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Analysis of Potential Risk Factors of Metabolic Syndrome in a Pediatric Population Comparing Normal Weight and Overweight Subjects

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Analysis of Potential Risk Factors of Metabolic Syndrome in a Pediatric Population Comparing Normal Weight and Overweight Subjects Sherrock 1 Senior Honors Thesis: Analysis of Potential Risk Factors of Metabolic Syndrome in a Pediatric Population Comparing Normal Weight and Overweight Subjects. Kaitlyn Sherrock Department of Biology, Wittenberg University, Springfield, OH 45501-0720 USA Sherrock 2 Abstract Metabolic syndrome is a collection of risk factors that increase the risk for cardiovascular disease. The objective of this study was to determine which of the following potential risk factors were significantly different between normal-weight and overweight children. Potential risk factors included: fasting blood glucose, blood glucose after consumption of food, the amount and type of food and beverage selected, blood pressure, height and weight (to calculate BMI), heart rate during inhalation and heart rate during exhalation, and fungiform papillae density. Those measures which showed significant differences between the normal-weight and overweight children should be included in the pediatric definition of metabolic syndrome in children. The results indicated that BMI, fasting blood glucose, and blood pressure are important risk factors in metabolic syndrome. Future studies could include triglycerides, cholesterol, and physical fitness as potential risk factors. Furthermore, additional studies should be conducted on taste receptor density as well as food selection in relation to metabolic syndrome. Introduction Metabolic syndrome is defined as a collection of risk factors that increase the risk for cardiovascular disease (CVD) (Grundy et al., 2004). According to Reaven (1988), people with CVD usually have a clustering of risk factors including obesity, atherogenic dyslipidemia, elevated blood pressure, insulin resistance and/or glucose intolerance, a proinflammatory state, and a prothrombotic state. Reaven called this syndrome X, but the name was changed to insulin resistance syndrome and later to metabolic syndrome to avoid the implication that insulin was solely responsible for the syndrome (Grundy et al., 2004). Obesity as a Risk Factor for Metabolic Syndrome Obesity is one of the main risk factors of metabolic syndrome (Grundy et al., 2004). It is the increase of body weight due to excessive accumulation of fat, usually measured by body mass index (BMI). BMI is an indicator of the weight-to-height ratio and is defined by the formula [body weight (kg)/height(m)2]. Cutoff points have been established for BMI: less than 18.5 is considered underweight; between 18.5 and 24.99 is considered normal weight; greater Sherrock 3 than or equal to 25 is considered overweight; and greater than or equal to 30 is considered obese (World Health Organization, 2010). There are three modes of fat accumulation (McGill, 2008). The first mode is pure energy overload, which involves consuming more calories than are being expended. The second mode of fat accumulation is nutritional imbalance, usually a lack of co-factors for efficient fat oxidation. The third mode is associated with the effect of stress hormones (McGill, 2008). Abdominal obesity, also known as central obesity, is the main form of obesity associated with metabolic syndrome (Grundy et al. 2004). Abdominal obesity is clinically recognized by an increase in waist circumference or an increase in waist-to-hip ratio. Ideally, the waist: hip ratio should be less than or equal to 0.8 for women and less than or equal to 0.95 for men (Collins, 2007). One of the main causes of the recent spike in diagnoses of the metabolic syndrome in the United States is the obesity epidemic (Chobanian et al., 2003). Atherogenic Dyslipidemia as a Risk Factor for Metabolic Syndrome Atherogenic dyslipidemia is a condition in which the artery wall thickens as the result of a build-up of fatty materials due to a disruption of the amount of lipids in the blood (Grundy et al., 2004). Atherogenic dyslipidemia is characterized by elevated triglycerides and low concentrations of HDL cholesterol. A more in-depth analysis reveals increased remnant lipoproteins, elevated apolipoprotein B and small LDL cholesterol particles. Atherogenic dyslipidemia results in inflammation and can lead to cardiovascular disease (Grundy et al., 2004). Elevated Blood Pressure as a Risk Factor for Metabolic Syndrome Elevated blood pressure, or hypertension, is strongly associated with obesity and also commonly occurs in insulin-resistant people. It is believed by some investigators to be less Sherrock 4 metabolic than other factors of the syndrome, but it is almost universally included in the syndrome definition. Blood pressure is the measure of the force of the blood on the walls of the arteries (Dugdale et al., 2009). Factors that determine this pressure are the amount of blood being pumped by the heart, the force that the heart is pumping, and the size and flexibility of the arteries. Blood pressure is measured with a stethoscope and a sphygmomanometer, commonly called the blood pressure cuff. Inflating the cuff to about 180 mmHg will cause all of the blood vessels to collapse. Slowly releasing air out of the cuff will allow the blood to rush back into the vessels, giving what is called the systolic blood pressure, or the maximum pressure exerted when the heart contracts. As the air is released from the cuff, eventually, there will be no sound heard in the stethoscope, and this is the diastolic blood pressure, or the minimum pressure in the arteries when the heart is at rest. A normal blood pressure is 120/80 mmHg (systolic/diastolic), hypertension is defined as 140/90 mmHg or greater (Dugdale et al., 2009). Hypertension has been shown to be linked to cardiovascular disease, and longitudinal studies have shown a more than two-fold increase in risk from CVD for those with blood pressure in the range of 130- 139/85-89 mmHg compared to those with blood pressure less than 120/80 mmHg (Chobanian et al., 2003). Insulin Resistance as a Risk Factor for Metabolic Syndrome Insulin is produced by the pancreas and aids in the movement of glucose across the cell membrane in fat and muscle cells (Baumann et al., 2000). Insulin resistance occurs when people become insensitive to their own insulin (Grundy et al., 2004). Individuals with chronic insulin resistance tend to develop glucose intolerance, which can lead to hyperglycemia, and eventually, if the blood sugar reaches a high enough concentration, type 2 diabetes (Grundy et al., 2004). Sherrock 5 Insulin resistance is strongly associated with CVD. Adiponectin is an adipokine secreted by the white adipose tissue (Kadowaki, 2008). Adiponectin has been shown to affect insulin sensitivity through modulation of insulin signaling pathway. There are two adiponectin receptors, adiponectin receptor 1 (found throughout the body) and adiponectin receptor 2 (found mainly in the liver). These receptors are both integral membrane proteins, with their n-terminus on the interior of the cell and the c-terminus on the exterior of the cell, which is the opposite orientation of all other G-protein coupled receptors. Increased fat accumulation in obesity results in decreased adiponectin secretion (Kadowaki, 2008). Leptin is a protein that is also produced by the adipose tissue ((Haynes, 2000). Leptin and adiponectin act in an antagonist fashion in a feedback loop with the hypothalamus to regulate food intake, maintain an adequate fat reserve, and maintain energy homeostasis (Haynes, 2000; Kadowaki, 2008). When adiposity shrinks, the leptin signal decreases and the adiponectin signal increases, which suppresses energy expenditure and promotes fat storage. When adiposity rises, the leptin signal is increased and the adiponectin signal is decreased which increases energy expenditure and inhibits fat storage. If this balance is disturbed in any way, obesity can develop (Haynes, 2000; Kadowaki, 2008). Proinflammatory and Prothrombotic States as Risk Factors for Metabolic Syndrome A proinflammatory state is a condition that supports inflammation in the body (Grundy et al., 2004). It is clinically diagnosed by elevated C-reactive protein. Multiple mechanisms are responsible for this increase in C-reactive protein, one of which is obesity. Excess adipose tissue releases inflammatory cytokines that raise C-reactive protein levels. A prothrombotic state is a condition that supports the formation of a blood clot. It is clinically recognized by an increase in plasma plasminogen activator inhibitor as well as fibrinogen. Fibrinogen is an acute-phase Sherrock 6 reactant like C-reactive protein, so it is also increased by the release of cytokines. This shows that the proinflammatory state and the prothrombotic state are related (Grundy et al., 2004). C-reactive protein (CRP) is produced by the body in response to injury or infection (Lambert, 2004). It is also a risk factor for type 2 diabetes; adult studies have shown that as CRP levels rise, the development of diabetes and CVD also increases. CRP is linked to most of the components of the metabolic syndrome including: body fat, blood pressure, insulin, triglycerides, and cholesterol. The link between CRP and BMI can be explained by the molecule interleukin- 6, which is a primary determinate of CRP production in the liver. Interleukin-6 is a type of cytokine that is released from subcutaneous adipose tissue. The amount of interleukin-6 released is directly proportional to the amount of fat present, so the more fat a person has accumulated, the more interleukin-6 released, and the more CRP that is produced by the liver (Lambert, 2004). Correlates of Metabolic Syndrome in Adults In adults, it is known that abdominal obesity is positively correlated to metabolic syndrome. There are many suggested mechanisms behind this, one of which is that abdominal adipose tissue has an increased amount of catecholamine-induced lipolysis primarily due to an increase in adipocyte B-adrenergic receptor function (Kelley et al., 2000). This lipolysis releases an abnormally high amount of free fatty acids into the circulatory system and causes the build-up of lipids in sites such as the muscle and liver. Elevated free fatty acid flow into the liver inhibits insulin binding and degradation, which leads to insulin resistance and dyslipidemia (Grundy et al., 2005, Wajchenberg 2000).
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