk of MS was positively associated with plasma concentration of 16:1n-7 and negatively associated with proportion of 20:4n-6 (OR 2.76; P = 0.004; OR 0.56, P = 0.030, respectively). Saturated FA in TG were associated with HOMA-IR (R = 0.349, P = 0.017) and 22:5n-6 with adiponectin (R = 0.336, P = 0.05). In conclusion, increased concentrations of 16:1n-7 and decreased proportions of 20:4n-6 and 22:5n-6 in plasma lipids appear to be early markers of MS in children at prepubertal age.
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ABSTRACT: With the increasing incidence of obesity today, related complications such as diabetes, insulin resistance and hepatic steatosis are also becoming major concerns. Since these conditions share a common factor, aberrations in lipid metabolism, understanding the molecular changes that lead to abnormal lipid partitioning has become key to combating the obesity epidemic. The enzyme stearoyl-coenzyme A desaturase 1 (SCD1) has been shown to be intimately involved in both the lipogenic as well as the lipid oxidative pathways. Our studies with the SCD1 mouse model have established that these animals are lean and protected from leptin deficiency-induced and diet-induced obesity. Consequently, they also show greater whole body insulin sensitivity than wild-type mice. SCD1 mice have decreased expression of genes of lipogenesis and increased expression of lipid oxidative genes. The main transcription factors controlling genes of lipid synthesis and oxidation are sterol regulatory element binding protein-1c and peroxisome proliferator-activated receptor-alpha (PPARalpha), respectively. Here, we review some studies that show that the effects of SCD1 deficiency on whole body adiposity may be partly dependent on sterol regulatory element binding protein-1c, but are most likely independent of peroxisome proliferator-activated receptor-alpha. Our findings indicate that SCD1 is a key controller of lipid partitioning between lipogenesis and oxidation. While some questions regarding the molecular changes downstream of SCD1 deletion are yet to be answered, the studies outlined below clearly point to SCD1 as a highly promising target in combating obesity as well as related complications.Current Opinion in Clinical Nutrition and Metabolic Care 04/2006; 9(2):84-8. · 4.52 Impact Factor
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ABSTRACT: The incidence rate of obesity in youth has continued to increase worldwide and about 30% of obese children display insulin resistance (IR) and other metabolic abnormalities. The present study reviews the mechanisms for development of IR in the obese child and possible links between IR and dietary factors in childhood and adolescence. Although increased concentrations of plasma free fatty acids (FFA) and their counter part at intracellular level, long-chain acyl-coenzyme A (LC acyl-CoA), have been related to the early onset of IR in childhood obesity, a new endocrine paradigm states that adipose tissue secretes a wide variety of hormones and cytokines that regulate lipid energy metabolism. These hormonal changes precede any changes in metabolites such as FFA and glucose and appear to be associated with early IR in childhood. Excessive caloric intake increases IR in children; opposite, substantial reduction of overweight achieved by a hypocaloric diet decreases it. Elevated consumption of animal protein, particularly in early life, as well as diets rich in saturated, trans, and n-6 polyunsaturated fatty acids, and diets with a high carbohydrate to fat ratio, besides a high glycaemic and low-fiber diet also appear to exacerbate adiposity and IR.European Journal of Nutrition 07/2007; 46(4):181-7. · 3.13 Impact Factor
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ABSTRACT: The aim of this study was to detect the presence and degree of impairment of cardiovascular disease (CVD) risk factors, grouped as metabolic cardiovascular syndrome (MCS), in obese prepubertal children. We also assessed the influence of high fasting insulin levels in this pathological status. A cross-sectional study was performed on obese children based on fasting blood samples. Subjects were 61 obese children (aged 6 to 9 years) and an equal number of non-obese children paired by age and sex. The obese children presented the following characteristics in comparison to the non-obese group: significantly high levels of insulin (8.2 +/- 0.52 v 6.12 +/- 0.34 microU/mL), triglycerides (TG) (0.79 +/- 0.04 v 0.60 +/- 0.02 mmol/L), uric acid (0.24 +/- 0.005 v 0.21 +/- 0.004 mmol/L), systolic (SBP) (94.59 +/- 1.06 v 88.85 +/- 1.2 mm Hg) and diastolic (56.49 +/- 1.07 v 52.21 +/- 1.06 mm Hg) blood pressure (DBP), and low levels of high-density lipoprotein cholesterol (HDL-C) (1.30 +/- 0.04 v 1.46 +/- 0.03 mmol/L), and nonesterified fatty acids (0.407 +/- 0.02 v 0.505 +/- 0.02 mmol/L). The hyperinsulinemic obese children showed the same types of differences when compared with the normoinsulinemic group. In the obese group, having adjusted for age, waist/hip ratio (WHR), body mass index (BMI), and sex hormone-binding globulin (SHBG), insulin was an independent prediction factor for triglycerides (P =.0004), apolipoprotein A-I (Apo-AI) (P =.005), and alanine aminotransferase (ALT) (P =.029). BMI was an independent prediction factor for HDL-C (P =.001) and triglycerides (P =.027). However, insulin was an independent prediction factor in the control group for triglycerides (P =.0002) and SBP (P =.012), just as BMI was for HDL-C (P =.011) and uric acid (P =.041). We conclude that the cluster of CVD risk factors associated with MCS and intra-abdominal fat is present in obese prepubertal children. This situation seems to depend, to a large extent, on the insulin basal level. The apparent association between BMI and MCS is due to the correlation between BMI and insulin, and to the fact that insulin associates with MCS. Within the obese group, hyperinsulinemic children present the greatest impairment in the parameters considered to be constituents of MCS.Metabolism 05/2002; 51(4):423-8. · 3.10 Impact Factor