Dose- and time-dependent effects of 17beta-oestradiol on insulin sensitivity in insulin-dependent tissues of rat: implications of IRS-1

González, Celestino; Alonso, Ana; Dı́az, Fernando; Am, Patterson

doi:10.1677/joe.0.1760367

Cited by 32 publications

(28 citation statements)

References 65 publications

(71 reference statements)

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“…Indeed, experimental studies confirm that the impact of estradiol on IRS-1 expression in adipocytes is dose and time dependent. 28 Low IRS-1 expression of subcutaneous adipocytes has been recently proposed as a marker of IR, low adiponectin expression/secretion, and accelerated atherogenesis. 27 Because centrally obese women in the present study had similarly high IR, low adiponectin, and signs of accelerated atherogenesis, it is tempting to postulate that the decreased expression of IRS-1 in subcutaneous adipocytes could reflect increased cellular exposure to estradiol.…”

Section: Discussionmentioning

confidence: 99%

Novel Associations Between Bioavailable Estradiol and Adipokines in Elderly Women With Different Phenotypes of Obesity

et al. 2004

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Background-Peripheral adiposity confers protection against diabetes and atherosclerosis in elderly women. The underlying mechanisms, however, remain to be elucidated. Methods and Results-On the basis on dual-energy X-ray absorptiometry measurements of central fat mass (CFM) and peripheral fat mass (PFM), we identified 290 elderly women with distinct forms of body fat distribution (lean, peripheral obesity, central obesity, or general obesity). Study parameters were plasma tumor necrosis factor-␣, interleukin (IL)-6, adiponectin, estradiol, sex hormone-binding globulin, insulin resistance, and aortic calcification, graded on lateral radiography. In peripherally and generally obese women, plasma estradiol and insulin resistance were significantly lower, whereas sex hormone-binding globulin and adiponectin were significantly higher compared with centrally obese women independent of age, body mass index, total fat mass, and smoking habits (all PϽ0.05). After adjustment for these confounders, IL-6 in centrally obese women was comparable with that seen in generally obese (similar high CFM%) but significantly higher than in peripherally obese women and lean women (low CFM%). Atherosclerosis was less severe in generally obese (2.5Ϯ0.3) compared with centrally obese women (5.0Ϯ0.7, Pϭ0.001). In multiple regression analysis, total fat mass, body fat distribution, insulin resistance, estradiol, current smoking, treated hyperlipidemia, and treated hypertension contributed independently to the variation of aortic calcification (Rϭ0.55, SEEϭ3.60, PϽ0.001). Conclusions-Abundant presence of PFM in generally obese women is associated with increased plasma adiponectin and higher insulin sensitivity, which could explain the apparent protection against the atherogenic effects of IL-6 derived from CFM. Low peripheral exposure to estradiol appears to be a sine qua non of maintained adiponectin secretion from

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Section: Discussionmentioning

confidence: 99%

Novel Associations Between Bioavailable Estradiol and Adipokines in Elderly Women With Different Phenotypes of Obesity

et al. 2004

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“…Experimental studies (González et al 2000(González et al , 2003Kumagai et al 1993) and clinical observations (Colacurci et al 1998;Karjalainen et al 2001) have demonstrated the importance of estrogen in the maintenance of insulin sensitivity in postmenopausal women. However, the route, dose and type of estrogen used appear to determine the efficacy of therapy.…”

Section: Introductionmentioning

confidence: 99%

Chronic 17β-estradiol treatment improves skeletal muscle insulin signaling pathway components in insulin resistance associated with aging

Moreno

Ordóñez

Alonso

et al. 2009

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Insulin resistance is a common feature of aging in both humans and rats. In the case of females, it seems to be related to loss of gonadal function, due mainly due to a decrease in plasma estrogen levels. Several causes have been postulated for this insulin resistance, among them changes in several steps of the insulin pathway. In view of these findings, the purpose of the present study was to examine the role of chronic 17β-estradiol treatment on insulin sensitivity during the aging process, and its effects on levels of the insulin-sensitive glucose transporter Glut4 (both total and plasma membrane localized), the interaction between p85α subunit of PI3-k and IRS-1, Tyr-and Ser-612 phosphorylation of IRS-1 levels, and Ser-473 phosphorylation of Akt. The present findings indicate that 17β-estradiol treatment is able to minimize the deleterious effect of aging on insulin sensitivity, at least at the level of plasma membrane localized Glut4. Nevertheless further research is needed to determine this conclusively.

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“…Estrogen effects also depend on dose and route of administration (53). Cell-specific delivery of E 2 stimulates beneficial activities without unwanted side effects.…”

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confidence: 99%

Estrogen Receptor α Regulates β-Cell Formation During Pancreas Development and Following Injury

et al. 2015

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Identifying pathways for b-cell generation is essential for cell therapy in diabetes. We investigated the potential of 17b-estradiol (E 2 ) and estrogen receptor (ER) signaling for stimulating b-cell generation during embryonic development and in the severely injured adult pancreas. E 2 concentration, ER activity, and number of ERa transcripts were enhanced in the pancreas injured by partial duct ligation (PDL) along with nuclear localization of ERa in b-cells. PDL-induced proliferation of b-cells depended on aromatase activity. The activation of Neurogenin3 (Ngn3) gene expression and b-cell growth in PDL pancreas were impaired when ERa was turned off chemically or genetically (ERa 2/2 ), whereas in situ delivery of E 2 promoted b-cell formation. In the embryonic pancreas, b-cell replication, number of Ngn3 + progenitor cells, and expression of key transcription factors of the endocrine lineage were decreased by ERa inactivation. The current study reveals that E 2 and ERa signaling can drive b-cell replication and formation in mouse pancreas.Decreased functional b-cell mass is the major cause for hyperglycemia in diabetes. Restoration of the endogenous b-cell mass as a therapeutic strategy, however, requires a better understanding of signaling pathways that control b-cell growth and differentiation. Embryonic b-cells are generated by a developmental program executed through the timed action of a number of key transcription factors among which Neurogenin3 (Ngn3) is key for endocrine specification. Ngn3 + cells delaminate from pancreatic epithelium, are mitotically quiescent, and give rise to endocrine cells. Ngn3 cells appear maximally competent for driving b-cell formation at embryonic day (E) 14.5. Formed b-cells expand through self-replication, already evident at E18.5, and continue into early postnatal life (1). Also in adult mice with severely injured pancreas by partial duct ligation (PDL), Ngn3 + cells are generated near duct epithelium and can differentiate into b-cells (2). b-Cells are vastly generated through replication in PDL (3,4), but some derive from acinar (5) and duct (6) cells, apparently through an Ngn3 + stage (2,5) as in embryonic pancreas. How the numbers of Ngn3 + endocrine progenitors and replicating b-cells are controlled in the embryonic or mature pancreas is uncertain. Identifying factors that control these processes and manipulating them may be of therapeutic advantage. What is known is that 17b-estradiol (E 2 ) enhances b-cell survival and glycemic control in various animal models (7,8) by signaling through estrogen receptor (ER) a (8,9) and/or ERb (10).However, little is known about the importance of estrogen and ER signaling for b-cell proliferation and differentiation. So far, no in vivo effects on b-cell formation have been reported for the ER antagonist tamoxifen (TAM), although this compound is used to conditionally activate Cre recombinase activity (Cre ERT ) in genetic

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Dose- and time-dependent effects of 17beta-oestradiol on insulin sensitivity in insulin-dependent tissues of rat: implications of IRS-1

Cited by 32 publications

References 65 publications

Novel Associations Between Bioavailable Estradiol and Adipokines in Elderly Women With Different Phenotypes of Obesity

Novel Associations Between Bioavailable Estradiol and Adipokines in Elderly Women With Different Phenotypes of Obesity

Chronic 17β-estradiol treatment improves skeletal muscle insulin signaling pathway components in insulin resistance associated with aging

Estrogen Receptor α Regulates β-Cell Formation During Pancreas Development and Following Injury

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