Fat Cell Diameter Research Articles

Plasma leptin in growing lambs as a potential predictor for carcass composition and daily gain

Leptin is an adipocyte derived hormone and correlates highly to the extent of body fat tissue. The aim of this study was to determine if leptin could serve as an early predictor for carcass composition and final growth rate in lambs with special emphasis on size and cellularity of the different body fat depots. Thirty intact male ad libitum fed lambs were blood sampled at 20, 25, 30, 35, and 40 kg live weight. After slaughtering at 40 kg, lean and the visceral, subcutaneous and intermuscular fat were measured by dissection. The fat cell diameter was determined in subcutaneous and perirenal fat. Average daily gain from birth to slaughter correlated to leptin only at 30 and 35 kg live weight ( r = −0.56 and −0.61, P < 0.01) and thus leptin cannot be regarded as a suitable early predictor for growth rate. That goes for the prediction of subcutaneous and intermuscular fat, too; because no relationships were detected between early leptin concentrations and the amount of these tissues. Leptin concentrations measured just before slaughter were related to all fat tissues except the pelvic and intramuscular fat. Among the visceral fat depots, omental fat expressed the highest correlations to leptin ( r = 0.60, P < 0.001). Additionally, leptin concentrations at 35 and 40 kg live weight increased with increasing fat cell diameters ( r = 0.38, P < 0.05 to r = 0.59, P < 0.001). This study indicates that leptin concentration measured in the slaughter weight range has the greatest potential to assess body fat content, whereas an earlier prediction does not seem to be feasible. Further studies should clarify if these results are reproducible for other breeds or species.

声帯内自家脂肪注入術の臨床・組織学的研究

Injection laryngoplasty is a reliable surgical procedure to correct laryngeal incompetence caused by vocal fold paralysis. Although autologous fat has become a popular injection material in recent times, there are numerous problems that need to be addressed in its application in laryngoplasty; such as, injection site of the vocal fold, quantity of injection material, possibility of improvement for glottal gap, and resorption of injected autologous fat. The purpose of this study is to investigate the problems of autologous fat injection in laryngoplasty.The clinical study involved 31 patients with unilateral vocal fold paralysis who had received treatment at the Kurume University Hospital between 2000 and 2003. The pathological study was comprised of 23 patients whose autologous fat harvested by liposuction was utilized as injection material during laryngoplasties between 2000 and 2005.In patients with a small degree of vocal fold bowing, autologous fat was injected locally into the thyroarytenoid muscle lateral to the oblong fovea of the arytenoid cartilage. As a result, the glottal gap decreased and postoperative voice functions, maximum phonation time (MPT) and mean airflow rate during phonation over comfortable duration (MFRc) improved. In patients with a large degree of vocal fold bowing, the autologous fat was injected not only into the thyroarytenoid muscle lateral to the ob-long fovea of the arytenoid cartilage but also into the thyroarytenoid muscle at the membranous portion of the vocal fold. As a result, the glottal gap decreased and postoperative voice functions, MPT and MFRc improved.The fat cell membranes had not been damaged during liposuction harvesting or microinjection by our technique. The diameters of fat cells ranged from 41.3±8-117.1±15.2μm. A few patients with large diameter fat cells showed less improvement compared to those with smaller diameters for the postoperative voice functions, MPT, MFRc, and pitch perturbation quotient (PPQ).These results indicate that fat injection into the thyroarytenoid muscle lateral to the oblong fovea of the arytenoid cartilage produced good postoperative voice function and this procedure can improve a large degree of glottal gap. Resorption of autologous fat may be related to not only the size and density of fat cells but also their proliferation.

Anti-lipolytic Action of AMP-activated Protein Kinase in Rodent Adipocytes

Despite its importance in terms of energy homeostasis, the role of AMP-activated protein kinase in adipose tissue remains controversial. Initial studies have described an anti-lipolytic role for AMP-activated protein kinase, whereas more recent studies have suggested the converse. Thus we have addressed the role of AMP-activated protein kinase in adipose tissue by modulating AMP-activated protein kinase activity in primary rodent adipocytes using pharmacological activators or by adenoviral expression of dominant negative or constitutively active forms of the kinase. We then studied the effects of AMP-activated protein kinase activity modulation on lipolytic mechanisms. Finally, we analyzed the consequences of a genetic deletion of AMP-activated protein kinase in mouse adipocytes. AMP-activated protein kinase activity in adipocytes is represented mainly by the alpha(1) isoform and is induced by all of the stimuli that increase cAMP in adipocytes, including fasting. When AMP-activated protein kinase activity is increased by 5-aminoimidazole-4-carboxamide-riboside, phenformin, or by the expression of a constitutively active form, isoproterenol-induced lipolysis is strongly reduced. Conversely, when AMP-activated protein kinase activity is decreased either by a dominant negative form or in AMP-activated protein kinase alpha(1) knock-out mice, lipolysis is increased. We present data suggesting that AMP-activated protein kinase acts on hormone-sensitive lipase by blocking its translocation to the lipid droplet. We conclude that, in mature adipocytes, AMP-activated protein kinase activation has a clear anti-lipolytic effect.

A quick, reliable, and automated method for fat cell sizing

Mean diameters of fat cells from abdominal tissues from 31 volunteers were determined by three methods based on fat cell isolation after collagenase digestion and methylene blue staining. The three methods were direct microscopy (Micro), manual measurement of diameters from digital images by using the public domain NIH Image program (Scion), and automated measurement of diameters from digital images using a customized program developed by Biomedical Imaging Resource at Mayo Clinic (AdCount). There was excellent agreement between the methods' measurement of mean abdominal fat cell diameter (concordance correlation coefficient >0.84). The Scion method gave slightly but systematically lower mean abdominal fat cell diameters than did either AdCount or Micro. The AdCount approach produced results that are comparable to those from Micro. Comparison of AdCount and Micro in measuring diameters of fat cells from thigh confirmed the good comparability between the two methods independent of fat depot. AdCount is very reliable, and the quickest and most objective of the three methods in measuring fat cell diameters from various depots.

Metabolic changes during the perinatal period in dairy sheep in relation to level of nutrition and breed. I. Late pregnancy

SummaryThe effects of level of nutrition during pregnancy on the development of the mammary gland, on various biochemical parameters, on feed intake and on body weight were investigated in Chios (CH) and Karagouniko (K) ewes. Thirty pregnant ewes of both breeds were randomly assigned to groups A and B, which received 110% of their energy requirements for maintenance plus pregnancy for two foetuses and 90% of their maintenance energy requirements, respectively. In a second experiment, 34 pregnant Chios ewes were assigned and fed as in the first trial, but they were slaughtered on day 140 of pregnancy to study udder characteristics. The feed intake and the body weight in pregnancy were higher in ewes of group A and K ewes than of groups B (p 0.001) and CH (p 0.01), respectively. Plasma glucose concentration tended to be higher in group A than group B. Group A ewes had significantly decreased plasma free fatty acids (p 0.001) and β‐hydrobutyric acid (p 0.05), but higher insulin (p 0.01) concentrations, whereas serum T4 concentrations were higher in K than in CH ewes (p 0.01), during the last 10 days of pregnancy. The fat cell diameter and the NADP‐isocitrate dehydrogenase activity of the adipose tissue were higher in ewes of group A than group B, on the day 7 before lambing. In the second experiment, the underfed CH ewes had significantly lower empty udder weight (p 0.05), smaller udder (p 0.05), smaller teat length (p 0.01), lower mammary gland weight (p 0.05), less total content of DNA (p 0.05) and less fat percentage of mammary gland (p 0.01) in comparison with the well‐fed CH ewes. It is concluded that undernutrition during pregnancy causes considerable changes in the ewe's metabolism, mainly in the adipose tissue. Furthermore, the level of nutrition significantly affected udder development.

Effects of porcine somatotropin on the chemical body composition and fat quality in growing-finishing pigs.

Seventy eight growing-finishing pigs (male castrates and females) of the cross-breed Pietrain x (Large White x German Landrace) were used to investigate the effects of pST treatment on the chemical composition of the body, the growth of adipocytes, and the fatty acid profile of the backfat. Intramuscular injections (1 or 3 mg pST) were administered daily from an average weight of 65 kg up to slaughter. After pST treatment significant changes in all studied characteristics were observed in barrows, whereas the females exhibited very small responses. The pST caused an increase of water and protein contents and a simultaneous decrease of lipid content especially in body parts rich in fat. Furthermore, the proportion of unsaturated fatty acids increased and the fat cell diameter decreased in the backfat.

Reproductive history in relation to relative weight and fat distribution

Department of Primary Health Care, Sahlgrenska University Hospital, Goteborg University, Gothenburg, Sweden. OBJECTIVE: To investigate the relationship between reproductive history and body composition. DESIGN: Prospective population study in Sweden. SUBJECTS: 1462 randomly selected women representing five separate age cohorts (38, 46, 50, 54 and 60 at the 1968-1969 baseline examination) have been followed longitudinally. MEASUREMENTS: Relative weight, fat distribution, and fat cellularity were related to menarche, parity, lactation, menopause and oestrogen medication. RESULTS: Age of menarche did not show any association with subsequent fat distribution, nor did length of lactation time. On the other hand parity was positively associated to total as well as central obesity, and lactation time was positively associated to abdominal fat cell diameter. Premenopausal women showed higher mean body weight and hip circumference than postmenopausal women of the same age. Change from pre- to postmenopausal status was associated with increase of waist circumference as well as reduction of hip circumference, resulting in an increased waist-hip ratio (WHR). Oestrogen replacement suggested some postponement of this increase. CONCLUSION: Parity and menopause are the reproductive factors most associated with gradual changes in body fat distribution. Oestrogen medication seems to play an additional role in diminishing waist circumference increase and could thus contribute to decreased cardiovascular morbidity in women. PMID: 8653141 [PubMed - indexed for MEDLINE]

Effects of β-agonist, L-644,969, on adipose depots in growing female rats

Growing female Sprague Dawley rats (n = 33) were used to determine the effects of β-agonist, L-644,969, on adipose depots, mammary growth and plasma ST and IGF-I levels. Fat-cell diameter in SF and PF, and mammary DNA content were studied. Rats were allocated to three groups to receive 0,4 or 8 mg kg−1 L-644,969 in powdered diet for 35 d. Compared with control, total mammary gland weight, as a proportion of final body weight, was reduced 14.6 (P &lt; 0.05) and 35.6% (P &lt; 0.01), PF was reduced 30 and 49.6% (both P &lt; 0.01) by 4 and 8 mg kg−1, respectively. The SF was reduced 22.3% (P &lt; 0.05) by β-agonist at 8 mg kg−1 only. In all fat depots, the reductions increased with increasing dose of β-agonist. Carcass fat percentage was reduced by 28.5 and 41.7% (both P &lt; 0.01) in rats fed β-agonist at 4 and 8 ppm, respectively. Fat-cell diameter in both SF and PF was reduced (P &lt; 0.05) (except at 4 ppm level in SF), and mammary DNA content was increased (P &lt; 0.01) in both treatment groups. There was a trend to increased ST concentration but to lower IGF-I concentration as β-agonist levels in diet increased (P &gt; 0.1). The results indicate that β-agonist is effective in reducing body fat deposition and fat-cell size and stimulating mammary gland growth, which may play a role in the control of mammogenesis in growing rats. Key words: Rats, β-agonist, mammary gland, adipose tissue

Fat cells in red bone marrow of human rib: their size and spatial distribution with respect to the radon-derived dose to the haemopoietic tissue.

Samples of human rib were collected at autopsy and 20 were selected for marrow fat cell measurement, representing an age range of 16-96 years. The mean diameter of fat cells in red bone marrow of human rib was found to increase from around 48 microns at ages 16-29 years to around 65 microns at ages 82-96 years. There was a greater number of fat cells of smaller size range in younger ages compared with that in older ones. The maximum size of fat cells was found to be 102 microns. Calculated radon-derived doses to haemopoietic tissue ranged from 60 to 162 microSv y-1 at average UK exposures of 20 Bq m-3. It was concluded that the bone marrow fat fraction is the important parameter as far as alpha-radiation dose from radon in fat is concerned. This updates the theoretical estimates of dose carried out by Richardson et al. (1991).

Comparison of two methods to assess the tissue/blood partition coefficient for xenon in subcutaneous adipose tissue in man

A new method to calculate the tissue/blood partition coefficient (lambda) for xenon in studies on the subcutaneous adipose tissue blood flow was compared with a previously reported method based on local skinfold thickness (lambda LST). The former method included needle biopsies from the abdominal and femoral subcutaneous adipose tissue, and the mean fat cell diameter was measured (lambda ECT). The extracellular tissue fraction in subcutaneous tissue was then estimated from a diagram. The tissue lipid content was approximated to equal the relative intracellular volume and Ostwald's solubility coefficients for 133Xe, based on the distribution of xenon in lipid, albumin and 0.9% saline were applied. Estimated lambda-values based on needle biopsies from the abdominal site were: 8.6 +/- 0.1 versus 9.9 +/- 0.4 ml g-1 (mean +/- SE) (P < 0.05) and from the femoral site: 9.1 +/- 0.1 versus 9.6 +/- 0.2 in lean (n = 10) and obese subjects (n = 10), respectively. The corresponding lambda-values obtained from skinfold measurements were: 6.2 +/- 0.5 versus 11.0 +/- 0.4 (P < 0.001) and 6.9 +/- 0.3 versus 11.4 +/- 0.4 (P < 0.001) in lean and obese subjects, respectively. Pooled lambda LST-values correlated positively with estimated adipose tissue blood flow (ATBF) (r: 0.34, P < 0.05, n = 40) whereas no such correlation was found for lambda ECT-values. In conclusion, a new method is presented which may allow an accurate determination of, and which may lead to reliable data on, subcutaneous ATBF in both lean and obese subjects.(ABSTRACT TRUNCATED AT 250 WORDS)

Validation of Indirect Measures of Body Fat in Lactating Cows

The objective of the study was to establish and compare equations that would estimate the body fat content of lactating dairy cows from different indirect techniques. The techniques used were body condition scoring, dilution of D2O in body water, and determination of mean fat cell size diameter of the subcutaneous, abdominal, and perirenal depots. Each technique was validated against direct determination of body fat content of the same lactating cows. To apply equations to high producing, lactating dairy cows, cows were from a herd producing more than 9500kg of FCM/305 d, were lactating, and were in less than average body condition. Eight days prior to slaughter, a single injection of D2O was injected into the jugular vein, and body dilution was followed for 4 d. Cows were scored for body condition on the day of injection and weighed daily for the 4 d prior to slaughter. Samples of subcutaneous, perirenal, and omental adipose depots were taken, and adipocyte size and number were determined. Body fat was not predicted well by D2O space alone, but inclusion of BW did improve the prediction of body fat from this variable. The best equations were derived from use of BW with body condition score or subcutaneous fat cell diameter: observed body fat = −122.1 + .21 × BW + 36.0 × body condition score, and −195.6 + .290 × BW + .927 × subcutaneous fat cell diameter; standard errors of the estimate were 4.6 and 5.5kg, respectively. Equations using diameters of abdominal and perirenal fat cells gave similar relationships. Equations using all four predictors (live BW, fat cell diameter, condition score, and D2O space) were only slightly improved over these equations. Thus, use of body condition score, adipocyte diameter, and BW in laboratory and field conditions may help in the study and management of the use of body fat in lactating dairy cows.

Reversal of high-fat diet-induced obesity in female rats.

The purpose of the present study was to test whether the degree of obesity or the duration of the obese state affects the reversibility of diet-induced obesity. This was accomplished by initially feeding adult female Wistar rats either a low-fat diet (Chow) or one of two high-fat diets (HFDs; 30 and 60% of total calories as dietary fat; 30% HFD and 60% HFD, respectively). Fifty-four days, reversal 1 (R1), or ninety-seven days, reversal 2 (R2), later the HFDs were substituted with the low-fat control diet in subgroups of rats. Animals from all groups were sampled at three intervals: the start of R1 (R1 start), and the completion of R1 (R1 end) and R2 (R2 end). At the end of each interval the 60% HFD-fed group had increased body weight, carcass lipid content, and retroperitoneal and parametrial white adipose tissue (RWAT and PWAT) pad weight, fat cell diameter, and fat cell volume, but not fat cell number (FCN), compared with the other groups. The 60% HFD-fed rats also exhibited a marked and persistent hyperphagia that continued even as most of the indexes of obesity approached their maximal values (R1 end). The 60% HFD group had a transient increase in RWAT and PWAT lipoprotein lipase activity that followed the development of most obesity indicators. A clear intermediate level of obesity did not develop in the 30% HFD-fed group. Instead, these animals had nonsignificant increases in these measures of adiposity, making it impossible to test whether the severity of the obesity affected its reversibility in age-matched groups.(ABSTRACT TRUNCATED AT 250 WORDS)

Age-Dependent Dose to Red Bone Marrow from Natural Radon, Thoron and 40K

The age-dependent radiation dose to the haematopoietic tissue of bone marrow has been calculated for exposure to radon, thoron and their daughter products, for the foetus, children and adults. The component of dose due to pure radon is dependent on the fat content of the marrow, since the solubility of radon in fat is about sixteen times that in tissue. The mean dose equivalent µSv to the total active marrow is estimated for a range of fat cell diameters from 25 to 200 µm, taking account of the percentage cellularity and distribution of active marrow as a function of age. Similarly the dose due to the inhalation of short-lived radon daughters was estimated, based on measurements in blood and marrow, modified to allow for the greater deposition of daughter products expected in children. An estimate of the age-dependent dose from long-lived radon daughters was made from uranium miners and natural exposure data. Dose estimates were made for the average UK indoor exposure to radon gas of 20 Bq.m-3 and an equilibrium equivalent thoron concentration of 0.3 Bq.m-3. The annual radon and thoron derived dose to the active marrow of the newborn was calculated as 30 and 40 µSv respectively. For a 10 year old child, the radon and thoron derived annual doses are 70 and 40 µSv and for the 40 year old adult 90 and 30 µSv, respectively.

Age-Dependent Dose to Red Bone Marrow from Natural Radon, Thoron and 40K

The age-dependent radiation dose to the haematopoietic tissue of bone marrow has been calculated for exposure to radon, thoron and their daughter products, for the foetus, children and adults. The component of dose due to pure radon is dependent on the fat content of the marrow, since the solubility of radon in fat is about sixteen times that in tissue. The mean dose equivalent µSv to the total active marrow is estimated for a range of fat cell diameters from 25 to 200 µm, taking account of the percentage cellularity and distribution of active marrow as a function of age. Similarly the dose due to the inhalation of short-lived radon daughters was estimated, based on measurements in blood and marrow, modified to allow for the greater deposition of daughter products expected in children. An estimate of the age-dependent dose from long-lived radon daughters was made from uranium miners and natural exposure data. Dose estimates were made for the average UK indoor exposure to radon gas of 20 Bq.m-3 and an equilibrium equivalent thoron concentration of 0.3 Bq.m-3. The annual radon and thoron derived dose to the active marrow of the newborn was calculated as 30 and 40 µSv respectively. For a 10 year old child, the radon and thoron derived annual doses are 70 and 40 µSv and for the 40 year old adult 90 and 30 µSv, respectively.

Dose to red bone marrow from natural radon and thoron exposure.

The age-dependent radiation dose to the haematopoietic tissue of bone marrow has been calculated for exposure to radon, thoron and their daughter products. The component of dose due to pure radon is dependent on the fat content of the marrow, since the solubility of radon in fat is about 16 times that in tissue. The mean dose equivalent muSv to the total active marrow is estimated for a range of fat cell diameters from 25 to 200 microns, taking account of the percentage cellularity and distribution of active marrow as a function of age. Similarly, the dose due to the inhalation of short-lived radon daughters was estimated, based on measurements in blood and marrow, modified to allow for the greater deposition of daughter products expected in children. An estimate of the age-dependent dose from long-lived radon daughters was made from uranium miner and natural exposure data. Dose estimates were made for the average UK indoor exposure to radon gas of 20 Bq/m3 and an equilibrium equivalent thoron concentration of 0.3 Bq/m3. The annual radon and thoron derived dose to the active marrow of the newborn was calculated as 30 and 40 muSv, respectively. For a 10-year-old child, the radon and thoron derived annual dose are 70 and 40 muSv, and for a 40-year-old adult 90 and 30 muSv, respectively. The above values exhibit wide range limits due principally to uncertainties in the accumulation of 210Pb in bone, and 210Po in marrow. These data indicate that at the average UK exposure, the alpha-particle dose to active marrow is dominated by that derived from inhaled radon and thoron compared with dietary intake. In infants the dose is dominated by thoron daughters. At the UK radon Action Limit of 200 Bq/m3, the radon and associated thoron derived dose is similar to that from all low LET sources. This work shows that the dose to red bone marrow from radon and thoron is significant, and that the possibility of leukaemia induced by these radiation sources warrants further investigation.

Effect of postweaning thyroid status on endocrine and adipose development in rats.

We previously reported that 6 wk after thyroidectomy, rat fat cell diameter and number were 86 and 32% of values in age-matched controls. This study aims to 1) determine the time course of these changes and of parallel changes in the levels of several hormones known to participate in adipose differentiation and 2) try to normalize the altered cellularity with thyroxine (T4) treatment. Rats were thyroidectomized (T) or sham-operated and studied 2, 5, or 6 wk later. At 5 wk some T rats received L-T4. Epididymal fat cells were sized and used to estimate fat cell number. Triiodothyronine (T3), T4, thyroid-stimulating hormone, somatotropin (GH), and insulin plasma levels were assayed. In T rats fat cell hypertrophia was blunted uniformly with time, whereas fat cell hyperplasia was slow for 2 wk and zero thereafter. Insulinemia was less drastically reduced than T4, T3, and GH levels. The fat cell number-to-body weight ratio always stayed close to the ratio present at thyroidectomy. In T rats receiving a T4 substitution dose for 1 wk, fat cell number and body weight increased, but not when the T4 dose was lower even though the plasma thyroid hormone levels were increased. These thyroid hormone effects on adipose tissue are probably secondary to other endocrine changes that occur in hypothyroidism.

Dietary influence on the insulin function in the epididymal fat cell of the Wistar rat. III. Effect of the ratio carbohydrate to fat.

Newly weaned male Wistar rats were fed semipurified diets containing sunflowerseed oil or palm oil. The fatty acid compositions of the phospholipid and triacylglycerol fractions either from whole epididymal fat pads or from fat cells isolated from the pads appeared to be nearly similar. Feeding the diets for a period of only 3-4 weeks after weaning was found to be sufficient to produce a difference in insulin response and insulin binding in the epididymal fat cells. A reduction in the dietary fat content from 30 to 15% of the energy had only minor effects on fat pad weight and on the fatty acid composition of the phospholipid- and triacylglycerol fractions isolated from the epididymal fat pads. There was no effect either on body weights or on average fat cell diameter but there was an increase in insulin response in the isolated fat cells, however. The difference in insulin response after a diet rich in polyunsaturated fatty acids (sunflowerseed oil) as compared to one rich in saturated fatty acids (palm oil) remained after the reduction of fat content.

Genotype-controlled changes in body composition and fat morphology following overfeeding in twins

This study investigated the effects of overfeeding on the body composition and fat morphology characteristics of 6 pairs of male monozygotic twins. Each participant was submitted to a 22-day overfeeding period, supplemented by an additional 1000 kcal/day. Significant changes were observed in body composition and fat morphology as shown by increases in body weight, fat mass, sum of 9 skinfolds, and fat cell diameter. Significant within-pair resemblance for absolute changes was observed for body weight, percent body fat, fat mass, sum of skinfolds, trunk skinfolds, and extremity skinfolds, suggesting a role for the genotype in determining the sensitivity of the response to an energy surplus. Significant within-pair resemblance was noted for the biceps, triceps, and thigh with less resemblance noted in the subscapular, abdomen, suprailiac, calf, axillary, and chest sites, suggesting a variation in genotype dependency for subcutaneous fat The results suggest that changes in body fat following short-term overfeeding appear to have a genetic basis.

Genotype dependency of adaptation in adipose tissue metabolism after short-term overfeeding.

The present study investigated the interaction of genotype and short-term overfeeding on adipose tissue metabolism of six pairs of male monozygotic twins. The sedentary nonobese twins were submitted to a 22-day overfeeding period in which their normal daily intake was supplemented by an additional 1,000 kcal/day. A fat tissue biopsy was performed in the suprailiac region before and after overfeeding to determine fat cell diameter and basal and maximal stimulated epinephrine, norepinephrine, and isoproterenol lipolysis from collagenase-isolated fat cells. Fat cell basal and maximal insulin-stimulated glucose conversion into triglycerides (basal and stimulated lipogenesis) were measured using [14C]glucose. Adipose tissue heparin-releasable lipoprotein lipase activity (LPL) was also determined. A repeated measures analysis of variance revealed overfeeding induced significant elevations in basal lipogenesis (P less than 0.05) and fat cell diameter (P less than 0.05). No significant group changes were noted in basal, epinephrine-, norepinephrine-, and isoproterenol-stimulated lipolysis, insulin-stimulated lipogenesis, and LPL activity due to large individual variation in the response to overfeeding. However, significant intrapair resemblance was noted in the changes of the aforementioned variables, suggesting a coherent within-twin pair response, despite large between-pair variation in response. Less within-pair similarity was noted in changes in basal lipogenesis and fat cell diameter. The results of the present study suggest that overfeeding induced a large range of adipose tissue metabolic responses and that the genotype plays a role in determining the sensitivity of adipose tissue adaptation to caloric affluence.

Abnormalities of islet B-cell function, insulin action, and fat distribution in women with histories of gestational diabetes: relationship to obesity.

Although obese women with histories of gestational diabetes mellitus (former GDM) are highly predisposed to develop noninsulin-dependent diabetes mellitus (NIDDM), lean former GDM women are less predisposed. To explore reasons for this difference, we performed measures of islet B-cell function and insulin action in eight lean former GDM women [ideal body weight (IBW), 107 +/- 2% (mean +/- SEM)], 11 obese former GDM (IBW, 161 +/- 11%), and 19 normal women subjects who were individually pair-matched to former GDM for % IBW and age. The first phase (0-10 min) insulin secretory response to iv glucose was significantly lower in both lean and obese former GDM compared to that in normal women (3,480 +/- 548% vs. 8,234 +/- 1,337% basal . min and 3,444 +/- 682 vs. 10,251 +/- 2,465). The second phase (10-60 min) insulin response to glucose was also significantly lower in lean former GDM women and tended to be lower in obese former GDM women compared to that in their respective controls. Insulin action was assessed by the insulin sensitivity index (SI) using Bergman's minimal modeling technique. SI values in lean former GDM women were similar to those in their controls (4.42 +/- 1.3 X 10(-4) ml min-1 microU-1 vs. 5.19 +/- 1.2 X 10(-4). In contrast, SI values in obese former GDM women were significantly lower than those in their controls (0.77 +/- 0.28 X 10(-4) vs. 2.04 +/- 0.43 X 10(-4). To assess whether differences in fat distribution and fat cell size were associated with these differences in insulin sensitivity, the waist to thigh circumference ratio, the waist to hip ratio, and abdominal fat cell diameter were measured. All three were significantly greater in the obese former GDM women than in controls. Thus, an abnormal central distribution of adiposity appears to be associated with the insulin action defect in obese former GDM women. We conclude that both lean and obese former GDM women have insulin secretion defects. Although a modest insulin action defect in lean former GDM women may have been missed by this technique, only in the obese former GDM women, who have a higher risk for future NIDDM, was an insulin action defect demonstrable. Thus, impairments of both insulin secretion and insulin action may be necessary to cause a marked predisposition toward NIDDM.