Role of 17β-estradiol administration on insulin sensitivity in the rat: implications for the insulin receptor

González, Celestino; Alonso, Ana; Grueso, Natalia Alvaraz; Dı́az, Fernando; Esteban, Manuel M.; Fernández, Sergio Tomé; Patterson, Ángeles M.

doi:10.1016/s0039-128x(02)00073-9

Cited by 45 publications

(44 citation statements)

References 43 publications

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“…In fact, Kinuta et al (32) indicated the key role of vitamin D on estrogen biosynthesis in general and more specifically a direct regulation of the expression of the aromatase gene. Our early results (33) revealed that diabetes induced a breakdown in plasmatic estradiol level (a hormone essential in the regulation of insulin secretion and the modulation of the insulin receptors (34)(35)(36) and administration of 1␣,25(OH)2VD3 may prevent the decline in estrogens levels, and consequently prevent diabetes acceleration. This study also shows that 1␣,25(OH)2VD3 exerts hypocholesterolemic and hypolipidemic effects, best explained by increased conversion of cholesterol into bile acids like phytoecdysteroids (37).…”

Section: Discussionmentioning

confidence: 99%

1α,25 Dihydroxyvitamin D3: Therapeutic and Preventive Effects against Oxidative Stress, Hepatic, Pancreatic and Renal Injury in Alloxan-Induced Diabetes in Rats

Hamden

Carreau

Jamoussi

et al. 2009

J Nutr Sci Vitaminol

119

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Summary Diabetes mellitus is a major endocrine disorder and a growing health problem in most countries which can be ameliorated by numerous bio-molecules such as 1 ␣ ,25 dihydroxyvitamin D3 [1 ␣ ,25(OH)2VD3]. With this in mind, the current study investigated the therapeutic and preventive effects of 1 ␣ ,25(OH)2VD3 on diabetes and its side effects: toxicity in liver, pancreas and kidneys. Our results show that administration of 1 ␣ ,25(OH)2VD3 in diabetic rats increased the plasmatic insulin level, favored the normal blood glucose levels and normalized the hepatic glycogen concentration. In addition, 1 ␣ ,25(OH)2VD3 enhanced superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GPX) (by 207, 52 and 72%, respectively) compared to diabetic rats. It also reduced lipid peroxidation and the indices of toxicity in liver and kidneys by significantly decreasing alkaline phosphatases (PAL), aspartate and lactate transaminase (AST and ALT) activities, total and direct bilirubin, triglycerides (TG), cholesterol, creatinine, urea and iron levels in diabetic rats. Moreover, the plasmatic non-enzymatic antioxidant level of HDL-cholesterol, magnesium (Mg), calcium (Ca) and copper (Cu) increased after 1 ␣ ,25(OH)2VD3 administration. The administration of 1 ␣ ,25(OH)2VD3 in diabetic rats protects against alloxan-induced histological changes in pancreas. Conclusion: from these data, it is concluded that 1 ␣ ,25(OH)2VD3 might be useful for the therapy and prevention of diabetes and the numerous side effects especially toxicity in liver, pancreas and kidneys and this protective effect is more obvious in our preventive experiment.

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Section: Discussionmentioning

confidence: 99%

1α,25 Dihydroxyvitamin D3: Therapeutic and Preventive Effects against Oxidative Stress, Hepatic, Pancreatic and Renal Injury in Alloxan-Induced Diabetes in Rats

Hamden

Carreau

Jamoussi

et al. 2009

J Nutr Sci Vitaminol

119

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“…Every 90 days, the pellets were replaced. This dosing regimen has resulted in physiological levels of plasma estradiol and has been shown to be neuroprotective in rats (Gonzalez et al 2000).…”

Section: Experimental Designmentioning

confidence: 99%

Aging and substitutive hormonal therapy influence in regional and subcellular distribution of ERα in female rat brain

Navarro

Valle

Ordóñez³

et al. 2012

AGE

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Estrogens are not only critical for sexual differentiation it is well-known for the role of 17β-estradiol (E2) in the adult brain modulating memory, learning, mood and acts as a neuroprotector. E2 exerts its actions through two classical receptors: estrogen receptor alpha (ERα) and estrogen receptor beta (ERβ). The distribution of both receptors changes from one brain area to another, E2 being able to modulate their expression. Among the classical features of aging in humans, we find cognitive impairment, dementia, memory loss, etc. As estrogen levels change with age, especially in females, it is important to know the effects of low E2 levels on ERα distribution; results from previous studies are controversial regarding this issue. In the present work, we have studied the effects of long-term E2 depletion as well as the ones of E2 treatment on ERα brain distribution of ovariectomized rats along aging in the diencephalon and in the telencephalon. We have found that ovariectomy causes downregulation and affects subcellular localization of ERα expression during aging, meanwhile prolonged estrogen treatment produces upregulation and overexpression of the receptor levels. Our results support the idea of the region-specific neuroprotection mechanisms mediated by estradiol.

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“…In contrast, oestrogen excess, as in oral contraceptive therapy or HRT with potent alkylated oestrogens or high-dose natural oestrogens, is associated with deterioration in glucose tolerance and insulin resistance. Interestingly, such gradations in response to oestrogens could be further determined at the level of insulin receptor gene expression [48]. Receptor binding for oestrogen present in the pancreas [31] Exposure of isolated pancreatic islets to oestrogen does not affect insulin release [33] Exposure of perfused pancreas to oestrogen augments insulin release [32] Oestrogen-induced increases in pancreatic islet progesterone receptors…”

Section: Oestrogen-induced Changes In Growth Hormonementioning

confidence: 99%

Oestrogens and insulin secretion

2005

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There is a persistent perception that oestrogens have an adverse effect on carbohydrate metabolism. It might therefore be expected that their use would result in a corresponding increase in the incidence of diabetes. Recent evidence from clinical trials suggesting that women on postmenopausal oestrogen hormone replacement therapy (HRT) have a reduced incidence of type 2 diabetes therefore appears paradoxical. Short-term supraphysiological oestrogen administration has an adverse effect on glucose tolerance, resulting from suppression of first-phase insulin secretion and increased insulin resistance. Oestrogen-induced increases in glucocorticoid activity could account for these effects. Oestrogen-induced deterioration in glucose tolerance is, however, accompanied by a reduction in fasting glucose, an effect that could be accounted for by glucagon antagonism. These short-term effects contrast with long-term preservation of insulin secretion and glucose homeostasis by oestrogens. In animal studies, ovariectomy is associated with decreased insulin secretion and increased risk of diabetes, whereas oestrogen administration protects against diabetes and increases the insulin response to glucose. The mechanism is uncertain, but direct effects on the pancreas via steroid receptors or indirect effects via oestrogen-induced glucagon antagonism and subclinical increases in glucocorticoids and growth hormone could all contribute. Recent evidence that HRT increases the risk of cardiovascular disease suggests that it should not be used for the prevention of diabetes, but the mechanism responsible for this benefit merits further investigation and might lead to new therapies.

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Role of 17β-estradiol administration on insulin sensitivity in the rat: implications for the insulin receptor

Cited by 45 publications

References 43 publications

1α,25 Dihydroxyvitamin D3: Therapeutic and Preventive Effects against Oxidative Stress, Hepatic, Pancreatic and Renal Injury in Alloxan-Induced Diabetes in Rats

1α,25 Dihydroxyvitamin D3: Therapeutic and Preventive Effects against Oxidative Stress, Hepatic, Pancreatic and Renal Injury in Alloxan-Induced Diabetes in Rats

Aging and substitutive hormonal therapy influence in regional and subcellular distribution of ERα in female rat brain

Oestrogens and insulin secretion

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