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The ability of cells from the stromal-vascular fraction of rat brown adipose tissue to develop into adipocytes in primary cell cultures was investigated. Comparison was made with precursor cells isolated by the same procedure from the white adipose tissue of the same animals and cultured in parallel under identical conditions. The culture procedure used allowed the cells isolated from both tissues to rapidly proliferate and differentiate. During the first week in culture the brown fat cells grew to confluence and accumulated fat in a multilocular way. During the second week, further fat was accumulated, but the cells remained multilocular. Analysis of the parallel white fat cell cultures revealed clear differences between the two adipocyte types, although the rates of cell growth were identical. Measurement of the size of the cellular lipid inclusions as a function of the time in culture indicated a much higher number of fat droplets larger than 30 micron in the white adipocytes. Moreover, after isolation of pelleting fractions of both cultured cell types, comparative functional analysis of their mitochondria by oxygen consumption measurement, as well as direct cytochrome-c-oxidase determinations, showed a significantly higher amount of mitochondria in the brown fat cell fractions than in the white fat cell fractions. It was concluded that mature brown fat contains precursor cells which can proliferate and develop into adipocytes in monolayer cell culture and which have inherent characteristics distinct from those of white fat precursor cells.
The relationship of fat mass, lean body mass (LBM), and fat distribution to blood pressure was examined in Japanese adult men and women. Percent body fat was estimated using two skinfold thicknesses, and fat mass and LBM were then calculated. Correlation coefficients showed that fat mass, fat distribution, and age were weakly associated with blood pressure levels, and that the correlation coefficients of LBM to blood pressure levels were nearly zero. Stepwise regression analysis revealed that fat mass and age contributed significantly to the variations in blood pressure levels. In addition, only in the case of men, trunk-extremity skinfolds ratio was also entered into the model for diastolic and mean arterial blood pressure. It thus has been concluded that fat mass may be the more predictive determinant of blood pressure level than LBM in the Japanese population, and that the independent correlation of fat distribution to blood pressure is rather small.
Fat tissues consist of fat cells, capillaries, and collagen fibers. In order to completely suppress the signals from fat tissues in clinical magnetic resonance imaging, the signal from capillaries and collagen fibers as well as from fat cells should all be suppressed. We have previously reported that fat signal can be uniformly suppressed by applying an optimized presaturation pulse. The inhomogeneously broadened fat peak of tissue spectrum is excited by the optimized pulse and dephased by a subsequent field gradient. The broadened water peak is not affected. In this paper we discuss a technique that suppresses signals from fat tissues completely as well as uniformly. This technique is based on the cancellation of fat and water signals in the same image voxel by combining the optimized selective excitation with the opposite phase imaging technique. Experimental and clinical images demonstrate that the new technique improves the delineation and depiction of anatomy in clinical fat suppression imaging.
Partition coefficients, K(fat), from air to human fat and to rat fat have been collected for 129 volatile organic compounds, VOCs. A linear free energy relationship, LFER, correlates the 129 values of log K(fat) with R(2)=0.958 and a standard deviation, S.D., of 0.194 log units. Use of training and test sets gives a predictive assessment of around 0.20 log units. Combination of log K(fat) with our previously listed values of log K(blood) enables blood/plasma to fat partition coefficients, as log P(fat), to be obtained for 126 VOCs. These values can be correlated with R(2)=0.847, S.D.=0.304 log units; the latter is also our assessment of the predictive capability of the LFER. Values of log P(fat) have been collected for 46 drugs, and can be fitted to an LFER with R(2)=0.811 and S.D.=0.355 log units. Unlike partition into brain or muscle, the data for VOCs and drugs cannot be combined. There are marked discrepancies for PCBs for which partition from blood/plasma into fat is very much less than that calculated from the data on VOCs or from the data on drugs.
A Trp64Arg mutation in the beta3-adrenergic receptor gene has been implicated in the pathophysiology of non-insulin-dependent diabetes mellitus and obesity. However, the findings have been controversial due to the use of different populations and different methods for the estimation of body fat. In the present study, the prevalence of Trp64Arg mutation of the beta3-adrenergic receptor gene was determined and its relation to body fat as assessed by dual-energy x-ray absorptiometry (DEXA) was evaluated in Thai men and women. The effect on insulin sensitivity as assessed by the serum insulin to glucose ratio was also examined. The subjects were 76 men and 135 women aged 20 to 80 years. Body fat and its regional distribution were assessed by DEXA. Mutation in the beta3-adrenergic receptor gene was determined by polymerase chain reaction (PCR)-restriction fragment length polymorphism. Data are expressed as the mean +/- SEM. Fifty-nine subjects (28.0%) had the Trp64Arg mutation in the beta3-adrenergic receptor gene; 54 (25.6%) were heterozygotes and five (2.4%) were homozygotes. The gene frequency of Trp64Arg mutation was 15.2% in these subjects. In women, Trp64Arg mutation was not associated with the difference in total body fat (Trp/Arg or Arg/Arg, 19.4 +/- 1.0 kg; Trp/Trp, 19.2 +/- 0.6 kg) or percent body fat (Trp/Arg or Arg/Arg, 34.6% +/- 1.2%; Trp/Trp, 34.3% +/- 0.6%). In contrast to the findings in women, men with Trp64Arg mutation had lower total body fat after controlling for age (Trp/Arg or Arg/Arg, 13.2 +/- 1.1 kg; Trp/Trp, 15.8 +/- 0.7 kg; P < .05). However, no difference was found in percent body fat (Trp/Arg or Arg/Arg, 20.9% +/- 1.3%; Trp/Trp, 23.3% +/- 0.7%). No difference in the fasting insulin resistance index (FIRI) was found between subjects with and without Trp64Arg mutation. The data suggest that Trp64Arg mutation of the beta3-adrenergic receptor is common in Thais and appears to exert effects on total body fat but not percent body fat in men. Trp64Arg mutation is not associated with insulin resistance as assessed by the FIRI in Thais.
BACKGROUND: It has been clarified that visceral fat accumulation leads to atherosclerosis through multiple risk factors such as insulin resistance, glucose intolerance, hyperlipidemia and hypertension. So far, it has been reported that a thaizolidinedione derivative, troglitazone, improves the insulin resistance in subjects with diabetes, glucose intolerance and obesity. However, it has not been reported yet that troglitazone affects fat distribution in subjects concomitant with visceral fat accumulation and multiple risk factors. METHODS: Twenty-nine subjects with visceral fat accumulation who had at least two risk factors including glucose intolerance, hyperlipidemia and hypertension were investigated. They were randomly assigned to receive either 200 or 400 mg per day of troglitazone or placebo for 12 weeks. A 75 g oral glucose tolerance test (OGTT) was performed before and after the treatment for 12 weeks. Fasting plasma glucose, insulin, HbA(1c), total serum cholesterol (T-chol), triglyceride (TG), HDL-cholesterol (HDL-C), and blood pressure, as well as the number of risk factors were measured periodically during the treatment. The change of the abdominal fat distribution was evaluated using computed tomographic scanning (CT scan) at the umbilicus level. RESULTS: After the treatment for 12 weeks, the area under the curve (AUC) of plasma glucose from a 75 g OGTT decreased dose-dependently. HbA(1c) and TG decreased significantly in the high-dose troglitazone group (400 mg per day) compared with the placebo group (P<0.05). Systolic blood pressure was significantly lower in subjects with hypertension in the pooled troglitazone group than in the placebo group (P<0.05). Therefore, the number of risk factors decreased with the troglitazone treatment. The ratio of visceral fat area (VFA) to subcutaneous fat area (SFA) (V/S ratio) decreased in the troglitazone groups due to decreased VFA and increased SFA. CONCLUSION: These results suggest that thiazolidinedione derivative may be a useful drug to improve multiple risk factors by changing the fat distribution in subjects with visceral fat accumulation.
Milk fat globule membranes (MFGM) were isolated from milk from cows injected intraperitoneally with dl-alpha-tocopherol acetate. The fatty acid composition and content, and the contents of tocopherols, retinol and beta-carotene were determined and compared with the composition and content in the original cream sample. Intraperitoneal injection of 10 g dl-alpha-tocopherol acetate elevated the alpha-tocopherol content in the milk fat from 13-30 to 50-70 micrograms alpha-tocopherol/g milk fat 2-3 d after injection. The increase depended on the alpha-tocopherol status of the cow prior to injection. The concentrations of retinol and beta-carotene in the milk fat were unchanged after the alpha-tocopherol injections. MFGM fatty acids made up 18-27 g/kg total fatty acids in the milk fat. However, the proportions of monounsaturated and polyunsaturated fatty acids were higher in MFGM than in total milk fat, while the proportion of saturated fatty acids was lower in MFGM (P < 0.001). Thus, the long-chain polyunsaturated fatty acids in MFGM constituted approximately 40-70 g/kg total milk fat. alpha-Tocopherol was the only fat-soluble vitamin detected in MFGM; gamma-tocopherol, retinol and beta-carotene were detected only in the cream. A significant relationship between alpha-tocopherol contents in cream and MFGM was found: (alpha-tocopherol in MFGM fatty acids) = -1652 x (1/ln(alpha-tocopherol in cream fatty acids)3) + 97 (r = 0.857, P < 0.001) when the contents of alpha-tocopherol were expressed as microgram/g fatty acid. According to this equation the upper limit for incorporation of alpha-tocopherol into MFGM is 97 +/- 5 micrograms/g MFGM fatty acids. Thus, under normal farming conditions the alpha-tocopherol content will be highest in MFGM. However, in cream with an alpha-tocopherol concentration < 15 micrograms/g cream fatty acids the concentration in MFGM will be lower and furthermore will decrease rapidly. The possible importance of this relationship in relation to the oxidation of milk fat is discussed.
OBJECTIVE: The purpose of the present study was to determine the impact of body fat mass and fat distribution on serum lipids, lipoproteins and apolipoproteins in African-American and Caucasian-American prepubertal children. SUBJECTS: Study participants included 62 African-American children (age 8.3+/-1.4 y; body mass 37.3+/-13.6 kg; height 133+/-11 cm) and 39 Caucasian children (age 8.6+/-1.2 y; body mass 34.1+/-11.0 kg; height 131+/-9 cm). METHODS: Venous blood samples were obtained after a 12 h overnight fast and serum was analyzed for total cholesterol (TC), high-density lipoprotein-cholesterol (HDL-C), triacylglycerol (TAG), apolipoprotein A-I (ApoA-I), apolipoprotein B (ApoB) and lipoprotein (a) (Lp(a)) concentrations. Body composition and body fat distribution were measured by dual-energy X-ray absorptiometry and computed tomography, respectively. RESULTS: African-American children had lower TAG (46+/-20 vs 61+/-32 mg/dl, P=0.015) and higher Lp(a) (34+/-25 vs 17+/-28 mg/dl, P=0.001) and HDL-C (44+/-11 vs 39+/-8 mg/dl, P=0.041). There were no ethnic differences in TC, ApoA-I and ApoB (P=0.535, P=0.218, P=0.418, respectively). The ethnic difference in TAG and Lp(a) was not explained by total fat or abdominal fat. The ethnic difference in HDL-C was explained by visceral fat and TAG. CONCLUSION: In prepubertal children, neither body fat nor fat distribution explain the ethnic difference in TAG or Lp(a), but visceral fat and TAG may contribute to differences in HDL-C.
The efficacy of cross-sectional fat areas in estimating total body fat was investigated in a sample of white American children and adults. Body density and total fat weight (kg) in the body were determined by hydrostatic weighing. Fat areas were calculated for the arm and calf using the appropriate limb circumferences and skinfolds measured at the triceps, biceps, and calf sites; also, a fat area was calculated using the average of triceps and biceps sites and arm circumference. Cross-sectional fat areas do not estimate body density (and percentage fat) any better than the corresponding skinfolds. In estimating weight of fat in the body, however, fat areas are systematically better estimators than corresponding skinfold thicknesses.
An ultrasonographic unit (A-scan mode) has been evaluated as a noninvasive method for estimating body fat in 25 dogs. Six anatomical sites were defined and subcutaneous fat thickness was measured by means of ultrasound and histology. Total body fat was subsequently calculated in 12 dogs. There was a high correlation between histology and ultrasound for the measurement of subcutaneous fat (r = 0.81; P less than 0.001). Total body fat was successfully predicted using measurements taken with ultrasound at the lumbar area (r = 0.87; P less than 0.001). Measurements of subcutaneous fat thickness from other anatomical sites did not estimate body fat with the same accuracy. These results suggest that ultrasound can reliably measure subcutaneous fat in dogs and that these measurements, when taken from the mid lumbar area, can be used to predict total body fat.
OBJECTIVE: Body fat and its distribution are determinants of cardiovascular disease but the underlying mechanisms of these adverse effects are poorly understood. We therefore investigated (1) the cross-sectional relationship between estimates of body fatness and its distribution on the one hand and carotid atherosclerosis and stiffness of the carotid, femoral and brachial arteries and the carotido-femoral segment on the other (336 subjects, 175 women); (2) the relationship between estimates of body fatness and its distribution during adolescence (13-16 years) and the same arterial properties at age 36- prospective analyses (subpopulation of 159 subjects, 84 girls). DESIGN: Cross-sectional and prospective analyses within an ongoing observational longitudinal study: The Amsterdam Growth and Health Longitudinal Study. METHODS: Body fatness and its distribution were assessed by anthropometry and dual-energy X-ray absorptiometry (DXA); arterial properties were assessed non-invasively by ultrasound imaging. RESULTS: Total adiposity and, in men, truncal subcutaneous fat accumulation during adolescence, were positively and independently associated with carotid intima-media thickness at age 36, a pre-clinical indicator of atherosclerosis. Adolescent truncal subcutaneous fat accumulation but not total adiposity was associated with increased arterial stiffness at age 36. At age 36, both abdominal and truncal subcutaneous fat were independently associated with arterial stiffness, while the associations between total adiposity and arterial stiffness appeared to be mediated by other cardiovascular risk factors. CONCLUSIONS: Body fatness and body fat distribution are associated with large artery structural and functional properties at age 36 and the roots of these associations may already be present in adolescence.
Investigations have been carried out to explain the heterogeneity of response to catecholamines of human fat cells from various deposits. Adipocytes from two subcutaneous sites (abdominal and femoral) were studied concomitantly in women while omental fat cells were taken from another group of patients undergoing abdominal surgery. Alpha-2 and beta sites were identified in fat-cell membranes with [3H]yohimbine and [3H]dihydroalprenolol, respectively. Lipolytic responses were tested with isoproterenol (beta agonist), clonidine (alpha-2 agonist) and epinephrine. There are clear differences in the relative number of beta and alpha-2 sites according to the origin of the fat deposit; beta sites are less numerous than alpha-2 sites in subcutaneous fat cells of both regions (alpha-2:beta sites are in a ratio of 3 +/- 0.4:2 +/- 0.4). However, in membranes of omental fat cells, beta sites are at least as numerous as alpha-2 sites (ratio 0.9 +/- 0.2). Epinephrine always has a higher affinity for alpha-2 sites than for beta sites in the subcutaneous and omental deposits. In lipolysis studies, epinephrine, in the absence of adenosine in the incubation medium, initiated an anti-lipolytic effect in femoral fat cells and promoted inhibition of lipolysis at lower concentrations in abdominal subcutaneous fat cells, the effect being reversed at higher doses; epinephrine, however, was always lipolytic in omental adipocytes. There was no striking differences in the sensitivity to isoproterenol in the various deposits. Clonidine had a higher affinity for alpha-2 sites in femoral fat cells and was equipotent in the omental and abdominal ones. Thus, the differences in the lipolytic responses to epinephrine in adipocytes from different sites are linked to a variable alpha-2 inhibiting effect (and alpha-2 site number) rather than to a modified beta driven increase in lipolysis initiated by the physiological amine.
BACKGROUND: Sex specific cross sectional reference values for lung function indices usually employ a linear model with terms for age and stature. The effects of also matching for body mass index (BMI = mass/stature(2)) or its components, fat percentage of body mass (fat%) and fat free mass index (FFMI = fat free mass/stature(2)) were studied. METHODS: The subjects were 458 asymptomatic male and female non-smokers (383 men) and 22 female ex-smokers. Measurements were made of ventilatory capacity, lung volumes, transfer factor (diffusing capacity, single breath CO method), and body composition (skinfold method). Linear and proportional regression models were used. RESULTS: Terms for fat% and FFMI significantly improved the accuracy of reference values for all the primary lung function indices. The improvements in subjects with atypical physiques (fat% and FFMI at the ends of the distributions for the subjects) were in the range 0.3-2.3 SD compared with conventional regression equations. The new partial regression coefficients on age were independent of age related changes in body fat. The coefficient for total lung capacity (TLC) on age in men was now positive. Most differences between the sexes were eliminated. A term for BMI improved the descriptions of subdivisions of TLC but lacked the other advantages. CONCLUSION: Allowance for fat% and FFMI increases the accuracy of reference equations for lung function, particularly for subjects with a lot of fat and little muscle or vice versa. Allowance for BMI is less informative.
We determined whether acquired obesity is associated with increases in liver or intra-abdominal fat or impaired insulin sensitivity by studying monozygotic (MZ) twin pairs discordant and concordant for obesity. We studied nineteen 24- to 27-yr-old MZ twin pairs, with intrapair differences in body weight ranging from 0.1 to 24.7 kg [body mass index (BMI) range 20.0-33.9 kg/m2], identified from a population-based FinnTwin16 sample. Fat distribution was determined by magnetic resonance imaging, percent body fat by dual-energy X-ray absorptiometry, liver fat by proton spectroscopy, insulin sensitivity by measuring the fasting insulin concentration, and whole body insulin sensitivity by the euglycemic insulin clamp technique. Intrapair differences in BMI were significantly correlated with those in intra-abdominal fat (r = 0.82, P < 0.001) and liver fat (r = 0.57, P = 0.010). Intrapair differences in fasting insulin correlated with those in subcutaneous abdominal (r = 0.60, P = 0.008), intra-abdominal (r = 0.75, P = 0.0001) and liver (r = 0.49, P = 0.048) fat. Intrapair differences in whole body insulin sensitivity correlated with those in subcutaneous abdominal (r = -0.72, P = 0.001) and intra-abdominal (r = -0.55, P = 0.015) but not liver (r = -0.20, P = 0.20) fat. We conclude that acquired obesity is associated with increases in intra-abdominal and liver fat and insulin resistance, independent of genetic factors.
To clarify further the independent relationships of body composition parameters to energy expenditure, resting metabolic rate (RMR) and postprandial thermogenesis were studied in four groups who were matched for absolute fat mass (study 1) and relative fatness (study 2). In study 1, five lean [group A, 15.4 +/- 0.6% (+/- SE) body fat] and five obese men (group B, 25.0 +/- 0.9% fat) were matched on body fat mass (13.0 +/- 0.9 vs. 14.4 +/- 0.8 kg, respectively). Fat-free mass (FFM) and total weight were greater for group A than B. RMR was measured for 3 h in the fasted state and after a 720-kcal mixed meal. RMR was greater for group A than B (1.38 +/- 0.08 vs. 1.14 +/- 0.04 kcal/min, P less than 0.05). The thermic effect of food, calculated as 3 h postprandial minus fasting RMR, was greater for group A than B (65 +/- 6 vs. 23 +/- 9 kcal/3 h; P less than 0.05). In study 2, two groups (n = 6 men/group) were matched for percent body fat (33 +/- 1% fat for both) but differed in lean, fat, and total weights: 50.8 +/- 3.1 kg FFM for the lighter (group C) vs. 68.0 +/- 2.8 kg FFM for the heavier (group D) group, P less than 0.05. RMR was lower for group C than D (1.17 +/- 0.06 vs. 1.33 +/- 0.04 kcal/min, P less than 0.05), but the thermic effect of food was not significantly different (31 +/- 3 vs. 20 +/- 6 kcal/3 h).(ABSTRACT TRUNCATED AT 250 WORDS)