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Biochemical and Hormonal Changes in Childhood Obesity

The prevalence of chronic or non communicable disease is escalating much more rapidly in developing countries than in industrialized countries. According to World Health Organization (WHO) estimates, by the 2020, non communicable diseases will account for approximately three quarter of all deaths in the developing countries (WHO. Global Strategy for non communicable disease prevention, 1997). In this regard, a potential emerging public health issue for the developing countries may be increasing incidence of childhood obesity with associated complications, which in turn is likely to create public health burden for poorer nations in the near future (Freedman et al, 2001). Lower to middle income nations face the double burden of having both malnourished and over nourished population, with most overweight and obese children being concentrated in urban areas. Rapid urbanization is associated with unhealthy lifestyle or “New World Syndrome”. In addition, in such communities, childhood obesity is still considered a sign of healthiness and high social class.

There is no universal consensus on a cut off points for defining overweight and obesity in children and adolescents, usually, for clinical practice and epidemiological studies, child overweight and obesity are assessed by means of indicators based on weight and height measurements, such as weight for height measures or body mass index (weight (kg)/height (m2))(WHO. Report series no.847, 1995).The US Centers for Disease Control and Prevention (CDC) defines obese as being at or above 95th percentile of body mass index for age (Kuczmarsk RJ et al, 2000).

History of obesity is both interesting and gives details of its progression. Obesity is an age-old health condition. Through out the history of obesity, its reputation varies from appreciation and opposite among cultures and in time. Ancient Egyptians are said to consider obesity as disease. Perhaps the most famous and earliest evidence of obesity is the Venus figurines, Statuettes of an obese female torso that probably had a major role in rituals. Ancient China has also been aware of obesity and dangers that come with it. They always were a believer of prevention as a key to longevity. The Aztecs believed that obesity was supernatural, an affliction of the gods. Hippocrates, the father of medicines was aware of sudden deaths being more common among obese men than lean ones as stated in his writings. In certain cultures and areas where food is scarce and poverty is prevalent, is viewed as symbol of wealth and social status. To date, an African tribe purposely plumps up a bride to prepare her for child bearing. Before a wedding can be set, a slim bride is pampered to gain weight until she reaches the suitable weight.

Through out the history of obesity, the public’s view and status of obesity changed considerably in the 1900’s. It was regarded as unfashionable by the French designer, Paul Poi ret who designed skin-revealing clothes for women. About the same time, the incidence of obesity began to increase and become wide spread. Later in 1940s’, Metropolitan life insurance published a chart of ideal weight for various heights. They also advocated that weight gain parallel to age is unhealthy. The government and medical society become more hands-on with obesity by imitating campaign against it. This was preceded by a study of risk factors for cardiovascular disease revealing obesity in the high ranks. Since then various diets and exercise programs have emerged. In 1996, the Body Mass Index (BMI) was published. This statistical calculation and index determined that a person is obese or not. At this time ,obesity incidence have soared, led by children and adolescent obesity, tripling in just a few short years, greater than any number in the history of obesity. This increase in the incidence of childhood obesity with associated cardiovascular risks, type 2 diabetes mellitus and stroke is supported by a considerable body of evidence.

The prevalence of overweight and obesity in childhood and adolescents has been increasing throughout much of the developed and developing world for the past few decades. It has become increasingly clear that excess adiposity in childhood predisposes individual not only to increased risk of adiposity and its sequaele as adults (Freedman et al, 2001), but also to increased risk of multiple chronic diseases in childhood and adolescence (Rosen bloom et al, 1999). Though mechanism not clearly delineated, excess body weight and adiposity is associated with type 2 diabetes mellitus and its complications, cardiovascular disease risk factors, non alcoholic fatty liver disease and asthma in youth.

Childhood Obesity 1930 – 1972

Risk factors for coronary heart disease (CHD) such as hypertension, dyslipidemia, impaired glucose tolerance and vascular abnormalities were present in overweight children. CHD is likely to be increased in overweight children when they become adults as a result of established risk factors. This study investigated whether excess weight in childhood was associated with CHD in adulthood among a very large cohort of persons born in Denmark in 1930 through 1972. They underwent mandatory annual health examination at public or private schools in Copenhagen. Each child was examined by school doctors or nurses and was assigned a health card bearing child’s name, date of birth, birth weight reported by parents. 10,235 men and 4,318 women, for whom childhood BMI data were available, received a diagnosis of CHD or died of CHD as adults. The risk of CHD event, a non fatal event, and a fatal event among adults was positively associated with BMI at 7-13 years of age for boys and 10 to 13 years of age as girls. The associations were linear for each age and risk increased across the entire BMI distribution.

Childhood Obesity 1930 – 1972

Risk factors for coronary heart disease (CHD) such as hypertension, dyslipidemia, impaired glucose tolerance and vascular abnormalities were present in overweight children. CHD is likely to be increased in overweight children when they become adults as a result of established risk factors. This study investigated whether excess weight in childhood was associated with CHD in adulthood among a very large cohort of persons born in Denmark in 1930 through 1972. They underwent mandatory annual health examination at public or private schools in Copenhagen. Each child was examined by school doctors or nurses and was assigned a health card bearing child’s name, date of birth, birth weight reported by parents. 10,235 men and 4,318 women, for whom childhood BMI data were available, received a diagnosis of CHD or died of CHD as adults. The risk of CHD event, a non fatal event, and a fatal event among adults was positively associated with BMI at 7-13 years of age for boys and 10 to 13 years of age as girls. The associations were linear for each age and risk increased across the entire BMI distribution.

Childhood Obesity and Economic Growth 1930-1983

Childhood obesity was related to the economic growth during the 50 years of economic growth in the industrialized world especially in Denmark. Annual measurements of height and weight were available for all children born between 1930 and 1983 attending primary schools in Copenhagen Municipality. 165,389 boys and 163,609 girls from the age of 7 through 13 years were included in this study. After computerization SBMI (kg/m2) were calculated and the prevalence of overweight and obesity according to international age and gender–specific criteria. Economics growth was indicated by the Gross National Product and the overall consumption per capita, adjusted for inflation. Prevalence of overweight and obesity among Danish children rose in phases, which were not paralleled by trends in economic growth. The microeconomics growth indicators seem inappropriate as proxies for the environmental exposures that have elicited the obesity epidemic.

Childhood obesity and television viewing

Children spend a substantial portion of their lives watching television (TV). Investigators have hypothesized that TV viewing cause’s obesity by one or more than three mechanisms:

      1. Displacement of physical activity.


          1. Increased calorie consumption while watching or caused by the effects of advertising.


            1. Reduced resting metabolism.

The relationship between TV viewing and obesity has been examined in a relatively large number of cross sectional epidemiological but few longitudinal studies. Many of them have found relatively weak, positive association or mixed results. Many experimental studies have found that reducing TV viewing may help to reduce the risk of obesity. One school based experimental study was designed specifically to test directly the casual relationship between TV viewing behaviors and body fatness. The results of this randomized controlled trial provide evidence that TV viewing is a cause of increased body fatness and that reducing the TV viewing is a promising strategy for preventing childhood obesity (Robinson; 2001).

The objective of another study (Utter J et al, 2006), was to explore how time spent watching television (TV) is associated with the dietary behavior of New Zealand children and young adolescents. Total number of participants was 3275 children aged 5-17 years. The findings suggest that longer duration of TV watching (thus more frequent exposure to advertising) influences the frequency of consumption of soft drinks, some sweets and snacks and some fast foods among children and young adolescents. Efforts to control the time spent watching TV may result in better dietary habits and weight control for children and adolescents.

Childhood Obesity US- A decade of progress, 1990-1999

Current data suggest that 20% of US children are overweight .An analysis of the secular trends suggest that 20% of US children are overweight, and a clear up ward trend in body weight in children of 0.2 Kg between 1973 and 1994. In addition, childhood obesity is more prevalent among minority sub groups such as African Americans. Obesity that begins early in life persists into adulthood and increases the risk of obesity related conditions later in life. There has been tremendous increase in the number of studies examining the etiology and health effects of obesity in children (Goran MI, 1990-1999).1980 (boys 0.2% girls 0.5%) and 1997 (boys 1.2%, girls 2.0%).

Ten years trends of childhood obesity in Israel 1990-2000

Cross sectional data was collected from 13284 second and fifth class school; children between 1990-2000. Prevalence of obesity was determined using Israeli and US reference values. BMI values at 95th percentile increased overtime in all ages and sex categories.

Between 1990 and 2000, 95th centile values were increased by 12.7%and 11.8% among second grade boys and girls respectively. Among fifth graders in 2000, 10.7% of boys and 11.1% of girls exceeded the 1990 BMI reference values. The proportion of obese children increased over time using both Israeli and US reference values (Huerta Michael et al, 2008).

Netherlands. Overweight, Obesity in 2003: V.1980-97.

Data on 90,071 children, aged 4-16 years were routinely collected by 11 Community Heath Services during 2002-2004. International cut -off points for BMI to determine overweight and obesity. On average, 14.5% of boys and 17.5% of the girls were overweight (including obesity), which is a substantial increase since 1980 (boys 3.9% and girls 6.9%) and 1997 (boys 9.7% and girls 13%). Similarly 2.6% of the boys and 3.3% 0f the girls aged 4-16 years were obese, which is much higher than in 1980 (boys 0.2% and girls 0.5%) and 1997 (boys 1.2% and girls 2.0%), (KatjaVan Den Husk, 2007).

Obesity trends in US. 2003-2006

Height and weight measurements were obtained from 8164 children and adolescents as apart of the 2003-2004 and 2005-2006 National Health and Nutrition Examination Survey (NHANES). Because no statistically significant differences in the prevalence of high BMI for age were found between the estimates for 2003-2004 and 2005-2006, data for four years were combined to provide more stable estimates for the most recent time period. Over all, in 2003-2006, 11.3% of children and adolescents aged 2 through years were at or above 97th percentile of the 2000 BMI- for- age growth charts, 16.3% were at or above 95th percentile. Prevalence estimates vary by age and by racial/ethnic group. Analysis of the trends in high BMI for age showed no statistically significant trend over the four time periods (1999-2000, 2001-2002, 2003-2004, and 2005-2006) for either boys or girls (Cynthia l.Ogden et al, 2008).

11-March 2005. Public Release Date: Consensus on Childhood Obesity, Recommends classification as disease

A common statement on childhood obesity was published to day in the journal of Chemical Endocrinology and Metabolism (one of the journals of Endocrine Society). The consensus statement reflects the conclusions from an international summit held in Israel last year (2004) and includes a controversial recommendation to classify obesity as a disease. This decision was based upon the available research on the diagnosis, prevalence, causes (including endocrine disorders), risks, prevention and treatment of childhood obesity. Pediatric obesity is now recognized as a major health problem all over the world. Researcher have found that children who are obese have a higher risks adult obesity, which is strongly associated with many serious medical complications that impair quality of life and lead to additional increased risks. The statement also noted the prevalence of overweight/obesity among children 6-11 years (in the US) doubled between the years 1980-2000. By classifying obesity as legitimate disease, public funding and in user s’reimbursement for obesity treatment becomes legalized (consensus on childhood obesity, 2005).

Serious health risks will likely to begin to appear in obese children and adolescents as they grow older. These may include diabetes mellitus, metabolic syndrome, hyperandrogenism, heart disease, hypertension, respiratory factors, and sleep disorders. Obese children are also at greater risk of anxiety and depression. It also recommended a number of measures that can be implemented by parents; schools, health providers and government and regulatory agencies to help to prevent the onset of childhood obesity

Endocrine Regulation of Energy Metabolism – Adipocytokines and Obesity

The mechanism underlying obesity was further explained by the discovery of adipocytokines, the role of peripheral thyroid hormones (T4, T3), thyroid stimulating hormone and insulin the regulation of energy metabolism. The levels of some of the adipocytokines were shown to be related to visceral obesity, type 2 diabetes mellitus and coronary artery disease. Plasma levels of all the adipocytokines increase with the obesity except adiponectin (Yuji Matsuzawa et al, 2003).

Recent studies point out to the adipose tissue as a highly active organ secreting a range of hormones, Leptin, Adiponectin, and Resistin. They are considered to take part in the regulation of energy metabolism. Leptin, Adiponectin and Resistin are produced by the adipose tissue. Leptin and Adiponectin are insulin sensitizing while Resistin increase the insulin resistance.


The notion that genetic abnormalities contribute to obesity gained important support with the identification of the Ob gene and its protein product in 1994 (Zhangy et al, 1996). The Ob gene termed “Leptin” from the Greek “Leptos”, meaning thin, is produced in adipose tissue and is thought to act as an afferent satiety signal in a feed back loop that affects the appetite and satiety centre in the hypothalamus of brain. The ultimate effect of this loop is to regulate body-fat mass. In human, as noted by Considine et al, 1996; caloric restriction reduces leptin concentrations and Ob mRNA levels in adipose tissue, and refeeding increases these levels. One fundamental mechanism of obesity is insensitivity to the action of Leptin, presumably in the hypothalamus. The Leptin’s primary physiological function is to provide a signal to suppress body fat by decreasing food intake or increasing energy expenditure. Serum leptin concentrations change more during weight loss than during weight gain (Rosenbaum M et al, 1997).


Adiponectin or Adipo Q, an adipocyte specific secreted protein with roles in glucose and lipid homeostasis (Insulin stimulates the secretion of adiponectin). Circulating adiponectin concentrations are high 500-30,000 µg/l (5-30mg/ml) accounting for 0.01% of total plasma proteins (Berget et al, 2002).

Adiponectin was discovered in the mid 1990s by four different groups of researchers (Hu E et al, 1996). Adiponectin has various biological functions including insulin sensitizing (Hotta K et al, 2000), antiatherogenic (Yamauchi T et al, 2003), anti-inflammatory (Ouchi N et al, 2003), antiangiogenic and anti tumor functions (Brakenhielm E et al, 2004). Adiponectin acts through Adiponectin receptors, Adipo R1 and Adipo R2. Adipo R1 is mostly expressed in skeletal muscles and Adipo R2 is abundant in liver. These receptors are also expressed by the pancreatic ß cells (Kharroubi et al, 2003), macrophages and atherosclerotic lesions (Chinetti et al, 2004) as well as in brain (Yamauchi et al, 2003). Circulating Adiponectin levels display diurnal variation with a nocturnal decline and maximum levels in the late morning (Gavrila et al, 2003). Adiponectin is also found in breast milk, which in turn is implicated in childhood obesity prevention (Savino et al, 2008).

Among the various adipocytokines, adiponectin, which is an abundant circulating protein (247 amino acids) synthesized purely in adipose tissue, appears to play a very important role in carbohydrates, lipid metabolism and vascular biology. Adiponectin appears to be a major modulator of insulin action and its levels are reduced in type 2 diabetes mellitus, which could contribute to peripheral insulin resistance in this condition. It has significant insulin sensitizing as well as anti inflammatory properties that include suppression of macrophage phagocytosis and TNF-a secretion and blockage of monocytes adhesion to endothelial cells in vitro. Although further investigations are required, Adiponectin administration, as well as regulation of the pathway controlling its production, represents a promising target for managing obesity, hyperlipidemia, insulin resistance, type 2 diabetes mellitus, and vascular inflammation (Manju Chandran et al, 2003).


Human resistin is 108 amino acids prepeptide and is cleaved before its secretion from the Adipose tissue. Resistin circulates in the blood as dimeric protein consisting of 92 amino acids polypeptides that are linked by a disulfide bridge. Holcomb et al, 2000 first described the gene family and its tissue specific distribution. Originally described as lung specific, is also produced by the adipose tissue and peripheral blood monocytes. It is also present in dividing epithelia of the intestine. Resistin increase blood glucose and insulin concentration in the mice and impairs hypoglycemic response to insulin infusion. In addition, anti resistin antibodies decrease blood glucose and insulin sensitivity in obese mice (Ukkalo O, 2002). The physiological role of resistin in human remains controversial. There more resistin protein in obese than lean individuals, with a significant positive correlation between resistin and BMI. BMI is a significant predictor of insulin resistance, but resistin adjusted for BMI is not. These data demonstrate that resistin protein is present in human adipose tissue and blood and that there is significantly more resistin in serum of obese individuals. Serum resistin is not a significant predictor of insulin resistance in human (Youn et al, 2003, Rear R and Donnelly R, 2004).

Tumor Necrosis Factor-a

It will be unreasonable not to mention the Tumor Necrosis Factor a and its role in vascular inflammation related to atherosclerosis especially in obesity.

It is a cytokine involved in systemic inflammation and is a member of a group of cytokines that stimulate the acute phase reaction. The primary role of TNF is in the regulation of immune cells. TNF is able to induce apoptotic cell death, to induce inflammation and to inhibit tumourgenesis and viral replication. Dysregulation and, in particular, over production of TNF have been implicated in a variety of human diseases, as well as cancer (Locksley et al, 2001).

The theory of antitumoural response of the immune system in vivo was recognized by the physician William B in 1968. Dr A Granger reported a cytotoxic factor produced by lymphocytes and named it Lymphotoxin (Kalli WB and Granger GA, 1968). Dr L Loyal old, in 1975 reported another cytotoxic factor produced by macrophages and named it Tumor Necrosis Factor (TNF) (Cars well et al, 1975).

Interleukin – 6 (IL-6)

Chronic inflammation is linked to endothelial dysfunction, atherosclerosis, and insulin resistance (Fernandez-Real JM and Ricart W, 2003 and Fernandez-Real JM, Ricart W, 2005). Plasma concentrations of proinflammatory cytokines, such as interleukin (IL) – 18, IL-6, and tumor necrosis factor (TNF)-a, and of several other inflammatory markers are increased in patients with ischemic heart disease (Fernandez-Real JM and Ricart W, 2003, Ridker PM et al, 2002, Engstrom G et al, 2004, Ridker PM et al, 1997, Pradham AD et al, 2002). Circulating cytokines also are elevated in type 2 diabetes, obesity, and insulin resistance syndrome and play a central role in the pathogenesis of these disorders (Fernandez-Real JM and Ricart W, 2003).

IL-6 is a mediator of the inflammatory response, and it is linked to dyslipidemia, type 2 diabetes, and risk of myocardial infarction (Fernandez-Real JM and Ricart W, 2003, Ridker PM et al, 2000, Esteve E et al, 2005, Yudkin JS et al, 2000). IL-6 is secreted by a variety of different cell types, including lymphoid and endothelial cells, fibroblasts, skeletal muscle, and adipose tissue. Circulating IL-6 levels correlate with obesity and insulin resistance and may predict the development of type 2 diabetes mellitus (Yudkin JS et al, 2000, Pradhan AD et al, 2001, Akira S et al, 1993, Mohamed-Ali V et al, 1997).

Endothelial dysfunction is regarded as a causal factor in the development of atherosclerosis (Hansson GK, 2005). It is one of the earliest abnormalities that can be detected in people at risk for cardiovascular events, and it is linked to insulin resistance and type 2 diabetes (Steinberg HO and Baron AD, 2002, Natali A et al, 2006). Cytokines have an important role in the endothelial injury induced by inflammation. The vascular endothelium is involved in the inflammatory response to atherosclerosis (Hansson GK, 2005, Steinberg HO and Baron AD, 2002, Natali A et al, 2006, Widlansky ME et al, 2003), and changes in endothelium function could underlie the association between cardiovascular disease and inflammation.

Obesity Related Insulin Resistance: Definition and Pathogenesis

Insulin resistance is a state in which a given amount of insulin produces a subnormal biological response (Kahn CR, 1978). In particular, it is characterized by a decrease in the ability of insulin to stimulate the use of glucose by muscles and adipose tissue and to suppress hepatic glucose production and output (Matthaei et al, 2000). Furthermore, it accounts a resistance to insulin action on protein and lipid metabolism and on vascular endothelial function and genes expression (Bajaj M and Defronzo RA, 2003).

Several defects in the insulin signaling cascade have been implicated in the pathogenesis of insulin resistance, Insulin resistance is believed to have both genetic and environmental factors implicated in its etiology (Matthaei et al, 2000 and Liu et al, 2004). The genetic component seems to be polygenic in nature, and several genes have been suggested as potential candidates (Matthaei et al, 2000). However, several other factors can influence insulin sensitivity, such as obesity, ethnicity, gender, perinatal factors, puberty, sedentary lifestyle and diet (Liu et al, 2004).

The Role of Fatty Acids and Adipocytokines

Obesity represents the major risk factor for the development of insulin resistance in children and adolescents (Caprio S, 2002), and insulin resistance/hyperinsulinemia is believed to be an important link between obesity and the associated metabolic abnormalities and cardiovascular risk (Weiss R and Kaufman FR, 2008). Approximately, 55% of the variance in insulin sensitivity in children can be explained by total adiposity, after adjusting for other confounders, such as age, gender, ethnicity and pubertal stage (Caprio S, 2002). Obese children have hyperinsulinemia and peripheral insulin resistance with an ~40% lower insulin-stimulated glucose metabolism than non-obese children (Caprio S et al, 19996).

Adipose tissue seems to play a key role in the pathogenesis of insulin resistance through several released metabolites, hormones and adipocytokines that can affect different steps in insulin action (Matsuzawa Y, 2005) (Fig. 1).

Adipocytes produce non-esterified fatty acids, which inhibit carbohydrate metabolism via substrate competition and impaired intracellular insulin signaling (Matsuzawa Y, 2005, Griffin ME et al 1999 and Randle PJ, 1998). In children, as in adults, several ‘adipocytokines’ have been related to adiposity indexes as well as to insulin resistance.

Adiponectin is one of the most common cytokines produced by adipose tissue, with an important insulin sensitizing effect associated with anti-atherogenetic properties (Despres JP, 2006 and Gil-Campos M et al, 2004). Whereas obesity is generally associated with an increased release of metabolites by adipose tissue, levels of Adiponectin are inversely related to adiposity (Matsuzawa Y, 2005). Therefore, reduced levels of this adipocytokine have been implicated in the pathogenesis of insulin resistance and metabolic syndrome (Matsuzawa Y, 2005). Decreased levels of Adiponectin have been detected across tertiles of insulin resistance in children and adolescents (Weiss R et al, 2004), where it is a good predictor of insulin sensitivity, independently of adiposity (Lee S et al, 2006). Adipose tissue also produces tumour necrosis factor-a, an inflammatory factor, which can alter insulin action at different levels in the intracellular pathway (Matsuzawa Y, 2005). Interleukin-6 (IL-6) is another inflammatory cytokine released by adipose tissue and its levels are increased in obesity (Matsuzawa Y, 2005). IL-6 stimulates the hepatic production of C-reactive protein and this can explain the state of inflammation associated with obesity, and could mediate, at least partially, obesity-related insulin resistance (Matsuzawa Y, 2005). Data based mainly on animal studies also suggest that increased levels of resistin, another molecule produced by adipose tissue, could impair insulin sensitivity (Matsuzawa Y, 2005). The close relationship between Leptin levels and insulin resistance in children has also been suggested by the data (Chu NF et al, 2000).

Serum levels of retinol-binding protein 4 (RBP4) correlate with insulin resistance in subjects with obesity as well as in those with impaired glucose tolerance (IGT) or type 2 diabetes mellitus, therefore suggesting that it could be useful in assessing insulin resistance and the associated risk for complications (Graham TE et al, 2006). Serum RBP4 is independently related to obesity as well as to components of the metabolic syndrome in normal weight and overweight children (Aeberli I et al, 2007).

Diet composition in obese children might be an additional factor promoting and/or worsening insulin resistance. Animal and human studies suggest that a high energy intake as well as a diet rich in fat and carbohydrates and low in fiber could increase the risk of developing insulin resistance (Canete R et al, 2007).

The Role of Fat Distribution

An altered partitioning of fat between subcutaneous and visceral or ectopic sites has been associated with insulin resistance (Weiss R and Kaufman FR, 2008). Visceral fat has a better correlation with insulin sensitivity than subcutaneous or total body fat (Caprio S et al, 1995), in both obese adults and children. Visceral fat has higher lipolytic activity compared with subcutaneous fat, therefore a greater amount of free fatty acids and glycerol gain entry or carried out to the liver (Matthaei et al, 2000). Visceral fat in girls is directly correlated to the glucose-stimulated insulin levels and inversely correlated with insulin sensitivity and the rate of glucose uptake. No correlation was found between abdominal subcutaneous fat (Caprio S et al, 1995).

Ectopic deposition of fat in the liver or muscle can also be responsible for insulin resistance in obese subjects, as the accumulation of fat in these sites impairs insulin signaling, with a reduced glucose uptake in the muscle and a decreased insulin-mediated suppression of hepatic glucose production (Weiss R and Kaufman FR, 2008).

Intramyocellular lipid (IMCL) accumulation has been shown as a factor related to decreased insulin sensitivity (Jacob S et al, 1999 and Thamer C et al, 2003). Obese insulin sensitive children and adolescents present lower levels of visceral fat and IMCL when compared with obese insulin resistant children (Weiss R et al, 2005).

Accumulation of fat in the liver has also been associated with insulin resistance, independently of adiposity (Kelley DE et al, 2003). It has also been suggested that deposits of fat around blood vessels can produce several cytokines and therefore contribute to the development of insulin resistance, through a so-called ‘vasocrine’ effect (Yudkin JS et al, 2005).

Insulin Resistance and Associated Complications

Insulin resistance in obesity is strictly related to the development of hypertension (Marcovecchio ML et al, 2006 and Cruz ML et al, 2002), dyslipidemia (Howard BV and Howard WJ, 1994), impaired glucose tolerance (IGT) (Sinha R et al, 2002), hepatic steatosis (D’Adamo E et al, 2008), as well as to the combination of these factors, also known as metabolic syndrome (Eckel RH et al, 2005). Furthermore, insulin resistance is associated with systemic inflammation, endothelial dysfunction, early atherosclerosis and disordered fibrinolysis (Dan Dona P et al, 2002). It is alarming that these metabolic and cardiovascular complications are already found in obese children and adolescents (Dietz WH, 2004). The presence of these alterations in prepubertal children is then particularly worrying, as insulin resistance and related complications might be further exacerbated by the influence of puberty, due to the physiological decrease in insulin sensitivity associated with normal pubertal development (Caprio S et al, 1989).

Insulin resistance in childhood can track in adult life (Sinaiko AR et al, 2006). Insulin resistance at the age of 13 years predicts insulin resistance at age 19 years, independently of BMI, and is also associated with cardiovascular risk in adulthood (Sinaiko AR et al, 2006).

The fundamental role of insulin resistance in human disease was already recognized in 1988 by Reaven (Reaven GM, 1988) who emphasized its role in the development of a grouping of metabolic abnormalities, which he defined as syndrome X. Later studies strengthened the concept of insulin resistance as a key component of the metabolic syndrome, a cluster of impaired glucose tolerance (IGT), dyslipidemia, hypertension, hyperinsulinemia, associated with an increased risk of type 2 diabetes mellitus and cardiovascular disease (Eckel RH et al, 2005).

Insulin resistance represents a serious and common complication of obesity during childhood and adolescence. A timely diagnosis and an appropriated prevention and treatment of obesity and insulin resistance are required in order to reduce the

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