Limits...
Estrogen signaling in metabolic inflammation.

Monteiro R, Teixeira D, Calhau C - Mediators Inflamm. (2014)

Bottom Line: However, the connection between these two fields of estrogen actions has been underacknowledged since little attention has been drawn towards the possible action of estrogens on the modulation of metabolism through their anti-inflammatory properties.In the present paper, we summarize knowledge on the modification inflammatory processes by estrogens with impact on metabolism and highlight major research questions on the field.Understanding the regulation of metabolic inflammation by estrogens may provide the basis for the development of therapeutic strategies to the management of metabolic dysfunctions.

View Article: PubMed Central - PubMed

Affiliation: Department of Biochemistry, Faculty of Medicine, University of Porto, Medical Investigation Center, 4200-319 Porto, Portugal.

ABSTRACT
There is extensive evidence supporting the interference of inflammatory activation with metabolism. Obesity, mainly visceral obesity, is associated with a low-grade inflammatory state, triggered by metabolic surplus where specialized metabolic cells such as adipocytes activate cellular stress initiating and sustaining the inflammatory program. The increasing prevalence of obesity, resulting in increased cardiometabolic risk and precipitating illness such as cardiovascular disease, type 2 diabetes, fatty liver, cirrhosis, and certain types of cancer, constitutes a good example of this association. The metabolic actions of estrogens have been studied extensively and there is also accumulating evidence that estrogens influence immune processes. However, the connection between these two fields of estrogen actions has been underacknowledged since little attention has been drawn towards the possible action of estrogens on the modulation of metabolism through their anti-inflammatory properties. In the present paper, we summarize knowledge on the modification inflammatory processes by estrogens with impact on metabolism and highlight major research questions on the field. Understanding the regulation of metabolic inflammation by estrogens may provide the basis for the development of therapeutic strategies to the management of metabolic dysfunctions.

Show MeSH

Related in: MedlinePlus

Different models have shown the influence of estrogens on metabolic-related inflammation. Loss of/decreased estrogen signaling through decreased production of estrogens or ERalpha, ERalpha/beta, or GPER inactivation promotes metabolic dysfunction revealed by visceral obesity, insulin resistance, dyslipidemia, inflammatory activation, and nonalcoholic fatty liver disease. On the other hand, promoting maintenance of estrogen signaling through hormone replacement therapy, blocking estrogen inactivation by estrogen sulfotransferase or increasing its reactivation from the estrogen-sulfate circulating pool by steroid sulfatase induction, tends to counteract metabolic dysfunction. Interestingly, inactivation of ERbeta also promotes metabolic health, showing the opposite metabolic effects mediated by both ER receptors. ER: estrogen receptor; GPER: G protein-coupled estrogen receptor; HRT: hormone replacement therapy; NAFLD: nonalcoholic fatty liver disease.
© Copyright Policy - open-access
Related In: Results  -  Collection


getmorefigures.php?uid=PMC4226184&req=5

fig3: Different models have shown the influence of estrogens on metabolic-related inflammation. Loss of/decreased estrogen signaling through decreased production of estrogens or ERalpha, ERalpha/beta, or GPER inactivation promotes metabolic dysfunction revealed by visceral obesity, insulin resistance, dyslipidemia, inflammatory activation, and nonalcoholic fatty liver disease. On the other hand, promoting maintenance of estrogen signaling through hormone replacement therapy, blocking estrogen inactivation by estrogen sulfotransferase or increasing its reactivation from the estrogen-sulfate circulating pool by steroid sulfatase induction, tends to counteract metabolic dysfunction. Interestingly, inactivation of ERbeta also promotes metabolic health, showing the opposite metabolic effects mediated by both ER receptors. ER: estrogen receptor; GPER: G protein-coupled estrogen receptor; HRT: hormone replacement therapy; NAFLD: nonalcoholic fatty liver disease.

Mentions: The absence of estrogens in animal and human models appears to favor the occurrence of the metabolic syndrome, starting with the facilitation of visceral AT deposition, which is reversed or prevented by estrogen reposition (Figure 3) [125].


Estrogen signaling in metabolic inflammation.

Monteiro R, Teixeira D, Calhau C - Mediators Inflamm. (2014)

Different models have shown the influence of estrogens on metabolic-related inflammation. Loss of/decreased estrogen signaling through decreased production of estrogens or ERalpha, ERalpha/beta, or GPER inactivation promotes metabolic dysfunction revealed by visceral obesity, insulin resistance, dyslipidemia, inflammatory activation, and nonalcoholic fatty liver disease. On the other hand, promoting maintenance of estrogen signaling through hormone replacement therapy, blocking estrogen inactivation by estrogen sulfotransferase or increasing its reactivation from the estrogen-sulfate circulating pool by steroid sulfatase induction, tends to counteract metabolic dysfunction. Interestingly, inactivation of ERbeta also promotes metabolic health, showing the opposite metabolic effects mediated by both ER receptors. ER: estrogen receptor; GPER: G protein-coupled estrogen receptor; HRT: hormone replacement therapy; NAFLD: nonalcoholic fatty liver disease.
© Copyright Policy - open-access
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC4226184&req=5

fig3: Different models have shown the influence of estrogens on metabolic-related inflammation. Loss of/decreased estrogen signaling through decreased production of estrogens or ERalpha, ERalpha/beta, or GPER inactivation promotes metabolic dysfunction revealed by visceral obesity, insulin resistance, dyslipidemia, inflammatory activation, and nonalcoholic fatty liver disease. On the other hand, promoting maintenance of estrogen signaling through hormone replacement therapy, blocking estrogen inactivation by estrogen sulfotransferase or increasing its reactivation from the estrogen-sulfate circulating pool by steroid sulfatase induction, tends to counteract metabolic dysfunction. Interestingly, inactivation of ERbeta also promotes metabolic health, showing the opposite metabolic effects mediated by both ER receptors. ER: estrogen receptor; GPER: G protein-coupled estrogen receptor; HRT: hormone replacement therapy; NAFLD: nonalcoholic fatty liver disease.
Mentions: The absence of estrogens in animal and human models appears to favor the occurrence of the metabolic syndrome, starting with the facilitation of visceral AT deposition, which is reversed or prevented by estrogen reposition (Figure 3) [125].

Bottom Line: However, the connection between these two fields of estrogen actions has been underacknowledged since little attention has been drawn towards the possible action of estrogens on the modulation of metabolism through their anti-inflammatory properties.In the present paper, we summarize knowledge on the modification inflammatory processes by estrogens with impact on metabolism and highlight major research questions on the field.Understanding the regulation of metabolic inflammation by estrogens may provide the basis for the development of therapeutic strategies to the management of metabolic dysfunctions.

View Article: PubMed Central - PubMed

Affiliation: Department of Biochemistry, Faculty of Medicine, University of Porto, Medical Investigation Center, 4200-319 Porto, Portugal.

ABSTRACT
There is extensive evidence supporting the interference of inflammatory activation with metabolism. Obesity, mainly visceral obesity, is associated with a low-grade inflammatory state, triggered by metabolic surplus where specialized metabolic cells such as adipocytes activate cellular stress initiating and sustaining the inflammatory program. The increasing prevalence of obesity, resulting in increased cardiometabolic risk and precipitating illness such as cardiovascular disease, type 2 diabetes, fatty liver, cirrhosis, and certain types of cancer, constitutes a good example of this association. The metabolic actions of estrogens have been studied extensively and there is also accumulating evidence that estrogens influence immune processes. However, the connection between these two fields of estrogen actions has been underacknowledged since little attention has been drawn towards the possible action of estrogens on the modulation of metabolism through their anti-inflammatory properties. In the present paper, we summarize knowledge on the modification inflammatory processes by estrogens with impact on metabolism and highlight major research questions on the field. Understanding the regulation of metabolic inflammation by estrogens may provide the basis for the development of therapeutic strategies to the management of metabolic dysfunctions.

Show MeSH
Related in: MedlinePlus