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The prevalence of obesity and severe obesity continues to increase in the developed world. Apart from obesity's strong association with a variety of health conditions, severely obese individuals (i.e. > or = 300 lb [136 kg]) sometimes have difficulty with ambulation, and often cannot use regular sized clothes, furniture, and assistive devices such as walkers and wheelchairs. The purpose of this study was to assess the relationship between linear body measurements (anthropometry) and weight in severely obese people in order to generate equations to predict such measurements from weight alone. Various body size measurements were obtained from three independent data sets (74 severely obese individuals evaluated at the New York Obesity Research Center, 103 severely obese individuals who participated in the National Center for Health Statistics' National Health and Nutrition Examination Survey III, and a further 90 severely obese individuals evaluated at the New York Obesity Research Center). Linear regression analyses revealed that for each increase of 10 kg (22.04 lb) above 136 kg (300 lb), body diameter measurements increase by 0.9-1.1 cm. These analyses provide body size-to-weight estimates that may help manufacturers develop products and services that are more appropriate for increasing numbers of severely obese individuals.

Visceral obesity is associated with resistance to the antilipolytic effect of insulin in vivo. We investigated whether subcutaneous abdominal and gluteal adipocytes from viscerally obese women exhibit insulin resistance in vitro. Subjects were obese black and white premenopausal nondiabetic women matched for visceral adipose tissue (VAT), total adiposity, and age. Independently of race and adipocyte size, increased VAT was associated with decreased sensitivity to insulin's antilipolytic effect in subcutaneous abdominal and gluteal adipocytes. Absolute lipolytic rates at physiologically relevant concentrations of insulin or the adenosine receptor agonist N(6)-(phenylisopropyl)adenosine were higher in subjects with the highest vs. lowest VAT area. Independently of cell size, abdominal adipocytes were less sensitive to the antilipolytic effect of insulin than gluteal adipocytes, which may partly explain increased nonesterified fatty acid fluxes in upper vs. lower body obese women. Moreover, increased VAT was associated with decreased responsiveness, but not decreased sensitivity, to insulin's stimulatory effect on glucose transport in abdominal adipocytes. These data suggest that insulin resistance of subcutaneous abdominal and, to a lesser extent, gluteal adipocytes may contribute to increased systemic lipolysis in both black and white viscerally obese women.

Although independent associations of visceral fat with the insulin resistance syndrome were previously reported in obese women, the importance of truncal subcutaneous fat in this syndrome is controversial. The method by which the various fat depots are measured may be the reason for the underlying controversy. In the past five years, we have used various methods to measure visceral versus subcutaneous fat distribution in Caucasian (C) and African-American (AA) women and have related it to insulin sensitivity (SI) and to blood lipids, particularly fasting serum triglyceride levels (TG). Elevated TG levels in obese women were best predicted by an increased amount of visceral fat, whereas the amounts of truncal and peripheral subcutaneous fat did not have an impact on them. These results were confirmed, regardless of the method used to measure the fat depots. Insulin resistance (low SI) in obese women was predicted by both an increase of visceral and of upper-body (truncal) subcutaneous fat. However, measurements of the entire visceral and truncal subcutaneous fat volumes may be needed to confirm this latter association.

This study was designed to determine the role of visceral adipose tissue (VAT) accumulation in systemic fat metabolism and to compare this in black and white women who differ in their manifestations of upper body obesity. Systemic glycerol and free fatty acid (FFA) turnover rates (rates of appearance, Ra) were measured in the basal state and during a pancreatic euglycemic clamp in nondiabetic, premenopausal, obese black and white women with a wide range of VAT accumulation. The slopes of the regression equations predicting basal and insulin-suppressed RaGlycerol and RaFFA from VAT area, age, and fat mass or fat-free mass did not significantly differ between black and white women. VAT area was the best predictor of the %-suppressed RaGlycerol and RaFFA during the pancreatic clamp (partial r = 0.76, P < 0.0001 and partial r = 0.60, P < 0.05, respectively). Basal R(a)Glycerol, but not RaFFA, was lower in black than in white women (P < 0.05). During the clamp, black women showed greater insulin suppression of RaGlycerol than of RaFFA (P < 0.0001) and greater insulin suppression of RaGlycerol (P < 0. 05) but similar suppression of RaFFA compared with white women. These differences were independent of age, fat mass, or fat-free mass and were partly explained by a lower VAT in black women. Thus, in both races, VAT accumulation was associated with systemic resistance to the antilipolytic effect of insulin and, in obese black women, systemic lipolysis measured as glycerol turnover rate was more responsive to insulin suppression than were systemic FFA turnover rates.

Although independent associations of visceral fat with the insulin resistance syndrome were previously reported in obese women, the importance of truncal subcutaneous fat with regard to insulin sensitivity is still controversial. We measured the insulin sensitivity index (S(I)), serum triglyceride (TG) level, and regional fat by two methods: (1) the sum of five truncal and four peripheral skinfolds (TrSUM and PerSUM) in 38 white and black obese nondiabetic premenopausal women, and (2) abdominal visceral (VFM) and subcutaneous fat mass (AbdSCFM) by a combination of magnetic resonance imaging (MRI) and dual x-ray absorptiometry (DXA) in a subset of 26 of these women. After adjusting for the total body fat mass, TrSUM and VFM were independently and negatively related to S(I) (n = 38, P < .012 and n = 26, P < .035, respectively), whereas PerSUM and AbdSCFM were not related (P > .50). Based on multiple regression modeling, TrSUM significantly predicted S(I) independently of the VFM (n = 26, P < .001). Black women had lower S(I) at all levels of TrSUM (n = 38, P = .061 for the slope and P = .03 for the intercept of the regression lines). After adjusting for the total body fat mass, only VFM showed an independent positive relation to serum TG, and race did not affect this relationship (n = 26, P < .001). In conclusion, (1) we confirmed the independent association of the VFM with insulin resistance and elevated TG in obese women; (2) the AbdSCFM measured by a combination of MRI and DXA did not show an independent association with S(I) in obese women; and (3) the independent association of TrSUM with S(I) suggests that truncal subcutaneous fat depots contribute to insulin resistance in obese women independently of the degree of visceral fat.

Our previous finding that a waist-to-hip ratio (WHR) >0.85 was not associated with similar health risks in black, compared with white, obese premenopausal non-diabetic women of similar fatness is attributed to either 1) a different relationship between WHR and visceral adiposity or 2) differences in the relationship between visceral adiposity and the metabolic abnormalities of obesity. We measured visceral (VAT) and subcutaneous adipose tissue (SCAT) areas at midwaist in 25 black and 25 white obese nondiabetic pre-menopausal women with similar BMI, percentage body fat, and wide range of WHR (0.7-0.95 for black women and 0.7-0.9 for white women) and then compared insulin sensitivity index (SI), glucose and insulin areas under the 2-h curve (AUCs) during an oral glucose tolerance test (OGTT), and blood lipids in the two groups before and after adjustments for total body and visceral adiposity. After adjusting for total body fat mass (FM), obese black women had significantly less VAT (by 32 cm2) and lower VAT/SCAT for any given WHR. The regression equations predicting the SI the glucose and insulin AUCs, and the triglyceride and HDL cholesterol levels from regional adipose tissue measurements (VAT, SCAT, or VAT/SCAT) and from total body fat (FM or percentage body fat) had slopes that were not significantly different for black and white women. LDL cholesterol levels were independently related to VAT in black but not in white women. The black women had a similar SI insulin AUC, and triglyceride levels but significantly lower glucose AUC and higher HDL cholesterol levels (P < 0.001), after adjusting for VAT and FM. Regression analysis of the pooled data showed that high VAT and high VAT/SCAT, but not SCAT, predicted lower SI higher glucose and insulin AUCs during OGTT, and higher triglyceride levels, independent of total adiposity. We conclude that while increases in VAT and VAT/SCAT adversely affect metabolism in both black and white obese premenopausal women, similar levels of total body and visceral adiposity are associated with different metabolic risk factors in these groups.