Assessment of Obesity

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Chapter: Biochemistry : Obesity

Because the amount of body fat is difficult to measure directly, it is usually determined from an indirect measure, the body mass index (BMI), which has been shown to correlate with the amount of body fat in most individuals.


Because the amount of body fat is difficult to measure directly, it is usually determined from an indirect measure, the body mass index (BMI), which has been shown to correlate with the amount of body fat in most individuals. [Note: Exceptions are athletes who have large amounts of lean muscle mass.] Measuring the waist size with a tape measure is also used to screen for obesity, because this measurement reflects the amount of fat in the central abdominal area of the body. The presence of excess central fat is associated with an increased risk for morbidity and mortality, independent of the BMI. [Note: A waist size ≥ 40 inches in men and ≥ 35 inches in women is considered a risk factor.]


A. Body mass index

The BMI (weight in kg)/(height in meters)2 provides a measure of relative weight, adjusted for height. This allows comparisons both within and between populations. The healthy range for the BMI is between 18.5 and 24.9. Individuals with a BMI between 25 and 29.9 are considered overweight, those with a BMI equal to or greater than 30 are defined as obese, and a BMI over 40 is considered extremely obese. Anyone more than 100 pounds overweight is considered severely (morbidly) obese (Figure 26.1). These cutoffs are based on the studies examining the relationship of BMI to premature death and are similar in men and women. Nearly two thirds of American adults are overweight, and more than one third of those are obese.

Figure 26.1 Body mass index (BMI) Chart. To use the BMI Chart, find height in the lefthand column. Move across the row to weight. Height and weight intersect at the individual’s BMI. [Note: To calculate BMI using inches and pounds, use BMI = [weight in pounds/ (height in inches)2] x 703.


B. Anatomic differences in fat deposition

The anatomic distribution of body fat has a major influence on associated health risks. A waist-to-hip ratio of more than 0.8 for women and more than 1.0 for men is defined as android, “apple-shaped,” or upper body obesity, and is associated with more fat deposition in the trunk (Figure 26.2A). In contrast, a lower waist/hip ratio reflects a preponderance of fat distributed in the hips and thighs and is called gynoid, “pear-shaped,” or lower body obesity. It is defined as a waist/hip ratio of less than 0.8 for women and less than 1.0 for men. The pear shape, more commonly found in women, presents a much lower risk of metabolic disease, and some studies indicate that it may actually be protective. Thus, the clinician can use simple indices of body shape to identify those who may be at higher risk for metabolic diseases associated with obesity.

About 80%–90% of the fat stored in the human body is in subcutaneous depots, just under the skin, in the abdominal (upper body) and the gluteal-femoral (lower body) regions. In addition, 10%–20% of body fat is stored in so-called visceral depots (omental and mesenteric), which are located within the abdominal cavity in close association with the digestive tract (Figure 26.2B). Excess fat in visceral and abdominal subcutaneous stores increases health risks associated with obesity.

Figure 26.2 A. Individuals with upper body obesity (left) have greater health risks than individuals with lower body obesity (right). B. Visceral fat is located inside the abdominal cavity, packed in between the internal organs. Subcutaneous fat is found underneath the skin.


C. Biochemical differences in regional fat depots

The regional types of fat described above are biochemically different. Subcutaneous adipocytes from the lower body (gluteal-femoral), particularly in women, are larger, very efficient at fat (triacylglycerol [TAG]) deposition, and tend to mobilize fatty acids more slowly than those from the abdominal subcutaneous depots. Visceral adipocytes are the most metabolically active. Both abdominal subcutaneous and visceral depots of obese subjects have high rates of lipolysis and contribute to increased availability of free fatty acids (FFAs). These metabolic differences may contribute to the higher risk found in individuals with upper body obesity.


1. Endocrine function: White adipose tissue, once thought to be a passive reservoir of TAGs, is now known to play an active role in body weight regulatory systems. For example, the adipocyte is an endocrine cell that secretes a number of protein regulators, such as the hormones leptin and adiponectin. Leptin regulates appetite as well as metabolism. Adiponectin reduces levels of FFAs in the blood and has been associated with improved lipid profiles, increased insulin sensitivity resulting in better glycemic control, and reduced inflammation in diabetic patients. [Note: Adiponectin levels decrease as body weight increases, and leptin levels increase.]


2. Importance of portal circulation: With obesity, there is increased release of FFAs and secretion of proinflammatory cytokines, such as interleukin 6 (IL-6), from adipose tissue. [Note: Cytokines are small proteins that regulate the immune system.] One reason that visceral and abdominal adipose depots may have such a large influence on metabolic dysfunction in obesity is that the FFAs and cytokines released from these depots enter the portal vein and, therefore, have direct access to the liver. In the liver, they may lead to insulin resistance and increased hepatic synthesis of TAGs, which are released as components of very-low-density lipoprotein particles and contribute to the hypertriacylglycerolemia associated with obesity. By contrast, FFAs from lower body subcutaneous adipose depots enter the general circulation, where they can be oxidized in muscle and, therefore, reach the liver in lower concentration.


D. Size and number of fat cells

As TAGs are stored, adipocytes can expand to an average of two to three times their normal volume. (Figure 26.3). However, the ability of a fat cell to expand is limited. With prolonged overnutrition, preadipocytes within adipose tissue are stimulated to proliferate and differentiate into mature fat cells, increasing the number of adipocytes. Thus, most obesity is due to a combination of increased fat cell size (hypertrophy) and number (hyperplasia). Like other tissues, the adipose tissue undergoes continuous remodeling. Contrary to early dogma, we now know that adipocytes can die. The estimated average lifespan of an adipocyte is 10 years.

 Obese individuals can have up to five times the normal number of fat cells. If excess calories cannot be accommodated within adipose tissue, the excess fatty acids “spill over” into other tissues, such as muscle and liver. The amount of this so-called “ectopic fat” is strongly associated with insulin resistance. With weight loss in an obese individual, the size of the fat cells is reduced, but the number of fat cells is not usually affected. Thus, a normal body fat is achieved by decreasing the size of the fat cell below normal. Small fat cells are very efficient at reaccumulating fat, and this may drive appetite and weight regain.

Figure 26.3 Hypertrophic (increased size) and hyperplastic (increased number) changes to adipocytes are thought to occur in severe obesity.

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