A SEMINAR PRESENTATION ON OBESITY BY IDI JUNAIDU BAKARI. ID: BC/10/0942

1.0 Introduction Obesity is a complex disorder involving an excessive amount of body fat. Obesity isn't just a cosmetic concern. It increases your risk of diseases and health problems, such as heart disease, diabetes and high blood pressure. The most commonly used definitions, established by the World Health Organization (WHO) in 1997 and published in 2000; provide the values listed in the table below. (WHO, 2000). Some modifications to the WHO definitions have been made by particular bodies. The surgical literature breaks down "class III" obesity into further categories whose exact values are still disputed. (Sturm R, 2007). Any BMI ≥ 35 or 40 kg/m2 is severe obesity. A BMI of ≥ 35 kg/m2 and experiencing obesity-related health conditions or ≥40–44.9 kg/m2 is morbid obesity. A BMI of ≥ 45 or 50 kg/m2 is super obesity. As Asian populations develop negative health consequences at a lower BMI than Caucasians, some nations have redefined obesity; the Japanese have defined obesity as any BMI greater than 25 kg/m2 (Kanazawa et al., 2002). While China uses a BMI of greater than 28 kg/m2. (Bei-Fan Z, 2002). Being extremely obese means you are especially likely to have health problems related to your weight. The good news is that even modest weight loss can improve or prevent the health problems associated with obesity. Dietary changes, increased physical activity and behavior changes can help you lose weight. Prescription medications and weight-loss surgery are additional options for treating obesity (Jensen et al., 2013). Obesity increases the likelihood of various diseases, particularly heart disease, type 2 diabetes, obstructive sleep apnea, certain types of cancer, and osteoarthritis. (Haslam , James , 2005). Obesity is most commonly caused by a combination of excessive food energy intake, lack of physical activity, and genetic susceptibility, although a few cases are caused primarily by genes, endocrine disorders, medications, or psychiatric illness. Evidence to support the view that some obese people eat little yet gain weight due to a slow metabolism is limited. On average, obese people have greater energy expenditure than their thin counterparts due to the energy required to maintain an increased body mass. (Kushner, Robert, 2007). (Adams, Murphy, 2000). Obesity is a leading preventable cause of death worldwide, with increasing rates in adults and children. Authorities view it as one of the most serious public health problems of the 21st century. (Barness et al., 2007). Obesity is stigmatized in much of the modern world (particularly in the Western world), though it was widely seen as a symbol of wealth and fertility at other times in history and still is in some parts of the world.( Haslam, James, 2005; Woodhouse R, 2008). In 2013, the American Medical Association classified obesity as a disease. (Pollack, Andrew, 2013), (Weinstock, Matthew, 2013). 1.1 Types of Obesity BMI Weight status Below 18.5 Underweight 18.5-24.9 Normal 25.0-29.9 Overweight 30.0-34.9 Obese (Class I) 35.0-39.9 Obese (Class II) 40.0 and higher Extreme obesity (Class III) For most people, BMI provides a reasonable estimate of body fat. However, BMI doesn't directly measure body fat, so some people, such as muscular athletes, may have a BMI in the obese category even though they don't have excess body fat. Ask your doctor if your BMI is a problem (Bray, 2015). 1.1 Symptoms Obesity is diagnosed when your body mass index (BMI) is 30 or higher. Your body mass index is calculated by dividing your weight in kilograms (kg) by your height in meters (m) squared. The most widely used formula for relating the height and weight of an individual is body mass index (BMI). BMI is defined as a ratio of weight (kilograms) and height2 (square meters) (Weisell, 2002). A BMI between 20-25 kg/m2 is normal and associated with lowest mortality, whereas a BMI of 25-30 kg/m2 is considered overweight. In adults a BMI above 30-40 kg/m2 is defined as obesity and BMI above 40 kg/m2 is severe obesity. Among the children and adolescent population with a BMI above the 95th percentile for age belong to the obese group (WHO, 2000). However, BMI does not discriminate between muscle and adipose tissue and does not directly assess regional adiposity (Stevens et al., 2008). Still, BMI primarily due to its simplicity often serves a guide in treatment selection. Regional fat distribution has a profound influence on health risks. In general, measures of fat distribution such as waist circumference and sagittal abdominal diameter are more highly correlated with cardiovascular disease risk factors and diabetes than BMI (Stevens et al., 2008). It appears that the typical male (android) or visceral obesity is closely associated with metabolic complications such as hypertension, insulin resistance, hyperuricemia, and dyslipoproteinemia. The typical female or gynecoid obesity, with fat deposited in hips, femoral and gluteal regions, has much less metabolic consequences. The waist-to-hip ratio has been used to determine these forms of obesity. A ratio above 1.0 in male subjects and above 0.6 in women suggests an undesirable obesity pattern (Krotkiewski et al., 1983). Fig. (1). Apple and pear shape weight comparison (American Cancer Society) 1.3 Causes of Obesity Although there are genetic, behavioral and hormonal influences on body weight, obesity occurs when you take in more calories than you burn through exercise and normal daily activities. Your body stores these excess calories as fat. Obesity can sometimes be traced to a medical cause, such as Prader-Willi syndrome, Cushing's syndrome, and other diseases and conditions (Bray GA., 2015). However, these disorders are rare and, in general, the principal causes of obesity are: i. Inactivity. If you're not very active, you don't burn as many calories. With a sedentary lifestyle, you can easily take in more calories every day than you use through exercise and normal daily activities. ii. Unhealthy diet and eating habits. Weight gain is inevitable if you regularly eat more calories than you burn. And most Americans' diets are too high in calories and are full of fast food and high-calorie beverages. Fig. (2). Demonstrating sedentary life style (American Cancer Society) 1.4 Mechanism of action of Obesity Central Obesity, Insulin Resistance and Comorbidities – Mechanisms of Association It is uncertain how obesity results in insulin resistance; however, several factors have been implicated as playing a pivotal role, as described in the following paragraphs and figure below: Insulin plays a vital role in the control of adipose tissue development and function. Insulin not only regulates lipogenesis but also the rate of lipolysis and NEFA efflux. Insulin control glucose uptake and causes fatty acid transport, translocation and enhanced fatty acid uptake in adipocytes (Stahl et al., 2002). Insulin inhibit basal and catecholamine stimulated lipolysis through phosphorylation via ser/thr protein kinase B(PKB) dependent action and activation of type 3 B phosphodiesterase (PDE-3B), leading to a decreased cAMP level, that prevent HSL activation. Insulin induced anti-lipolysis and activation of NEFA re-esterification are bunted in omental compared to subcutaneous fat cells. Various functional deference has been identified at the receptor level and the post receptor level of insulin signaling cascade. Other substances possibly playing a role in lipolytic pathways are a trial antiuretic peptide (ANP), growth hormone (GH) and miscellaneous agents such as nitric oxide (NO). ANP stimulation of human fat cells activates cyclic GMP (cGMP)-dependent protein kinase (cGK-I type), which phosphorylates perilipin and HSL, thus explaining lipolytic action (Sengenes et al., 2002). Although GH treatments in adults reduce visceral obesity and affect insulin sensitivity, the physiological contribution of GH to the control of human adipose tissue in lipid mobilization remains elusive (Lafontan et al., 2005). GH dependent modification of the relationship between adenylyl cyclase and Gi Protein removes inhibition of cAMP production and consequently increases lipolysis (Yip et al., 1999). NO or related redox. Fig. (3). Energy balance and etiology of obesity. Energy balance and etiology of obesity .Energy balance is determined by the interplay between food intake, energy expenditure and energy storage. Obesity is a multifactorial disorder resulting from combination of several environmental and genetic factors. Reduction in physical activity, metabolic rate and thermo genesis eventually decrease energy expenditure leading to increased energy storage and obesity. Availability of palatable food as well as hypothalamic injury and different drugs stimulate food intake. A growing list of genetic factors including dysmorphic syndromes, leptin/receptor mutation, _-3 AR mutation and over expression of NPY contribute to development of obesity. Fig.(4). Physiologic regulation and metabolic effects of leptin and adiponectin. Leptin is a peptide hormone that provides signals to the brain about the amount of fat stores and is secreted mainly by the adipose tissue (Strosberg et al.,2009). Leptin is found in the blood of normal mice but not of genetically obese ob/ob mice. If recombinant leptin is injected into the third or the lateral ventricle of the ob/ob mouse, it reduces food intake and weight gain, acting on neural networks of the brain involved in the control of food intake and energy expenditure. In addition, leptin increases the level of activity in the recipient mice, normalizes body temperature and restores reproductive function. Leptin mRNA is expressed exclusively in fat cells. The concentration of leptin in the circulation is proportional to fat stores and BMI in normal subjects and its secretion is pulsatile and inversely related to hydrocortisone levels (G. Frühbeck et al., 1998). The generation of leptin is enhanced by glucocorticoids, estrogens and insulin and is reduced by

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