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At least 19 recordsLinked to original sources
PubMed1994

Adipose tissue density, estimated adipose lipid fraction and whole body adiposity in male cadavers.

Lipid and water together typically make up more than 90% of the body's adipose tissue mass. Although some reports have shown that the fraction of lipid in adipose tissue is greater in obese people than in lean ones, the quantitative relationship between adipose lipid fraction and overall adiposity of the body has never been investigated. We dissected six male unembalmed cadavers and weighed all adipose tissue (range 9.7-25.7 kg), allowing the calculation of percentage adiposity as 100 x total adipose mass/body mass (range 17.8-43.9%). Adipose tissue volume was determined by hydrostatic weighing of all portions of the dissected adipose tissue. For the six cadavers, whole body adipose tissue density ranged from 0.925-0.970 g/ml. Based on a three-component model of adipose tissue (lipid, water and dry fat-free solids), an expression for lipid fraction, F, was derived. After assuming densities for adipose lipid (0.905 g/ml), water at 36 degrees C (0.997 g/ml) and the dry fat-free component (1.38 g/ml), the equation simplified to F = 6.256/D-5.912, where D is adipose tissue density (g/ml). Lipid fraction was then calculated for each of the six cadavers: the range (0.54-0.85) was in excellent agreement with published data. There was a significant correlation (r = 0.95, P < 0.005) between calculated lipid fraction and percentage adiposity. The regression equation predicting lipid fraction from percentage adiposity was y = 0.327 + 0.0124x. We conclude that the estimated fraction of lipid in human adipose tissue shows both a wide range and a strong positive linear relationship with overall body fatness.

Adipose Tissue↗
PubMed2005

Increased adiposity and reduced adipose tissue mRNA expression of uncoupling protein-2 in first-degree relatives of type 2 diabetic patients: evidence for insulin stimulation of UCP-2 and UCP-3 gene expression in adipose tissue.

The mitochondrial uncoupling proteins (UCP-2 and UCP-3), which have been suggested to be involved in the development of obesity by controlling the energy expenditure (EE), were studied in 22 healthy first-degree relatives (FDRs) of patients with type 2 diabetes and 13 body mass index (BMI)- and age-matched healthy control subjects. Abdominal subcutaneous adipose tissue biopsies were obtained before and after 150-min hyperinsulinaemic clamp (average serum insulin 250 pM). Basal adipose tissue UCP-2 mRNA levels in the FDR group were significantly lower than that in the control group. After the hyperinsulinaemic clamp, adipose tissue UCP-2 mRNA levels were increased by 32% in the control group (p < 0.05) and 32% in the FDR group (p < 0.05). The basal adipose tissue UCP-3 mRNA level was similar in the two groups and increased in both the groups during hyperinsulinaemia (p < 0.001). Dual energy X-ray absorptiometry showed that despite similar BMI the FDR group had significantly higher fat mass (FM) per cent compared to that of the control group (p < 0.01). The UCP-2 mRNA expression was inversely correlated with the amount of adipose tissue (r = -0.53, p < 0.001), and multiple regression analysis revealed that only the amount of FM was independently correlated with basal UCP-2 mRNA levels, whereas age, gender nor family history of type 2 diabetes contributed independently to the variation in UCP-2 mRNA levels. No differences in EE were observed between the two groups, and no association between EE and UCP mRNA expression was found. In conclusion, we have demonstrated that adipose tissue UCP-2 and UCP-3 mRNA levels are significantly increased during a 150-min hyperinsulinaemic clamp. The UCP-2 mRNA levels were expressed at a significantly lower level FDR to type 2 diabetes compared to control subjects. However, in multiple regression analysis controlling for amount of adipose tissue, the difference between the two groups disappeared. Thus, only the amount of adipose tissue contributed independently to the variation in UCP-2 mRNA expression.

Adipose Tissue↗
PubMed2004

Comparison of the release of adipokines by adipose tissue, adipose tissue matrix, and adipocytes from visceral and subcutaneous abdominal adipose tissues of obese humans.

The purpose of this study was to examine the source of adipokines released by the visceral and sc adipose tissues of obese humans. Human adipose tissue incubated in primary culture for 48 h released more prostaglandin E(2), IL-8, and IL-6 than adiponectin, whereas the release of plasminogen activator inhibitor 1 and hepatocyte growth factor was less than that of adiponectin but greater than that of leptin. IL-10 and TNFalpha were released in amounts less than those of leptin, whereas vascular endothelial growth factor and IL1-beta were released in much lower amounts. The accumulation of adipokines was also examined in the three fractions (adipose tissue matrix, isolated stromovascular cells, and adipocytes) obtained by collagenase digestion of adipose tissue. Over 90% of the adipokine release by adipose tissue, except for adiponectin and leptin, could be attributed to nonfat cells. Visceral adipose tissue released greater amounts of vascular endothelial growth factor, IL-6, and plasminogen activator inhibitor 1 compared with abdominal sc tissue. The greatly enhanced total release of TNFalpha, IL-8, and IL-10 by adipose tissue from individuals with a body mass index of 45 compared with 32 was due to nonfat cells. Furthermore, most of the adipokine release by the nonfat cells of adipose tissue was due to cells retained in the tissue matrix after collagenase digestion.

Abdomen↗
PubMed2005

Ghrelin regulates adiposity in white adipose tissue and UCP1 mRNA expression in brown adipose tissue in mice.

To examine the involvement of ghrelin in obesity, we investigated the effects of treatment with peripherally administered ghrelin on food intake, adiposity, and expression of uncoupling protein (UCP) mRNA in brown (BAT) and white (WAT) adipose tissue in mice. Acute bolus administration of ghrelin at a dose of 120 nmol/kg increased cumulative food intake over 4 and 24 h as compared to controls (p<0.05 for each), whereas 12 nmol/kg/day ghrelin showed no remarkable effect (p>0.1). Chronic repeated treatment with 12 nmol/kg/day ghrelin for 7 days increased body weight and adiposity assessed by the weight of adipose tissue, triglyceride content in WAT (p<0.05 for each versus control). In addition, the same treatment decreased and increased mRNA expression of BAT UCP1 and WAT UCP2, respectively (p<0.05 for each). In conclusion, ghrelin can regulate body weight, adiposity and UCPs mRNA expression in mice. The present results provide evidence for a new regulatory loop involving ghrelin and UCP, and add novel insights into the regulatory mechanisms of obesity.

Adipose Tissue↗
PubMed1978

Glycerolipid biosynthesis in rat adipose tissue. Influence of adipose-cell size and site of adipose tissue on triacylglycerol formation in lean and obese rats.

The rates of lipid formation were compared in different fat-depots from lean and obese rats by using [14C]glycerol 3-phosphate, [14C]glucose or [14C]acetate as substrates. In lean animals, subcutaneous adipose tissue showed significantly lower rates of lipid synthesis than did perirenal and gonadal fat-tissue. In obese animals, the rates of lipid synthesis were significantly higher and did not vary from one fat-depot to another. Differences in the rates of lipid formation between lean and obese rats disappeared during dietary restriction of obese animals. The isolated adipocyte preparation did not reflect the true metabolic activity of the adipose organ, since this preparation was mainly derived from smaller adipocytes that were metabolically less active than larger adipocytes. The present study suggests that it is better to use whole tissue preparations to measure lipogenesis and esterification reactions, because these measurements represent the contribution of both larger and smaller adipocytes towards lipid formation.

Acetates↗
PubMedDate not supplied

Waist-to-hip ratio and adipose tissue distribution: contribution of subcutaneous adiposity.

The waist-to-hip ratio (WHR) reflects the relative distribution of adipose tissue in the human body. However, whether this is due to the musculoskeletal structures of the waist and hip or the overlying subcutaneous adipose tissue has been disputed. We measured waist and hip girths in 11 male and 11 female cadavers, aged 55-94 years, before and after complete removal of skin and subcutaneous adipose tissue. Girths measured following removal of subcutaneous adipose tissue were termed "waist gx" and "hip gx", and their ratio "WHRx". Masses of regional adipose tissue segments were obtained by complete dissection, and the adipose mass ratios "trunk/arm-plus-leg", "trunk/leg", "internal/arm-plus-leg", and "internal/leg" were derived. As assessed by analysis of variance, WHR accounted for significant (P < 0.05) portions of the variance in all adipose mass ratios; adjustment for internal adipose mass increased the significance of all these relationships (P < 0.005). The ratio WHRx was not related to any ratio of regional adipose masses. Waist girth was related to trunk (P < 0.001) and internal (P < 0.05) adipose masses, and hip girth was related to arm-plus-leg adipose mass (P < 0.0001) and leg adipose mass (P < 0.0001), but waist gx and hip gx were not related to dependent variables. The results indicate that the ability of WHR and waist and hip girths to reflect the regional distribution of adipose tissue in the body is dependent upon the subcutaneous adipose tissue mass of the waist hip area, not its musculoskeletal constituency.

Adipose Tissue↗
PubMed1977

Cellularity of porcine adipose tissue: effects of growth and adiposity.

Adipose tissue, from two depots in pigs of three breeding groups with different propensities to fatten, was characterized in terms of weight of the adipose tissue organ, adipose cell number, and mean cell volume as determined by electronic counting of adipose cells fixed with osmium tetroxide. Perirenal and extramuscular adipose tissue growth was accompanied by progressive adipose cell enlargement along with an increase in cell number. By approximately 18-20 weeks of life, adipose tissue growth in both lean Hampshire x Yorkshire and fat Minnesota 3 x 1 pigs occurred exclusively by cellular hypertrophy. By 24 weeks of life (37 kg), hyperplasia was complete in Hormel Miniature pigs, which contained about one-third as many extramuscular adipose cells as the conventional pigs. Adiposity in the pig was due to cellular hypertrophy rather than cellular hyperplasia, since during growth, the leaner conventional pigs (30.6% extramuscular fat) contained more adipose cells than the fatter pigs (46.6% extramuscular fat). The number of adipose cells per animal or per adipose organ was directly related to the true body size (weight of fat-free carcass) of the animal. Fat Minnesota 3 x 1 pigs had fewer adipose cells than lean Hampshire x Yorkshire pigs at an equivalent live weight due to the smaller true body size of these animals. In young animals (28 and 54 kg), growth rate was positively correlated with adipose cell number. However, growth rate was unrelated to the total number of cells in the more mature animals (83 and 109 kg). Therefore a slow, normal growth rate may delay but not alter the final cell number.

Adipose Tissue↗
PubMed1995

Heterogeneity in adipose tissue metabolism: causes, implications and management of regional adiposity.

The observation that different patterns of adipose tissue distribution are associated with different metabolic abnormalities, has recently given new impetus to research in obesity. Due to several methodologic problems, however, many aspects of regional excess of adipose tissue are still poorly understood. Among them, the causes and the metabolic consequences of regional adiposity are particularly important. Heterogeneity in adipose tissue distribution may be determined by a combination of genetic and hormonal causes. Both factors may determine differences in metabolism of various adipose tissue compartments primarily by regulating LPL production, storage and release of triacylglycerols, and aromatization of androgens. Furthermore, changes in adipocyte sensitivity to hormones such as, sex steroids, glucocorticoids, insulin and adrenergic hormones may also regulate fat distribution in various adipose tissue compartments. The metabolic heterogeneity of adipose tissue from various compartments, particularly the differences between the "portal" and subcutaneous adipose tissues, may account for several metabolic abnormalities associated with "upper body adiposity". However, no direct evidence is available to confirm this hypothesis. Recent advances in the methodology to study adipose tissue distribution (mainly CT and MRI) may provide the necessary tools to evaluate the true impact of adiposity in various compartments on intermediary metabolism and to identify a "morbid" adipose tissue compartment. These observations may help in designing better therapeutic strategies targeted towards regional adiposity and its metabolic complications.

Adipose Tissue↗
PubMed2005

A correlation study of organochlorine levels in serum, breast adipose tissue, and gluteal adipose tissue among breast cancer cases in India.

We used data from a breast cancer pilot study carried out in Kerala, India in 1997, for which organochlorine levels were measured in three biological media, blood serum, breast adipose tissue, and gluteal adipose tissue, of 37 fasting breast cancer cases (pretreatment). Our objective was to investigate the relationships between organochlorine concentrations in different biological media. Gas-liquid chromatography determined serum, breast adipose, and gluteal adipose tissue levels of dichlorodiphenyltricholorethane, dichlorodiphenyldichloroethane, beta-benzene hexachloride, and polychlorinated biphenyl (PCB) congeners, PCB-153 and PCB-180. Correlation plots were made and Spearman correlation coefficients (r) calculated for breast adipose tissue versus serum, gluteal adipose tissue versus serum, and breast adipose versus gluteal adipose tissue. We also examined paired ratios of all summary statistics. There were strong correlations among serum, breast adipose tissue, and gluteal adipose tissue concentrations for most organochlorines analyzed, one exception being gluteal versus serum for PCB-153. The correlations for all other comparisons ranged from r = 0.65 to 0.94. Serum (ng/g) versus adipose ratios approached 1:1 for most of the organochlorine pesticide comparisons and did not vary by summary statistic. To our knowledge, this is the first study to use three different media from fasting subjects and to comprehensively investigate the relationship between organochlorines measured across the three media for both organochlorine pesticides and PCBs. These data indicate that blood serum reflects the present body burden of a range of organochlorines to the same extent as adipose tissue, and they support the view that serum may be collected in lieu of adipose tissue to obtain similar information. However, such measurements are a combination of both recent exposures and past exposures, which have metabolized slowly and may still persist. Therefore, investigators should use caution when assigning a level as lifetime body burden.

Adipose Tissue↗
PubMed2003

Effects of dietary fat and zinc on adiposity, serum leptin and adipose fatty acid composition in C57BL/6J mice.

Zinc (Zn) has been implicated in altered adipose metabolism, insulin resistance and obesity. The objective of this study was to investigate the effects dietary Zn deficiency and supplementation on adiposity, serum leptin and fatty acid composition of adipose triglycerides and phospholipid in C57BL/6J mice fed low-fat (LF) or high-fat (HF) diets for a 16 week period. Weanling C57BL/6J mice were fed LF (16% kcal from soybean oil) or HF (39% kcal from lard and 16% kcal from soybean oil) diets containing 3, 30 or 150 mg Zn/kg diet (ZD = Zn-deficient, ZC = Zn control and ZS = Zn-supplemented, respectively). HF-fed mice had higher fat pad weights and lower adipose Zn concentrations than the LF-fed mice. The ZD and ZS groups had a reduced content of fatty acids in adipose triglycerides compared to the ZC group, suggesting that zinc status may influence fatty acid accumulation in adipose tissue. Serum leptin concentration was positively correlated with body weight and body fat, and negatively correlated with adipose Zn concentration. Dietary fat, but not dietary Zn, altered the fatty acid composition of adipose tissue phospholipid and triglyceride despite differences in Zn status assessed by femur Zn concentrations. The fatty acid profile of adipose triglycerides generally reflected the diets. HF-fed mice had a higher percentage of C20:4 n-6, elevated ratio of n-6/n-3, lower ratio of PUFA/SAT and reduced percentage of total n-3 fatty acids in adipose phospholipid, a fatty acid profile associated with obesity-induced risks for insulin resistance and impaired glucose transport. In summary, the reduced adipose Zn concentrations in HF-fed mice and the negative correlation between serum leptin and adipose Zn concentrations support an interrelationship among obesity, leptin and Zn metabolism.

Adipose Tissue↗
PubMed1973

Studies of human adipose tissue. Adipose cell size and number in nonobese and obese patients.

The cellular character of the adipose tissue of 21 nonobese and 78 obese patients has been examined. Adipose cell size (lipid per cell) was determined in three different subcutaneous and deep fat depots in each patient and the total number of adipose cells in the body estimated by division of total body fat by various combinations of the adipose cell sizes at six different sites. Cell number has also been estimated on the basis of various assumed distribution of total fat between the subcutaneous and deep fat depots. Obese patients, as a group, have larger adipose cells than do nonobese patients; cell size, however, varies considerably among the fat depots of individuals of either group. The variation in cell size exists not only between, but also within subcutaneous and deep sites. Estimates of total adipose cell number for a given individual based upon cell size can, therefore, vary by as much as 85%. On the basis of these studies it is suggested that the total adipose number of an individual is best and most practically estimated, at this time, by division of total body fat by the mean of the adipose cell sizes of at least three subcutaneous sites. IRRESPECTIVE OF THE METHOD BY WHICH TOTAL ADIPOSE CELL NUMBER IS ESTIMATED, TWO PATTERNS OF OBESITY EMERGE WITH RESPECT TO THE CELLULAR CHARACTER OF THE ADIPOSE TISSUE MASS OF THESE PATIENTS: hyperplastic, with increased adipose cell number and normal or increased size, and hypertrophic, with increased cell size alone. These two cellular patterns of obesity are independent of a variety of assumed distributions of fat among the subcutaneous and deep depots. When these different cellular patterns are examined in terms of various aspects of body size, body composition, and the degree, duration, and age of onset of obesity, only the latter uniquely distinguishes the hyperplastic from the hypertrophic: hyperplastic obesity is characterized by an early age of onset, hypertrophic, by a late age of onset. These studies indicate that there are two distinct periods early in life during which hypercellularity of the adipose tissue are most likely to occur: very early within the first few years, and again from age 9 to 13 yr.

Adipose Tissue↗
PubMed1968

The role of adipose cell size and adipose tissue insulin sensitivity in the carbohydrate intolerance of human obesity.

Glucose metabolism and insulin sensitivity of isolated human adipose tissue was studied as a function of adipose cell size and number. Glucose metabolism by these tissues was closely related to the number of cells in the fragment, irrespective of cell size. Adipose cells of obese individuals metabolized glucose to carbon dioxide and triglyceride at rates similar to adipose cells of nonobese subjects. In contrast, insulin responsiveness of adipose tissue was dependent upon adipose cell size. The larger its adipose cells the less insulin sensitive was the tissue. Thus, adipose tissue of obese subjects, with enlarged cells, showed a diminished response to insulin. After weight loss and reduction in adipose cell size, insulin sensitivity of the adipose tissue of obese patients was restored to normal. When adipose tissue of obese individuals showed impaired responsiveness to insulin, their plasma insulin levels, after oral glucose, were elevated. Weight loss and reduction in adipose cell size restored plasma insulin concentration to normal, concomitant with the return of normal tissue insulin sensitivity.

Journal Article↗
PubMed1996

Characterization and regulation of angiotensin II receptors in rat adipose tissue. Angiotensin receptors in adipose tissue.

Characterization and regulation of angiotensin II (AII) receptor binding sites was performed in rat membrane preparations from nonadipose (liver, lung) and adipose (interscapular (ISBAT) and periaortic (PA) brown adipose tissue; epididymal (EF) and retroperitoneal (RPF) white adipose tissue). In membrane preparations from brown and white adipose sources, [125I]AII saturation binding revealed a single, high affinity (Kd range of 0.3 -0.6 nM) binding site with a modest AII receptor density (Bmax range of 17-120 fmol/mg protein) comparable to rat lung (130 fmol/mg protein). White adipose tissue contained a greater number of AII receptor sites than brown adipose tissue. Competition displacement studies demonstrated the AT1 receptor is the only angiotensin receptor subtype localized in adipose tissue, with the rank order for competition of [125I]AII binding in all adipose tissues examined AIII > AII > losartan > angiotensin I (AI) > PD123319. The AT2 specific receptor antagonist, PD123319, was ineffective at displacing [125I]AII binding in all adipose tissues examined. Since components of the renin-angiotensin system are regulated in adipose tissue, we determined if the AII receptor is also regulated in the obese state. AII receptor binding characteristics were determined in liver, lung, ISBAT and EF membrane preparations from adult Zucker obese (fa/fa) and lean (Fa/?) rats. AII receptor density was decreased in liver from obese rats. In contrast, the affinity for [125I]AII binding was not altered in tissues from obese rats. In a separate group of obese and lean rats, regulation of the AII receptor by phenobarbital (PB) was examined. Administration of PB restored AII receptor density in liver from obese rats to levels obtained in lean rats. In summary, these results demonstrate the presence of AT1 receptor sites in brown and white adipose tissue. Moreover, AII receptor density is decreased in tissues from obese rats, with restoration of receptor density by administration of PB. Future studies will determine if PB regulates the AT1 receptor at the level of gene expression.

Adipose Tissue↗
PubMed1981

Fatty acid synthesis in mouse brown adipose tissue. The influence of environmental temperature on the proportion of whole-body fatty acid synthesis in brown adipose tissue and the liver.

Fatty acid synthesis has been measured in vivo with 3H2O in mice acclimated at different environmental temperatures (33, 22, 4 degrees C), and the importance of brown adipose tissue and the liver to whole-body fatty acid synthesis at each temperature assessed. At 33 degrees C, when non-shivering thermogenesis is minimal, the rate of fatty acid synthesis in interscapular brown adipose tissue was lower than in the liver, but higher than in white adipose tissue and the carcass. At 4 degrees C, when non-shivering thermogenesis is maximal, the fatty acid synthesis rate in interscapular brown adipose tissue was many times greater than in any other tissue. High fatty acid synthesis rates were also found in other brown adipose tissue depots--subscapular, dorsocervical and axillary--of cold-acclimated mice. In mice maintained at 22 degrees C the rate of fatty acid synthesis was also higher in brown adipose tissue than in other tissues. Overall, the relative importance of brown adipose tissue as a site of fatty acid synthesis increased with lower environmental temperatures, while that of the liver decreased. It was calculated that brown adipose tissue in total accounted for approx. 5% of whole-body fatty acid synthesis at 33 degrees C, 10% at 22 degrees C and 30% at 4 degrees C. In contrast, hepatic synthesis amounted to 32% of whole-body fatty acid synthesis at 33 degrees C, 16% at 22 degrees C and only 11% at 4 degrees C. An estimate of the contribution that de novo synthesis makes to total fatty acid utilization by interscapular brown adipose tissue suggests that fatty acid synthesis and breakdown constitutes a significant heat-dissipating 'cycle' in brown adipose tissue of cold-acclimated mice. Such a cycle is not evident in suckling animals since fatty acid synthesis in brown adipose tissue is very low during early development.

Adaptation, Physiological↗
PubMed2001

Demonstration of estrogen receptor subtypes alpha and beta in human adipose tissue: influences of adipose cell differentiation and fat depot localization.

A novel ER-subtype, the ER-beta has recently been characterized in various tissues, furthermore five isoforms of the ER-beta are known (ER-beta1--ER-beta5). Using immunoblotting and real- time RT-PCR, ER-alpha and beta were studied in human adipose tissue. The expression of ER-alpha mRNA was equal in subcutaneous gluteal adipose tissue, subcutaneous abdominal and intra-abdominal adipose tissue, similar findings were obtained at the protein level. In contrast the amount of ER-beta1 (protein and mRNA) was significantly lower in intra-abdominal adipose tissue as compared with the subcutaneous adipose tissue (five-fold lower in women, P<0.005 and three-fold lower in men, P<0.005) whereas the expression of ER-beta4 and -beta5 mRNA isoforms were significantly higher in gluteal adipose tissue compared to subcutaneous abdominal adipose tissue. No significant gender differences in ER expression was detected in any of the fat depots investigated. During adipocyte differentiation the expression of ER-alpha, -beta4 and -beta5 mRNA declined, whereas, the expression of ER-beta1 mRNA was constant. In conclusion, the existence of ER-beta isoforms in human adipose tissue was demonstrated and the amount of these receptors was dependent upon fat depot localization, with much reduced expression of ER-beta1 in intra-abdominal adipose tissue compared to subcutaneous adipose tissue. These findings may indicate that estrogens could have differentiation and depot specific effects in human adipose tissue.

Abdomen↗
PubMed2004

Expression and activity of steroid aldoketoreductases 1C in omental adipose tissue are positive correlates of adiposity in women.

We examined expression and activity of steroid aldoketoreductase (AKR) 1C enzymes in adipose tissue in women. AKR1C1 (20alpha-hydroxysteroid dehydrogenase; 20alpha-HSD), AKR1C2 (3alpha-HSD-3), and AKR1C3 (17beta-HSD-5) are involved mainly in conversion of progesterone to 20alpha-hydroxyprogesterone and inactivation of dihydrotestosterone to 5alpha-androstane-3alpha,17beta-diol. Abdominal subcutaneous and omental adipose tissue biopsies were obtained during abdominal hysterectomies in seven women with low visceral adipose tissue (VAT) area and seven age- and total body fat mass-matched women with visceral obesity. Women with elevated VAT areas were characterized by significantly higher omental adipose tissue 20alpha-HSD and 3alpha-HSD-3 mRNA abundance compared with women with low VAT accumulations (1.4- and 1.6-fold differences, respectively; P < 0.05). Omental and subcutaneous adipose tissue 3alpha-HSD activities were significantly higher in women with high vs. low VAT areas (P < 0.05 for both comparisons). Total and visceral adiposities were positively associated with omental 20alpha-HSD mRNA level (r = 0.75, P < 0.003 for fat mass; r = 0.57, P < 0.04 for VAT area) and omental 3alpha-HSD-3 mRNA level (r = 0.68, P < 0.01 for fat mass; r = 0.74, P < 0.003 for VAT area). Enzyme activities in both depots were also positively correlated with adiposity measures. Omental adipose tissue enzyme expression and activity were positively associated with omental adipocyte size and LPL activity. In conclusion, mRNA abundance and activity of AKR1C enzymes in abdominal adipose tissue compartments are positive correlates of adiposity in women. Increased progesterone and/or dihydrotestosterone reduction in abdominal adipose tissue may impact locally on fat cell metabolism.

20-Hydroxysteroid Dehydrogenases↗
PubMed1974

Glucose metabolism and the response to insulin by human adipose tissue in spontaneous and experimental obesity. Effects of dietary composition and adipose cell size.

[1-(14)C]glucose oxidation to CO(2) and conversion into glyceride by adipose tissue from nonobese and obese subjects has been studied in vitro in the presence of varying medium glucose and insulin concentrations as functions of adipose cell size, the composition of the diet, and antecedent weight gain or loss. Increasing medium glucose concentrations enhance the incorporation of glucose carbons by human adipose tissue into CO(2) and glyceride-glycerol. Insulin further stimulates the conversion of glucose carbons into CO(2), but not into glyceride-glycerol. Incorporation of [1-(14)C]glucose into glyceride-fatty acids by these tissues could not be demonstrated under any of the conditions tested. Both adipose cell size and dietary composition influence the in vitro metabolism of glucose in, and the response to insulin by, human adipose tissue. During periods of ingestion of weight-maintenance isocaloric diets of similar carbohydrate, fat, and protein composition, increasing adipose cell size is associated with (a) unchanging rates of glucose oxidation and increasing rates of glucose carbon incorporation into glyceride-glycerol in the absence of insulin, but (b) decreasing stimulation of glucose oxidation by insulin. On the other hand, when cell size is kept constant, increasing dietary carbohydrate intake is associated with an increased basal rate of glucose metabolism and response to insulin by both small and large adipose cells. Thus, the rate of glucose oxidation and the magnitude of the insulin response of large adipose cells from individuals ingesting a high carbohydrate diet may be similar to or greater than that in smaller cells from individuals ingesting an isocaloric lower carbohydrate diet.The alterations in basal glucose metabolism and insulin response observed in adipose tissue from patients with spontaneous obesity are reproduced by weight gain induced experimentally in nonobese volunteers; these metabolic changes are reversible with weight loss. The relationships among adipose cell size, dietary composition, and the metabolism of adipose tissue are similar in spontaneous and in experimental obesity.

Adipose Tissue↗