Estrogen Controls Lipolysis by Up-Regulating α2A-Adrenergic Receptors Directly in Human Adipose Tissue through the Estrogen Receptor α. Implications for the Female Fat Distribution

Pedersen, Steen B.; Kristensen, Kurt; Hermann, Pernille; Katzenellenbogen, John A.; Richelsen, Bjørn

doi:10.1210/jc.2003-031327

Cited by 226 publications

(200 citation statements)

References 43 publications

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“…30,31 Estrogen may also decrease lipolysis in adipose tissues by increasing the number of antilipolytic a2A-adrenergic receptors. 20,32 Besides, it was suggested that estrogen may attenuate growth hormone (GH) signaling 33 and GH was reported to increase lipid oxidation 34 and reduce body fatness. 35 In sum, estrogen can affect obesity phenotypes through different pathways which may interact with each other, and much work is needed to understand its precise role in obesity.…”

Section: Discussionmentioning

confidence: 99%

Genetic and environmental correlations between obesity phenotypes and age at menarche

Wang

Zhao

et al. 2006

Int J Obes

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Objective: To assess the extent that the genetic and environmental factors contribute to the phenotypic correlations between obesity traits and age at menarche (AAM), and also to examine the influence of AAM on obesity in both pre-and postmenopausal women. Methods: Five hundred and twelve pedigrees with 2667 Caucasian female subjects from two to four generations were recruited. Fat mass and lean mass (both in kg) were measured by dual-energy X-ray absorptiometry scanner. Body mass index (BMI) (kg/m 2 ) was calculated. We performed bivariate quantitative genetic analyses in the total sample containing 2667 Caucasian women. We also selected 206 unrelated premenopausal women and 140 unrelated postmenopausal women from the total sample, and computed the respective phenotypic correlation between obesity and AAM in these two subgroups. Results: For fat mass, lean mass and BMI, we detected their significant negative genetic correlations with AAM after adjustment for significant covariates, which were À0.3170 (Po0.001), À0.1721 (Po0.05) and À0.3665 (Po0.001), respectively. However, their environmental correlations with AAM were all nonsignificant (P40.05), ranging from À0.0016 to 0.0192. In the premenopausal subgroup, significant associations were observed between fat mass and AAM (r ¼ À0.231, Po0.01) as well as between BMI and AAM (r ¼ À0.257, Po0.01). In the postmenopausal subgroup, no such associations were observed. Conclusion: Our results for the first time suggested that significant phenotypic association between obesity phenotypes and AAM is mainly attributable to shared genetic rather than environmental factors, and AAM may have stronger effects on obesity phenotypes in pre-than in postmenopausal women.

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Section: Discussionmentioning

confidence: 99%

Genetic and environmental correlations between obesity phenotypes and age at menarche

Wang

Zhao

et al. 2006

Int J Obes

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“…Real-time quantitation of target gene to -actin mRNA was performed with a SYBR-Green real-time PCR assay using an ICycler from BioRad (Hercules, CA, USA) as described previously. 12 The target gene and -actin mRNA were amplified in separate tubes. The increase in fluorescence was measured in real time during the extension step.…”

Section: Lipolysismentioning

confidence: 99%

Low Sirt1 expression, which is upregulated by fasting, in human adipose tissue from obese women

et al. 2008

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Objective: Calorie restriction increases the life span in a number of different organisms. This effect is dependent upon activation of the Sirt1 enzyme, and many of the beneficial effects of calorie restriction can be mimicked using resveratrol, which activates the Sirt1 enzyme. Nothing is known about this system in human adipose tissue; therefore, we investigated this system in human adipose tissue. Design: Sirt1 mRNA was measured in adipose tissue biopsies from human volunteers before and after 6 days of total fasting. In addition, adipose tissue from lean and obese individuals was compared and in vitro investigations were performed. Results: Long-term total fasting (6 days) of nine human volunteers increased Sirt1 mRNA expression in subcutaneous adipose tissue more than twofold (0.197-0.454 arbitrary units, Po0.05). Likewise, lean women (n ¼ 12) had more than twofold higher Sirt1 expression in subcutaneous adipose tissue compared to obese women (n ¼ 12; 0.33-0.73 arbitrary units, Po0.05). Sirt1 was equally expressed in the stroma-vascular fraction and the isolated adipocyte fraction. Finally, in vitro, we demonstrated that resveratrol (a Sirt1 activator) significantly enhanced the lipolytic effect of epinephrine in human adipose tissue (Po0.05). Conclusion: Human adipose tissue contains Sirt1 and the expression of Sirt1 can be regulated by calorie restriction as in other species. Furthermore, we demonstrated that resveratrol affects human fat-cell metabolism similar to the effects in rodents (that is, increased epinephrine induced lipolysis). These findings indicated that the beneficial effects of calorie restriction in humans might involve the activation of Sirt1. Thus, based on these findings, we propose that Sirt1 might play important roles for the beneficial effects of calorie restriction in humans.

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“…Trying to explain how estrogen promotes and maintains the typical female type of fat distribution, Pedersen et al [20] studied the effects of estradiol in vivo and in vitro on human adipose tissue metabolism and observed that estradiol administration attenuates lipolytic response in subcutaneous abdominal adipocytes, but not in intra-abdominal adipocytes. They found that estradiol directly increases the number of antilipolytic α-2A-adrenergic receptors in subcutaneous adipocytes and, in contrast, no effect of estrogen on α-2A-adrenergic receptor messenger RNA expression was observed in adipocytes from the visceral fat depots.…”

Section: Sex Hormones and Abdominal Obesitymentioning

confidence: 99%

Abdominal Obesity and Metabolic Alterations in the Menopausal Transition

Berg

Mesch

Siseles

2012

Curr Obstet Gynecol Rep

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The prevalence of overweight and obesity is strikingly increasing worldwide. Obesity is a major risk factor for non-insulin-dependent diabetes mellitus, cardiovascular diseases, and cancer, and is also associated with various psychosocial consequences. Menopausal transition is associated with unfavorable changes in body composition and abdominal fat deposition, which is accompanied by an increment of insulin resistance/hyperinsulinemia, a decrease in sex hormone-binding globulin levels and, consequently, an increase in free testosterone and greater androgenicity. Central body fat also correlates with deleterious changes in adipokines and inflammation markers like leptin, C-reactive protein, and adiponectin. In addition, the greater deposition of visceral fat in the menopausal transition contributes to the development of an atherogenic lipoprotein profile, which includes high triglyceride and low high-density lipoprotein (HDL) cholesterol concentrations, as well as an increment of small dense low-density lipoprotein (LDL) subfraction, intermediate density lipoproteins (IDL), apolipoprotein (apo) B/apo A-I ratio and lipoprotein(a).

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Estrogen Controls Lipolysis by Up-Regulating α2A-Adrenergic Receptors Directly in Human Adipose Tissue through the Estrogen Receptor α. Implications for the Female Fat Distribution

Cited by 226 publications

References 43 publications

Genetic and environmental correlations between obesity phenotypes and age at menarche

Genetic and environmental correlations between obesity phenotypes and age at menarche

Low Sirt1 expression, which is upregulated by fasting, in human adipose tissue from obese women

Abdominal Obesity and Metabolic Alterations in the Menopausal Transition

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