Body Fat Distribution

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The traditional view of adipose tissue is simply a reservoir for desposition of excess calories only has not been valid for years. It is very true that adipocytes serve as a major tissue for energy storage and there is

Table 3.2 Medical

complications associated with obesity. From reference 1, with permission

Gastrointestinal

Gallstones, pancreatitis, abdominal hernia, NAFLD* (steatosis, steatohepatitis, and cirrhosis), and possibly GERDf

Endocrine/metabolic

Metabolic syndrome, insulin resistance, impaired glucose tolerance, type 2 diabetes mellitus, dyslipidemia, polycystic ovary syndrome

Cardiovascular

Hypertension, coronary heart disease, congestive heart failure, dysrhythmias, pulmonary hypertension, ischemic stroke, venous stasis, deep vein thrombosis, pulmonary embolus

Respiratory

Abnormal pulmonary function, obstructive sleep apnea, obesity hypoventilation syndrome

Musculoskeletal

Osteoarthritis, gout, low back pain

Gyneoco logic

Abnormal menses, infertility

Genitourinary

Urinary stress incontinence

Ophthalmologic

Cataracts

Neurologic

Idiopathic intracranial hypertension (pseudotumor cerebri)

Cancer

Esophagus, colon, gallbladder, prostate, breast, uterus, cervix, kidney

Postoperative events

Atelectasis, pneumonia, deep vein thrombosis, pulmonary embolus

'Non-alcoholic fatty liver disease; gastroesophageal reflux disease

'Non-alcoholic fatty liver disease; gastroesophageal reflux disease

Insulin Resistance Images
Figure 3.3 Relationship of insulin sensitivity to body mass index. With increasing obesity as assessed by the increase in BMI, obese individuals are characterized as insulin resistant, whereas lean individuals with BMI <25 may be markedly insulin sensitive. From reference 7, with permission

a growing science demonstrating that size, differentiation, and secretions from the adipocyte are all important functions8-10 (Figure 3.4).

Individuals who are obese and have a high concentration of visceral adipose tissue tend to have dyslipi-demia in the form of elevated levels of triglycerides and decreased levels of high-density lipoprotein cholesterol (HDL-C), which place them at higher risk for cardiovascular disease. As obesity is a major factor to increase metabolic risk, the relevancy of managing obesity to prevent and/or ameliorate chronic diseases such as cardiovascular disease and type 2 diabetes is undeniable11.

The body weight and BMI have served an important purpose in stratifying individuals at high risk. However, the assessment of the specific distribution of the body fat may be considered an even more important assessment. In past studies, body fat distribution has been generally assessed by anthropometric measurements consisting of waist circumference, the waist-to-hip ratio (WHR), or skin fold thicknesses (Figure 3.5). When using skin fold measures, the most commonly utilized has been the subscapular-to-triceps ratio, or a sum of central-to-peripheral skinfolds12. Regardless of which is utilized, these measures are used to classify the subject as having either upper body, i.e. 'central' or abdominal obesity, or lower body obesity. In lay terms, these body types have been referred to as the 'apple-' or 'pear-shape' phenotypes (Figure 3.6). Abdominal adiposity, in addition to being significantly associated with the metabolic abnormalities that constitute the cardiometabolic syndrome, is

Large insulin-resistant adipocytes

Adrenergic receptors |

Insulin-mediated antilipolysis

Catecholamine-mediated lipolysis |

Insulin Resistance Images

Small insulin-sensitive adipocytes

Adrenergic receptors

Small insulin-sensitive adipocytes

Adrenergic receptors

Fatty acids |

Figure 3.4 There is strong evidence suggesting adipose tissue has a central role in contributing to insulin resistance. New evidence suggests that insulin resistance is partly the result of the inability of the adipose organ to expand to accommodate excess calories. Increased fat cell size may represent the failure of the adipose tissue mass to expand, i.e. proliferate and differentiate, resulting in a reduced ability to accommodate an increased energy influx. When combined with reduced fat oxidation in adipose tissue, these pathophysiologic changes will contribute to a decrease in fat storage in adipocytes and an increase peripheral deposition of lipids in tissues, i.e. increased 'ectopic fat'. Individuals who have a low capacity for proliferation and/or differentiation of precursors into mature fat-storing adipocytes are susceptible to hypertrophy of the existing adipocytes under conditions of energy excess. Thus, adipocyte hypertrophy (i.e. large fat cells) is indicative of a failure to proliferate and/or differentiate; a failure to accommodate an increased energy flux resulting in ectopic (intracellular) storage in sites such as muscle, liver and pancreas; and correlates better with insulin resistance than with any other measure of adiposity. Courtesy of Center for Obesity Research and Education

Insulin Resistance Images

Figure 3.5 Visceral adiposity: the critical adipose depot. Epidemiologic and metabolic studies conducted over the past 15 years have noted that complications frequently found in obese patients appear to be associated with the location of excess fat rather than to excess weight per se, specifically abdominally distributed obesity. The patient with abdominal obesity, or excess visceral adipose tissue, has a high cardiometabolic risk. A simple and practical screening tool such as a measurement of the waist circumference can be used to assess risk by monitoring the accumulation or loss of visceral fat between office visits. Courtesy of Center for Obesity Research and Education

Figure 3.5 Visceral adiposity: the critical adipose depot. Epidemiologic and metabolic studies conducted over the past 15 years have noted that complications frequently found in obese patients appear to be associated with the location of excess fat rather than to excess weight per se, specifically abdominally distributed obesity. The patient with abdominal obesity, or excess visceral adipose tissue, has a high cardiometabolic risk. A simple and practical screening tool such as a measurement of the waist circumference can be used to assess risk by monitoring the accumulation or loss of visceral fat between office visits. Courtesy of Center for Obesity Research and Education

Insulin Resistance Images
Figure 3.6 Schematic demonstrating use of anthropometric measures such as waist-to-hip ratio (WHR) in classifying central or upper-body (abdominal) obesity ('apple-shaped') versus lower-body peripheral obesity ('pear-shaped')
Insulin Resistance Images
Age (years)

Figure 3.7 Risk of diabetes mellitus during 13 years in relation to WHR at baseline. Comparison between risk in upper and lower 10% of WHR distribution. From reference 16, with permission also considered to be a significant risk factor for coronary heart disease in both men and women14-16. There is disagreement, however, between some investigators, whether this relationship holds after adjusting for total adiposity, as measured by BMI. It has been shown, however, that use of a very easily measured clinical tool such as waist circumference or WHR appears to be highly associated with development of type 2 diabetes (Figure 3.7 and Table 3.3). As it relates to cardiovascular mortality, there appears to be significant evidence that although obesity per se is well recognized to be a major risk factor for coronary heart disease in both men and women, several lines of evidence suggest that measures of regional fat distribution are independently associated with risk of cardiovascular disease (Table 3.3 and Figure 3.8).

In the recent past, more sophisticated techniques, such as computed tomography (CT) or magnetic resonance imaging (MRI) scans, have been utilized to assess central obesity. The advantage of these techniques is apparent in that specific and precise quantification of abdominal fat depots can be readily assessed (Figure 3.9)12,13. Specifically, with use of these techniques, the amount of visceral or intraabdominal fat can be compared with the amount of

Table 3.3 The use of waist sizes in both men and women were highly associated with disease risk. Specifically, a waist circumference of 40 inches, as opposed to 37 inches, in men was associated with a 4-fold greater risk for development of type 2 diabetes and a 3—4-fold greater risk for any cardiovascular event. Similar findings were noted for women comparing waist circumference of 34 inches versus 31 inches. Data from reference 17, with permission

Men: waist size >40 vs. < 37 inches Women: waist size > 34 vs. < 31 inches 4-fold greater risk for type 2 diabetes 3- to 4-fold greater risk for major cardiovascular event subcutaneous fat at the same level or 'cut' of the scan12. As such, it is now possible to appreciate the differences in fat depots in the abdominal area (Figure 3.10). Using these techniques, the relationship between fat distribution, e.g. visceral fat depots, and peripheral muscle insulin resistance has been shown to be highly correlated in both men and women (Figures 3.11-3.13)19-21. The pathophysiologic basis as to why central obesity, and particularly visceral fat,

Waist circumference tertiles (cm) | Low (38.1 —< 73.7) | Middle (73.7-< 81.8) | High (8l.8-< 139.7)

High (25.2-< 48.8) Middle (22.2-< 25.2) Low (l2.2-< 22.2)

Body mass index tertiles (kg/m2)

120-

100-

Waist circumference tertiles (cm) | Low (< 91.4) | Middle (9l.4-< 99.1) | High (a 99.1)

Body mass index tertiles (kg/m2)

Figure 3.8 Age-adjusted incidence rates for coronary heart disease according to body mass index and waist circumference ter-tiles for women (a) and men (b), and according to body mass index and waist-to-hip ratio tertiles for women (c) and men (d). Adapted from references 14 and 15, with permission

Waist-to-hip ratio tertiles | | Low (0.37-0.75) | Middle (0.75-< 0.80) High (0.80-< 1.90)

High (25.2-< 48.8) Middle (22.2-< 25.2) Low (l2.2-< 22.2)

Body mass index tertiles (kg/m2)

Waist-to-hip ratio tertiles I Low (< G.92) I Middle (G.92-< G.96) I High (a G.96)

Body mass index tertiles (kg/m2)

Figure 3.8 Continued

Insulin Resistance ImagesInsulin Resistance Images
Figure 3.9 (a) Schematic demonstrating abdominal fat depots that can be measured using NMR or CT scans. (b) Scan showing subcutaneous fat and visceral fat patterning. Courtesy of Dr Steven Smith, from reference 13, with permission
Visceral Fat Cat Scan

VF = 76 cm2; SF = 391cm2; DSF = 201cm2; SSF = 190 cm2

VF = 76 cm2; SF = 391cm2; DSF = 201cm2; SSF = 190 cm2

Insulin Resistance Images

VF = II4 cm2; SF = 530 cm2; DSF = 262 cm2; SSF = 268 cm2

Figure 3.10 Magnetic resonance imaging (MRI) of distribution of abdominal fat demonstrating transverse cross-sectional magnetic resonance image at the L4-6 vertebral level. The various abdominal fat depots, i.e. visceral fat, subcutaneous fat areas, abdominal deep and superficial subcutaneous fat areas can be appreciated. The fascia (arrows) separating the superficial subcutaneous and deep subcutaneous depots is easily visualized. Despite similar body mass index (BMI) measurements for the male (a), and female (b) subjects, there are significant differences in abdominal fat distribution. BW, body weight; VF, visceral fat; SF, superficial fat; DSF, deep subcutaneous fat; SSF, superficial subcutaneous fat. From reference 18, with permission

Body Fat Distribution
Figure 3.11 Relationship between visceral adipose tissue and skeletal muscle insulin action in both men and women. LBM, lean body mass. From reference 19, with permission
Insulin Resistance Images

Figure 3.12 Relationship between aging and accumulation of visceral fat. As shown in left panel, this study evaluated both men and women through seven decades. There appeared to be no significant increase in BMI with age for either men or women in this cohort. However, as seen in the right panel, intra-abdominal fat, expressed per kg of body weight, was significantly association with aging in this cohort. The data does suggest redistribution of body fat associated with the aging process. From reference 20 with permission

Figure 3.12 Relationship between aging and accumulation of visceral fat. As shown in left panel, this study evaluated both men and women through seven decades. There appeared to be no significant increase in BMI with age for either men or women in this cohort. However, as seen in the right panel, intra-abdominal fat, expressed per kg of body weight, was significantly association with aging in this cohort. The data does suggest redistribution of body fat associated with the aging process. From reference 20 with permission

Insulin Resistance Images

Figure 3.13 Insulin sensitivity is related to intra-abdominal fat accumulation regardless of age or gender. In this study, individuals ranging in age from 20 to 80 years had visceral fat assessed by magnetic resonance imaging and had insulin sensitivity assessed by the modified minimal model. As shown, the greater the visceral fat, the lower the insulin sensitivity. From reference 19, with permission

Figure 3.13 Insulin sensitivity is related to intra-abdominal fat accumulation regardless of age or gender. In this study, individuals ranging in age from 20 to 80 years had visceral fat assessed by magnetic resonance imaging and had insulin sensitivity assessed by the modified minimal model. As shown, the greater the visceral fat, the lower the insulin sensitivity. From reference 19, with permission

Insulin resistance

| Constriction i Relaxation

Vasculature

i Glucose uptake

Insulin resistance

Glucose release

Insulin Resistance Images

Figure 3.14 Central obesity and insulin resistance are integrally related. There are several possible links between adipose tissue function and insulin resistance determined in other organs such as skeletal muscle or liver. One such link is the regulation of free fatty acid delivery to peripheral tissues. It has been suggested that an expanded adipose tissue mass delivers more free fatty acids to the systemic circulation and to the peripheral tissues. These fatty acids are proposed to compete for substrate utilization in skeletal muscle, which in turn reduces glucose utilization. This increases blood glucose concentration and provides the stimulus for increased insulin secretion and hyperinsulinemia which is a key feature of the insulin-resistance syndrome. Courtesy of Center for Obesity Research and Education

I TG

| Insulin secretion

Figure 3.14 Central obesity and insulin resistance are integrally related. There are several possible links between adipose tissue function and insulin resistance determined in other organs such as skeletal muscle or liver. One such link is the regulation of free fatty acid delivery to peripheral tissues. It has been suggested that an expanded adipose tissue mass delivers more free fatty acids to the systemic circulation and to the peripheral tissues. These fatty acids are proposed to compete for substrate utilization in skeletal muscle, which in turn reduces glucose utilization. This increases blood glucose concentration and provides the stimulus for increased insulin secretion and hyperinsulinemia which is a key feature of the insulin-resistance syndrome. Courtesy of Center for Obesity Research and Education sc attenuates insulin action has been a topic of great debate. It has also been suggested that the association between abdominal fat and insulin resistance does not prove causality, as it is possible that environmental, biological, or inherited factors that induce insulin resistance also cause abdominal fat accumulation. Nonetheless, it has been proposed that alterations in fatty acid metabolism associated with abdominal obesity may be responsible for the attenuation in insulin action because excessive circulating free fatty acids (FFAs) inhibit the ability of insulin to stimulate muscle glucose uptake and to suppress hepatic glucose production. As such, the notion of a link between abdominal fat, FFA metabolism, and insulin resistance is supported by the observation that basal whole-body FFA flux rates are greater in upper-body obese than in lower-body obese and lean subjects and that diet-induced weight loss decreases whole-body FFA flux and improves insulin sensitivity (Figures 3.14 and 3.15). Furthermore, the adipose tissue excess, particularly in the visceral compartment, is associated with other co-morbidities including dyslipidemia, hypertension, prothrombotic and proinflammatory states.

Finally, the most recent data regarding the significance of obesity stem from the findings that adipose tissue acts not only as a passive reservoir for energy storage, but also serves as a well known endocrine organ8. Specifically, adipose tissue has been shown to express and secrete a number of bioactive proteins referred to as adipocytokines in addition to expressing numerous receptors that allow it to respond to different hormonal signals (Figure 3.16). Thus, in addition to its function to store and release energy, adipose tissue is able to communicate metabolically with other organ systems, and in this way, contributes significantly

Ve nous circulation

Lean 78% Obese 60%

Arterial circulation

Ve nous circulation

Arterial circulation

Increased Risk Intra Abdominal Fat

Figure 3.15 It is well established that excessive visceral fat is associated with insulin resistance and other co-morbidities associated with increasing cardiometabolic risk. Furthermore, increased plasma fatty acid concentrations have been postulated to contribute greatly to the metabolic abnormalities associated with abdominal obesity. Visceral fat has been suggested to be more harmful than excess subcutaneous fat, because lipolysis of visceral adipose tissue triglycerides releases free fatty acids (FFAs) into the portal vein, which are then delivered directly to the liver. This schematic demonstrates the approximate relative contributions of FFAs released from lower- and upper-body subcutaneous fat depots and from splanchnic tissues to the systemic venous circulation, and FFAs from visceral fat and the systemic arterial circulation to the portal circulation in lean and obese subjects. From reference 21 with permission

Upper-body subcutaneous fat

Lower-body subcutaneous fat

Visceral fat

Figure 3.15 It is well established that excessive visceral fat is associated with insulin resistance and other co-morbidities associated with increasing cardiometabolic risk. Furthermore, increased plasma fatty acid concentrations have been postulated to contribute greatly to the metabolic abnormalities associated with abdominal obesity. Visceral fat has been suggested to be more harmful than excess subcutaneous fat, because lipolysis of visceral adipose tissue triglycerides releases free fatty acids (FFAs) into the portal vein, which are then delivered directly to the liver. This schematic demonstrates the approximate relative contributions of FFAs released from lower- and upper-body subcutaneous fat depots and from splanchnic tissues to the systemic venous circulation, and FFAs from visceral fat and the systemic arterial circulation to the portal circulation in lean and obese subjects. From reference 21 with permission

Adipocyte-derived proteins

Receptors expressed in adipose tissuse

Leptin

^ Insulin receptor

Tumor necrosis factor-a (TNF-a)

Glucagon receptor

Interleukin-6 (IL-6)

Growth hormone (GH) receptor

Monocyte chemoattractant protein-1 (MCP-1)

Thyroid stimulating hormone (TSH) receptor

Plasminogen activator inhibitor-1 (PAI-1)

Gastrin/cholecystokinin BN (CCK-B) receptor

Tissue factor

Glucagon-like peptide-I receptor

Adipsin (complement factor D)

Angiotensin II receptors type I and 2

Complement factor B

Glucocorticoid receptor

Acylation stimulating protein (ASP)

Vitamin D receptor

Adiponectin

Thyroid hormone receptor

Lipoprotein lipase (LPL)

Androgen receptor

Cholesterol ester transfer protein (CETP)

Estrogen receptor

Apolipoprotein E

Progesterone receptor

Non-esterified fatty acids (NEFAs)

Leptin receptor

Cytochrome P450-dependent aromatase

Interleukin-6 (IL-6) receptor

I7ß-hydroxysteriod dehydrogenase

Tumor necrosis factor-a (TNF-a) receptor

II ß-hydroxysteriod dehydrogenase-I

ß I, ß2, ß3 receptors

Angiotensin (AGT)

a I, a2 receptors

Resistin ._

Figure 3.16 Adipose tissue has been shown to express and secrete a number of bloactive proteins referred to as adipocytokines in addition to expressing numerous receptors that allow it to respond to different hormonal signals. Data from reference 8, with permission to biological processes that include energy metabolism, neuroendocrine, and immune function8.

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