Signal crosstalk between estrogen and peroxisome proliferator-activated receptor α on adiposity

Kim, Bang Hyun; Won, Young Suk; Kim, Dae Yong; Kim, Bora; Kim, Eun Young; Yoon, Mijung; Oh, Goo Taeg

doi:10.5483/bmbrep.2009.42.2.091

Cited by 17 publications

(9 citation statements)

References 27 publications

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“…Normally, ovariectomization results in significant gains in adipose tissue mass, while subsequent treatment with exogenous estradiol relieves this effect. However, in PPARa-null mice, no significant changes in adipose tissue are observed upon ovariectomization and subsequent estradiol administration, suggesting that the effect estrogen has on fat oxidation is dependent on the presence of PPARa [134]. Circulating leptin concentrations decrease in PPARa-null mice as compared with control mice, with a sex-specific effect in the leptin response to feeding as leptin was increased in female PPARa-null mice as compared with male PPARa-null mice [135].…”

Section: Estrogen and Pparamentioning

confidence: 82%

Elevated Production of Docosahexaenoic Acid in Females: Potential Molecular Mechanisms

Kitson

Stroud

Stark

2010

Lipids

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Observational evidence suggests that in populations consuming low levels of n-3 highly unsaturated fatty acids, women have higher blood levels of docosahexaenoic acid (DHA; 22:3n-6) as compared with men. Increased conversion of alpha-linolenic acid (ALA; 18:3n-3) to DHA by females has been confirmed in fatty acid stable isotope studies. This difference in conversion appears to be associated with estrogen and some evidence indicates that the expression of enzymes involved in synthesis of DHA from ALA, including desaturases and elongases, is elevated in females. An estrogen-associated effect may be mediated by peroxisome proliferator activated receptor-alpha (PPARalpha), as activation of this nuclear receptor increases the expression of these enzymes. However, because estrogens are weak ligands for PPARalpha, estrogen-mediated increases in PPARalpha activity likely occur through an indirect mechanism involving membrane-bound estrogen receptors and estrogen-sensitive G-proteins. The protein kinases activated by these receptors phosphorylate and increase the activity of PPARalpha, as well as phospholipase A(2) and cyclooxygenase 2 that increase the intracellular concentration of PPARalpha ligands. This review will outline current knowledge regarding elevated DHA production in females, as well as highlight interactions between estrogen signaling and PPARalpha activity that may mediate this effect.

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Section: Estrogen and Pparamentioning

confidence: 82%

Elevated Production of Docosahexaenoic Acid in Females: Potential Molecular Mechanisms

Kitson

Stroud

Stark

2010

Lipids

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“…ERβ is involved in the regulation of metabolic rate and can suppress diet- and ovariectomy-induced obesity in mice [88]. In obese ovariectomized mice, E2 effects depend on Ppara [89]. Downstream mechanisms by which ERα regulates these processes are also poorly understood and may involve regulation of the transcriptional co-activator of PPARγ, PGC-1α (nomenclature PPARGC1) [90].…”

Section: Review Sectionmentioning

confidence: 99%

Aldehyde Dehydrogenase 1A1: Friend or Foe to Female Metabolism?

2014

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In this review, we summarize recent advances in understanding vitamin A-dependent regulation of sex-specific differences in metabolic diseases, inflammation, and certain cancers. We focus on the characterization of the aldehyde dehydrogenase-1 family of enzymes (ALDH1A1, ALDH1A2, ALDH1A3) that catalyze conversion of retinaldehyde to retinoic acid. Additionally, we propose a “horizontal transfer of signaling” from estrogen to retinoids through the action of ALDH1A1. Although estrogen does not directly influence expression of Aldh1a1, it has the ability to suppress Aldh1a2 and Aldh1a3, thereby establishing a female-specific mechanism for retinoic acid generation in target tissues. ALDH1A1 regulates adipogenesis, abdominal fat formation, glucose tolerance, and suppression of thermogenesis in adipocytes; in B cells, ALDH1A1 plays a protective role by inducing oncogene suppressors Rara and Pparg. Considering the conflicting responses of Aldh1a1 in a multitude of physiological processes, only tissue-specific regulation of Aldh1a1 can result in therapeutic effects. We have shown through successful implantation of tissue-specific Aldh1a1−/− preadipocytes that thermogenesis can be induced in wild-type adipose tissues to resolve diet-induced visceral obesity in females. We will briefly discuss the emerging role of ALDH1A1 in multiple myeloma, the regulation of reproduction, and immune responses, and conclude by discussing the role of ALDH1A1 in future therapeutic applications.

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“…(25) Compared with control, TNF-α treatment completely prevented the induction of both C/EBPα and PPARγ2 (Fig. 1G).…”

Section: Effects Of Tnf-α On Differentiation Of Porcine Preadipocytesmentioning

confidence: 99%

β-catenin protein utilized by Tumour necrosis factor-α in porcine preadipocytes to suppress differentiation

Luο

Li²,

Liu³

et al. 2009

BMB Reports

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Signal crosstalk between estrogen and peroxisome proliferator-activated receptor α on adiposity

Cited by 17 publications

References 27 publications

Elevated Production of Docosahexaenoic Acid in Females: Potential Molecular Mechanisms

Elevated Production of Docosahexaenoic Acid in Females: Potential Molecular Mechanisms

Aldehyde Dehydrogenase 1A1: Friend or Foe to Female Metabolism?

β-catenin protein utilized by Tumour necrosis factor-α in porcine preadipocytes to suppress differentiation

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