scholarly journals Estradiol acutely inhibits whole body lipid oxidation and attenuates lipolysis in subcutaneous adipose tissue: a randomized, placebo-controlled study in postmenopausal women

2012 ◽  
Vol 167 (4) ◽  
pp. 543-551 ◽  
Author(s):  
Lars Christian Gormsen ◽  
Christian Høst ◽  
Britta Eilersen Hjerrild ◽  
Steen Bønløkke Pedersen ◽  
Søren Nielsen ◽  
...  

ContextEstradiol (E2) promotes and maintains the female phenotype characterized by subcutaneous fat accumulation. There is evidence to suggest that this effect is due to increased anti-lipolytic α2A-adrenergic receptors, but whether this requires long-term exposure to E2or is an immediate effect is not clear.ObjectiveTo study acute effects of a single dose (4 mg) of 17β-E2on regional and systemic lipolysis.MethodsSixteen postmenopausal women (age, 59±5 years; weight, 67±10 kg; and BMI, 24.8±2.9) were studied in a crossover design: i) placebo and ii) 4 mg E2. Basal and adrenaline-stimulated regional lipolysis was assessed by microdialysis and substrate oxidation rates by indirect calorimetry. Tissue biopsies were obtained to assess lipoprotein lipase activity and mRNA expression of adrenergic, estrogen, cytokine, and vascular reactivity receptors.ResultsAcute E2stimulation significantly attenuated catecholamine-stimulated lipolysis in femoral subcutaneous adipose tissue (interstitial glycerol concentration (micromole/liter) ANOVA time vs treatment interaction,P=0.01) and lipolysis in general in abdominal adipose tissue (ANOVA treatment alone,P<0.05). E2also reduced basal lipid oxidation ((mg/kg per min) placebo, 0.58±0.06 vs E2, 0.45±0.03;P=0.03) and induced a significantly higher expression of anti-lipolytic α2A-adrenergic receptor mRNA (P=0.02) in skeletal muscle tissue as well as an upregulation ofeNOS(NOS3) mRNA (P=0.02).ConclusionE2acutely attenuates the lipolytic response to catecholamines in subcutaneous adipose tissue, shifts muscular adrenergic receptor mRNA toward anti-lipolytic α2A-receptors, decreases whole body lipid oxidation, and enhances expression of markers of vascular reactivity.

2009 ◽  
Vol 297 (5) ◽  
pp. E999-E1003 ◽  
Author(s):  
Birgit Gustafson ◽  
Silvia Gogg ◽  
Shahram Hedjazifar ◽  
Lachmi Jenndahl ◽  
Ann Hammarstedt ◽  
...  

Obesity is associated mainly with adipose cell enlargement in adult man (hypertrophic obesity), whereas the formation of new fat cells (hyperplastic obesity) predominates in the prepubertal age. Adipose cell size, independent of body mass index, is negatively correlated with whole body insulin sensitivity. Here, we review recent findings linking hypertrophic obesity with inflammation and a dysregulated adipose tissue, including local cellular insulin resistance with reduced IRS-1 and GLUT4 protein content. In addition, the number of preadipocytes in the abdominal subcutaneous adipose tissue capable of undergoing differentiation to adipose cells is reduced in hypertrophic obesity. This is likely to promote ectopic lipid accumulation, a well-known finding in these individuals and one that promotes insulin resistance and cardiometabolic risk. We also review recent results showing that TNFα, but not MCP-1, resistin, or IL-6, completely prevents normal adipogenesis in preadipocytes, activates Wnt signaling, and induces a macrophage-like phenotype in the preadipocytes. In fact, activated preadipocytes, rather than macrophages, may completely account for the increased release of chemokines and cytokines by the adipose tissue in obesity. Understanding the molecular mechanisms for the impaired preadipocyte differentiation in the subcutaneous adipose tissue in hypertrophic obesity is a priority since it may lead to new ways of treating obesity and its associated metabolic complications.


1992 ◽  
Vol 263 (5) ◽  
pp. E850-E855 ◽  
Author(s):  
L. Simonsen ◽  
J. Bulow ◽  
J. Madsen ◽  
N. J. Christensen

Whole body energy expenditure, thermogenic and metabolic changes in the forearm, and intercellular glucose concentrations in subcutaneous adipose tissue on the abdomen determined by microdialysis were measured during epinephrine infusion in healthy subjects. After a control period, epinephrine was infused at rates of 0.2 and 0.4 nmol.kg-1 x min-1. Whole body resting energy expenditure was 4.36 +/- 0.56 (SD) kJ/min. Energy expenditure increased to 5.14 +/- 0.74 and 5.46 +/- 0.79 kJ/min, respectively (P < 0.001), during the epinephrine infusions. Respiratory exchange ratio was 0.80 +/- 0.04 in the resting state and did not change. Local forearm oxygen uptake was 3.9 +/- 1.3 mumol.100 g-1 x min-1 in the basal period. During epinephrine infusion, it increased to 5.8 +/- 2.1 (P < 0.03) and 7.5 +/- 2.3 mumol.100 g-1 x min-1 (P < 0.001). Local forearm glucose uptake was 0.160 +/- 0.105 mumol.100 g-1 x min-1 and increased to 0.586 +/- 0.445 and 0.760 +/- 0.534 mumol.100 g-1 x min-1 (P < 0.025). The intercellular glucose concentration in the subcutaneous adipose tissue on the abdomen was equal to the arterial concentration in the basal period but did not increase as much during infusion of epinephrine, indicating glucose uptake in adipose tissue in this condition. If it is assumed that forearm skeletal muscle is representative for the average skeletal muscle, it can be calculated that on average 40% of the enhanced whole body oxygen uptake induced by infusion of epinephrine is taking place in skeletal muscle. It is proposed that adipose tissue may contribute to epinephrine-induced thermogenesis.


Obesity ◽  
2014 ◽  
Vol 22 (6) ◽  
pp. 1458-1463 ◽  
Author(s):  
Beret A. Casey ◽  
Wendy M. Kohrt ◽  
Robert S. Schwartz ◽  
Rachael E. Van Pelt

2001 ◽  
Vol 90 (1) ◽  
pp. 99-104 ◽  
Author(s):  
Nicole A. Lynch ◽  
Barbara J. Nicklas ◽  
Dora M. Berman ◽  
Karen E. Dennis ◽  
Andrew P. Goldberg

The accumulation of visceral fat is independently associated with an increased risk for cardiovascular disease. The aim of this study was to determine whether the loss of visceral adipose tissue area (VAT; computed tomography) is related to improvements in maximal O2 uptake (V˙o 2 max) during a weight loss (250–350 kcal/day deficit) and walking (3 days/wk, 30–40 min) intervention. Forty obese [body fat 47 ± 1 (SE) %], sedentary (V˙o 2 max 19 ± 1 ml · kg−1 · min−1) postmenopausal women (age 62 ± 1 yr) participated in the study. The intervention resulted in significant declines in body weight (−8%), total fat mass (dual-energy X-ray absorptiometry; −17%), VAT (−17%), and subcutaneous adipose tissue area (−17%) with no change in lean body mass (all P < 0.001). Women with an average 10% increase in V˙o 2 max reduced VAT by an average of 20%, whereas those who did not increaseV˙o 2 max decreased VAT by only 10%, despite comparable reductions in body fat, fat mass, and subcutaneous adipose tissue area. The decrease in VAT was independently related to the change in V˙o 2 max( r 2 = 0.22; P < 0.01) and fat mass ( r 2 = 0.08; P = 0.05). These data indicate that greater improvements inV˙o 2 max with weight loss and walking are associated with greater reductions in visceral adiposity in obese postmenopausal women.


1994 ◽  
Vol 266 (1) ◽  
pp. E151-E154 ◽  
Author(s):  
T. J. Kowalski ◽  
M. Watford

Information about adipose tissue amino acid metabolism is limited, with most data derived from studies in vitro. The purpose of this study was to further characterize the role of adipose tissue in glutamine metabolism in the rat in vivo. The extracellular concentrations of glutamine, glutamate, alanine, and ammonia were measured in the rat inguinal fat pad using a microdialysis sampling technique. A calibration method was used to accurately assess the extracellular levels of metabolites, and a comparison of these concentrations with those in arterial blood allowed determination of the net flux of each compound. The adipose tissue-arterial blood concentration differences were 122 +/- 19, 54 +/- 37, -61 +/- 21, and -28 +/- 13 microM for glutamine, alanine, glutamate, and ammonia, respectively, indicating a production of glutamine and an uptake of glutamate by subcutaneous adipose tissue. The magnitude of glutamine production suggests that adipose tissue may play a significant role in whole body glutamine homeostasis.


2007 ◽  
Vol 88 (1) ◽  
pp. 100-106 ◽  
Author(s):  
Hong Zang ◽  
Mikael Rydén ◽  
Kerstin Wåhlen ◽  
Karin Dahlman-Wright ◽  
Peter Arner ◽  
...  

2005 ◽  
Vol 288 (5) ◽  
pp. E930-E934 ◽  
Author(s):  
Neda Rasouli ◽  
Ulrika Raue ◽  
Leslie M. Miles ◽  
Tong Lu ◽  
Gina B. Di Gregorio ◽  
...  

Patients with insulin resistance often manifest increased intramyocellular lipid (IMCL) along with increased visceral adipose tissue. This study was designed to determine whether the insulin sensitizer drugs pioglitazone and metformin would improve glucose intolerance and insulin sensitivity by decreasing IMCL. In this study, 23 generally healthy subjects with impaired glucose tolerance were randomized to receive either pioglitazone 45 mg/day or metformin 2,000 mg/day for 10 wk. Before and after treatment, we measured insulin sensitivity and abdominal subcutaneous and visceral adipose tissue with CT scanning. In addition, muscle biopsies were performed for measurement of IMCL and muscle oxidative enzymes. After treatment with pioglitazone, 2-h glucose fell from 9.6 mmol/l (172 mg/dl) to 6.1 mmol/l (119 mg/dl), whereas there was no change in 2-h glucose with metformin. With pioglitazone treatment, there was a 65% increase in insulin sensitivity along with a 34% decrease in IMCL (both P ≤ 0.002). This decrease in IMCL was not due to increased muscle lipid oxidation, as there were no changes in muscle lipid oxidative enzymes. However, pioglitazone resulted in a 2.6-kg weight gain along with a significant decrease in the visceral-to-subcutaneous adipose tissue ratio. In contrast, metformin treatment resulted in no change in insulin sensitivity, IMCL, oxidative enzymes, or adipose tissue volumes. Pioglitazone improved glucose tolerance and insulin sensitivity by reducing IMCL. This reduction in IMCL was not due to an increase in muscle lipid oxidation but to a diversion of lipid from ectopic sites into subcutaneous adipose tissue.


Imaging ◽  
2021 ◽  
Author(s):  
Takashi Abe ◽  
Vickie Wong ◽  
Zachary W. Bell ◽  
Robert W. Spitz ◽  
Scott J. Dankel ◽  
...  

Background:It has been observed that gluteal-femoral adipose tissue has a protective effect against risk factors for cardiovascular disease but has not yet been concluded how different evaluation methods of fat distribution affect the results.Methods:To test the hypothesis that B-mode ultrasound-measured subcutaneous adipose tissue distribution is associated with cardiovascular risk factors, 326 Japanese unmedicated postmenopausal women aged 50-70 years were analyzed. Subcutaneous adipose tissue thickness at 6 sites (anterior and posterior aspects of trunk, upper-arm, and thigh) and serum total (TC) and high-density lipoprotein cholesterol (HDLC) was measured, and a ratio of HDLC to TC (HDLC/TC) was calculated. We used Bayesian linear regression with 4 separate models with each model predicting HDLC/TC.Results:Our first model provided evidence for an inverse correlation (r = –0.23) between ultrasound measured body fat (6 site measurement) and HDLC/TC. The second model noted evidence for an inverse correlation between trunk fat and HDLC/TC and found evidence for the null with respect to the correlation between thigh fat and HDLC/TC. Therefore, we added thigh fat to the null model to produce Distribution Model 2. Within this model, we noted an inverse correlation (r = –0.353) between trunk fat and HDLC/TC. Our last model determined that within the trunk fatness, the abdominal area (anterior trunk) was a larger predictor than the subscapular site (posterior trunk).Conclusion:These results support the evidence that ultrasound-measured abdominal subcutaneous adipose tissue thickness is a non-invasive predictor for monitoring the risk for dyslipidemia in postmenopausal women.


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