Erratum to “Obesity and disturbed lipoprotein profile in estrogen receptor-α-deficient male mice” [Biochem. Biophys. Res. Commun. 278 (2000) 640–645]

Ohlsson, Claes; Hellberg, Nina; Parini, Paolo; Vidal, Olle; Bohlooly‐Y, Mohammad; Rudling, Mats; Lindberg, Mattias F.; Warner, Margaret; Angelin, Bo; Gustafsson, Jan-Ã...ke

doi:10.1016/j.bbrc.2006.07.058

Cited by 3 publications

(2 citation statements)

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“…The predominant biological effects of estradiol are mediated through two members of the nuclear receptor family, ER␣ and ER␤ (9). We focused on ER␣ because no significant role of ER␤ has been demonstrated in energy metabolism (13). Using qualitative and real-time quantitative RT-PCR, we confirmed that the full-length ER␣ mRNA was expressed (see Fig.…”

Section: Er␣ Is Expressedmentioning

confidence: 63%

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Estrogens protect pancreatic β-cells from apoptosis and prevent insulin-deficient diabetes mellitus in mice

May

Chu

et al. 2006

Proc. Natl. Acad. Sci. U.S.A.

420

252

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In diabetes, the death of insulin-producing ␤-cells by apoptosis leads to insulin deficiency. The lower prevalence of diabetes in females suggests that female sex steroids protect from ␤-cell injury. Consistent with this hypothesis, 17␤-estradiol (estradiol) manifests antidiabetic actions in humans and rodents. In addition, estradiol has antiapoptotic actions in cells that are mediated by the estrogen receptor-a (ER␣), raising the prospect that estradiol antidiabetic function may be due, in part, to a protection of ␤-cell apoptosis via ER␣. To address this question, we have used mice that were rendered estradiol-deficient or estradiol-resistant by targeted disruption of aromatase (ArKO) or ER␣ (␣ERKO) respectively. We show here that in both genders, ArKO ؊/؊ mice are vulnerable to ␤-cell apoptosis and prone to insulin-deficient diabetes after exposure to acute oxidative stress with streptozotocin. In these mice, estradiol treatment rescues streptozotocin-induced ␤-cell apoptosis, helps sustain insulin production, and prevents diabetes. In vitro, in mouse pancreatic islets and ␤-cells exposed to oxidative stress, estradiol prevents apoptosis and protects insulin secretion. Estradiol protection is partially lost in ␤-cells and islets treated with an ER␣ antagonist and in ␣ERKO islets. Accordingly, ␣ERKO mice are no longer protected by estradiol and display a gender nonspecific susceptibility to oxidative injury, precipitating ␤-cell apoptosis and insulin-deficient diabetes. Finally, the predisposition to insulin deficiency can be mimicked in WT mice by pharmacological inhibition of ER␣ by using the antagonist tamoxifen. This study demonstrates that estradiol, acting, at least in part, through ER␣, protects ␤-cells from oxidative injury and prevents diabetes in mice of both genders.estradiol ͉ oxidative stress

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Section: Er␣ Is Expressedmentioning

confidence: 63%

“…The analysis of human and rodent models of aromatase or ER␣ deficiency has challenged the traditional belief of gender-specificity in sex steroid actions and has revealed critical functions of the estradiol-ER␣ axis in the prevention of obesity and insulin resistance in mammals of both sexes (9,13,(15)(16)(17)(18).…”

Section: Discussionmentioning

confidence: 99%

Estrogens protect pancreatic β-cells from apoptosis and prevent insulin-deficient diabetes mellitus in mice

May

Chu

et al. 2006

Proc. Natl. Acad. Sci. U.S.A.

420

252

View full text Add to dashboard Cite

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Inhibitor of Differentiation-3 and Estrogenic Endocrine Disruptors: Implications for Susceptibility to Obesity and Metabolic Disorders

Doke

Avecilla

Felty

2018

BioMed Research International

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The rising global incidence of obesity cannot be fully explained within the context of traditional risk factors such as an unhealthy diet, physical inactivity, aging, or genetics. Adipose tissue is an endocrine as well as a metabolic organ that may be susceptible to disruption by environmental estrogenic chemicals. Since some of the endocrine disruptors are lipophilic chemicals with long half-lives, they tend to bioaccumulate in the adipose tissue of exposed populations. Elevated exposure to these chemicals may predispose susceptible individuals to weight gain by increasing the number and size of fat cells. Genetic studies have demonstrated that the transcriptional regulator inhibitor of differentiation-3 (ID3) promotes high fat diet-induced obesity in vivo. We have shown previously that PCB153 and natural estrogen 17β-estradiol increase ID3 expression. Based on our findings, we postulate that ID3 is a molecular target of estrogenic endocrine disruptors (EEDs) in the adipose tissue and a better understanding of this relationship may help to explain how EEDs can lead to the transcriptional programming of deviant fat cells. This review will discuss the current understanding of ID3 in excess fat accumulation and the potential for EEDs to influence susceptibility to obesity or metabolic disorders via ID3 signaling.

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Sex differences in non-alcoholic fatty liver disease: hints for future management of the disease

Salvoza

Giraudi

Tiribelli

et al. 2020

Exploration of Medicine

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Non-alcoholic fatty liver disease (NAFLD) remains a major cause of chronic liver disease worldwide. Despite extensive studies, the heterogeneity of the risk factors as well as different disease mechanisms complicate the goals toward effective diagnosis and management. Recently, it has been shown that sex differences play a role in the prevalence and progression of NAFLD. In vitro, in vivo, and clinical studies revealed that the lower prevalence of NAFLD in premenopausal as compared to postmenopausal women and men is mainly due to the protective effects of estrogen and body fat distribution. It has been also described that males and females present differential pathogenic features in terms of biochemical profiles and histological characteristics. However, the exact molecular mechanisms for the gender differences that exist in the pathogenesis of NAFLD are still elusive. Lipogenesis, oxidative stress, and inflammation play a key role in the progression of NAFLD. For NAFLD, only a few studies characterized these mechanisms at the molecular level. Therefore, we aim to review the reported differential molecular mechanisms that trigger such different pathogenesis in both sexes. Differences in lipid metabolism, glucose homeostasis, oxidative stress, inflammation, and fibrosis were discussed based on the evidence reported in recent publications. In conclusion, with this review, we hope to provide a new perspective for the development of future practice guidelines as well as a new avenue for the management of the disease.

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Erratum to “Obesity and disturbed lipoprotein profile in estrogen receptor-α-deficient male mice” [Biochem. Biophys. Res. Commun. 278 (2000) 640–645]

Cited by 3 publications

References 0 publications

Estrogens protect pancreatic β-cells from apoptosis and prevent insulin-deficient diabetes mellitus in mice

Estrogens protect pancreatic β-cells from apoptosis and prevent insulin-deficient diabetes mellitus in mice

Inhibitor of Differentiation-3 and Estrogenic Endocrine Disruptors: Implications for Susceptibility to Obesity and Metabolic Disorders

Sex differences in non-alcoholic fatty liver disease: hints for future management of the disease

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