**2. Dyslipidemia in childhood obesity**

The dyslipidemia pattern usually associated with childhood obesity consists of a combina‐ tion of elevated triglyceridemia, decreased plasma level high-density lipoprotein cholester‐ ol (HDL-c) concentration, and low-density lipoprotein cholesterol (LDL-c) concentration at the upper limit of the normal range. According to the nuclear magnetic resonance spectro‐ scopy results, this type of dyslipidemia is associated with dense and small LDL, less stable HDL, a reduction in total HDL-c, and in large HDL particles [3]. Small and dense LDL particles are associated also with visceral fat and insulin resistance. In school-age chil‐ dren, greater total and central adiposity are associated with smaller LDL particle size and lower HDL-c plasma levels [4].

The LDL can be easily oxidized; they have low affinity for LDL receptors and they penetrate the intima [5]. The macrophages from the vessel wall take the oxidized LDL and they are transformed into foam cells, and so the process of atherosclerosis starts. GGT (Gamma Glutamyl Transpeptidase), an enzyme known to modulate the redox status of the thiol proteins, can also catalyze the oxidation of LDL from the circulation, augmenting the devel‐ opment of atherosclerosis [6]. In the plasma, GGT constitutes complexes with albumin and lipoproteins [7]; while in the atheromatous plaques, GGT is colocalized with oxidized LDL and foam cells [8].

the Sea buckthorn berry, including flavonols, carotenoids, fatty acids, tocopherols and phytosterols can affect the metabolic profile. Special features of the berry oils are high proportions of palmitoleic acid as well as vitamin E, carotenoids, and sterols. The palmitoleic acid stimulates muscle insulin action, suppresses hepatosteatosis and prevent the deleterious effects of saturated fatty acids and high glucose on human pancreatic beta-cell turnover and function. Phenolic compounds and flavonoids from sea buckthorn ameliorate bodyweight, blood glucose, and serum lipid profile. By reducing triglyceridemia and by improving the blood pressure levels, sea buckthorn pulp oil may prevent metabolic syndrome in obese children. The treatment is recommended in hypertriglyceridemic waist phenotype obese children. Omega-3 supplements and sea buckthorn pulp oil supplements reversed the carotid intima media thickness values in obese children and they have beneficial effects in childhood

The World Health Organization (WHO) regards childhood obesity as one of the most serious global public health challenges for the 21st century. Childhood obesity is associated with a higher chance of obesity, premature death, and disability in adulthood. But in addition to increased future risks, overweight and obese children are at an increased risk of developing various health problems. Visceral obesity leads to insulin resistance, mediated by free fatty

The present review deals with the management of obesity and dyslipoproteinemia in child‐ hood and emphasis the beneficial effects of supplements with Omega-3 fatty acids and Sea-

The dyslipidemia pattern usually associated with childhood obesity consists of a combina‐ tion of elevated triglyceridemia, decreased plasma level high-density lipoprotein cholester‐ ol (HDL-c) concentration, and low-density lipoprotein cholesterol (LDL-c) concentration at the upper limit of the normal range. According to the nuclear magnetic resonance spectro‐ scopy results, this type of dyslipidemia is associated with dense and small LDL, less stable HDL, a reduction in total HDL-c, and in large HDL particles [3]. Small and dense LDL particles are associated also with visceral fat and insulin resistance. In school-age chil‐ dren, greater total and central adiposity are associated with smaller LDL particle size and

buckthorn (Hippophae rhamnoides) pulp oil obtained by cold pressing.

obesity

60 Lipoproteins - From Bench to Bedside

**1. Introduction**

acids and adipokines [1, 2].

lower HDL-c plasma levels [4].

**2. Dyslipidemia in childhood obesity**

**Keywords:** MIFA, PUFA, childhood obesity

HDL inhibits LDL oxidation. The antioxidant activity of HDL can be explained by its proteins, which link transitional metals, and by two intrinsic enzymatic systems: acetylhydrolase and paraoxonase [9].

High circulating levels of oxidized LDL were described in extreme pediatric obesity [10] in children with high fructose intake [11] and are associated with insulin resistance [12].

More than half of the obese children have dyslipidemia. Improper dietary habits, such as fast foods and snacks, rich in saturated and trans-fatty acids have an important contribution for dyslipidemia. Decreased physical activity and unhealthy eating habits are noticed to have higher incidence in adolescents. These lifestyle modifications, increased susceptibility to insulin resistance, and hormonal changes make pubertal subjects prone to metabolic syn‐ drome. Dyslipidemia present in metabolic syndrome (hypertriglyceridemia and low HDL-c) is associated with insulin resistance, with inflammatory markers (C reactive protein) and with a protrombotic status [13, 14, 15].

In a recent study [16] done on 139 children, the prevalence of dyslipidemia among overweight and obese children was 50.4%. Dyslipidemia patterns were: hypertriglyceridemia 31.9%, low HDL-c 29.7%, high non-HDL-c 15.8%, hypercholesterolemia 11.9%, and elevated LDL-c 10.7%. The dyslipidemia was often (> 50%) present among those with increased waist circumference and family history of dyslipidemia.

The consumption of fructose has recently increased and it seems that in adolescents, fructose represents 12% of the total daily intake [11]. In overweight children, higher fructose intake from sweets and sweetened drinks predicts smaller LDL particle size [4].

Although the caloric intake from fat and different types of fatty acids influence the plasma lipid profile, the amount of total energy intake plays a more important role in lipid profiles [17].

The worst effect on blood lipids have trans and saturated fatty acids [18]. Partially hydrogen‐ ated vegetable oil or fish oil are very rich in trans fatty acids that increase LDL-c and decrease HDL-c, so they must be avoided in the diet. C12-16 saturated fatty acids increase both LDL-c and HDL-c levels, but stearic acid has a neutral effect on the plasma lipid profile comparable to that of oleic acid [19].

Replacement of saturated fatty acids by polyunsaturated fatty acids (PUFA) or monounsatu‐ rated fatty acids (MUFA) lowers both LDL-c and HDL-c [20].

Supplementation with MUFA is supported by authoritative bodies. When MUFA replaces saturated fatty acids it reduces total cholesterol, and when MUFA replaces carbohydrates it decreases triglycerides and increases HDL [21].

The atherogenic lipid profile is more severe in obese children, especially in boys, who are insulinoresistent. The severity of obesity estimated by the value of body mass index (BMI) is of a lesser importance in comparison with insulin resistance on the atherogenic lipid profile [22].

The atherogenic index can be calculated in many ways, but the most used procedures are: as the ratio between total cholesterol to HDL cholesterol or as a ratio apoB/apoA1. By assessing atherogenic indexes, it has been demonstrated that overweight and obese children have twice higher risk of atherosclerosis [23] and that advancing puberty and advancing age are athero‐ genic risk factors for obese boys [24].

The relation between plasma lipids and prediabetes in obese prepubertal children is proved by the association of saturated fatty acids in triglycerides with the HOMA-IR (homeostatic model assessment of insulin resistance) [25].

In children, the process of atherosclerosis starts at an early age and is linked to visceral obesity [26]. The common carotid artery intima-media thickness (C-IMT) measured by ultrasound imaging is a marker of preclinical atherosclerosis. C-IMT relates to the severity and extent of coronary artery disease and predicts the likelihood of cardiovascular events in adults.

True primary prevention of atherosclerosis, as contrasted with primary prevention of clinically manifest atherosclerotic disease, must begin in childhood or adolescence [27].

Results from the Young Finns Study have shown that conventional childhood risk factors, such as dyslipidemia, obesity, elevated blood pressure, and smoking, are predictive of subclinical atherosclerosis in young adults [28]. The same authors of the study underline the good news that the adverse cardiometabolic effects of childhood overweight/obesity are reversed among those who become nonobese adults.

The relation cause-effect between dyslipidemia and insulin resistance is not well established but they are interdependent. Most of the researchers consider that insulin resistance precedes the development of the metabolic syndrome feature, including dyslipidemia [29].

Insulin resistance increases free fatty acid flux to the liver by decreased inhibition of lipolysis and also by increased de novo lipogenesis [30].

Supplements with docosahexaenoic acid (DHA) reduce plasma concentrations of free fatty acids of LDL-c and the ratio triacylglycerols/HDL-c, improving insulin resistance [31].

Eicosapentaenoic acid (EPA) increases the anti-inflammatory monocyte cytokine IL-10 expression and reduces arterial stiffness, which may contribute to the antiatherogenic effect of EPA in obese dyslipidemic patients [32].
