Estrogens Protect against High-Fat Diet-Induced Insulin Resistance and Glucose Intolerance in Mice

Riant, Élodie; Waget, Aurélie; Cogo, Haude; Arnal, Jean‐François; Burcelin, Rémy; Gourdy, Pierre

doi:10.1210/jcem.94.3.9995

Cited by 67 publications

(91 citation statements)

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“…Thus, elevated FA in AdS of HFD groups could have contributed to the inhibition of VSMC proliferation. Finally, ERα, known to improve insulin sensitivity and glucose tolerance 25) , showed decreased mRNA in adipocytes of HFD-fed mice groups with a 4 times higher rate in females than in males 19) . In females, therefore, the higher ERα expression level in adipocytes may have contributed to maintaining better sensitivity to insulin and glucose stimulation, which inhibits lipolysis and reduces FA release.…”

Section: Fundingmentioning

confidence: 94%

Vascular Smooth Muscle Cell Alterations Triggered by Mice Adipocytes: Role of High-Fat Diet

Akoum

Cloutier

Tanguay

2012

JAT

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Aim: Inherent mechanisms leading to vascular smooth muscle cells (VSMC) alterations in obesitylinked type 2 diabetes (T2D) situation remain to be clarified. This study evaluates the impact of supernatant of adipocytes extracted from mice fed high-fat-diets (HFD) on the proliferation and apoptosis of VSMC. Methods: Adipocytes were extracted from visceral white fat pads of male and female C57Bl6 mice showing different stages of metabolic alterations after 20 weeks of vegetal or animal HFD feeding. These cells were stimulated or not with insulin or glucose to condition VSMC media. After 24h of stimulation with adipocyte supernatants (AdS), VSMC proliferation and sustainability were assessed in the absence and presence of AdS. CD36 and insulin receptor mRNA levels were also evaluated. Results: Proliferation and viability of VSMC were significantly modulated by the nature of the AdS used and the gender of mice from which adipocytes have been extracted. The most extensive effects on VSMC were triggered by adipocytes from males fed animal HFD and females fed vegetal HFD. These effects were concurrent with increased leptin concentration and decreased adiponectin levels in AdS. In addition, adipocytes of HFD-fed mice increased caspase-3 activity and apoptosis in VSMC. Significant up-regulation of CD36 mRNA was also found in these cells. Conclusion: Adipocytes of HFD-fed mice induce VSMC alterations. These changes involved mouse gender, most probably correlated to the diet-induced adipocyte secretion profile. Greater sensitivity to AdS effects in VSMC raises concerns about the more frequent cardiovascular events associated with obesity in the presence of T2D, which impairs adipocyte activity.

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Section: Fundingmentioning

confidence: 94%

Vascular Smooth Muscle Cell Alterations Triggered by Mice Adipocytes: Role of High-Fat Diet

Akoum

Cloutier

Tanguay

2012

JAT

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“…Imporantly, our data reveal that E 2 treatment partially restores translocation of GLUT4 (but not GLUT1) to the PM which is likely to have a positive influence on myocardial metabolism. Previous studies have shown that in OVX mice fed with HF diet E 2 treatment improved insulin sensitivity and glucose transport (Riant et al 2009, Zhu et al 2013. Furthermore, ERα knockout mice have decreased GLUT4 mRNA level in skeletal muscle linking the E 2 with the regulation of glucose transporters (Barros et al 2006).…”

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confidence: 97%

17β-Estradiol protects against the effects of a high fat diet on cardiac glucose, lipid and nitric oxide metabolism in rats

Zafirović

Obradović

Sudar-Milovanović

et al. 2017

Molecular and Cellular Endocrinology

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Please cite this article as: Zafirovic, S., Obradovic, M., Sudar-Milovanovic, E., Jovanovic, A., Stanimirovic, J., Stewart, A.J., Pitt, S.J., Isenovic, E.R., 17β-Estradiol protects against the effects of a high fat diet on cardiac glucose, lipid and nitric oxide metabolism in rats, Molecular and Cellular Endocrinology (2017), doi: 10.1016/j.mce.2017 This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain. AbstractThe aim of this study was to investigate the in vivo effects of estradiol (E 2 ) on myocardial metabolism and inducible nitric oxide synthase (iNOS) expression/activity in obese rats. MaleWistar rats were fed with a normal or a high fat (HF) diet (42% fat) for 10 weeks. Half of the HF fed rats were treated with a single dose of E 2 while the other half were placebo-treated. 24h after treatment animals were sacrificed. E 2 reduced cardiac free fatty acid (FFA Akt, protein kinase B; AS160, Akt substrate of 160 kDa; CD36, fatty acid transporters; E 2 ,

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“…Oestrogens, the primary female sex hormones, are suggested to reduce visceral adiposity and prevent insulin resistance and glucose intolerance in rodents [27,28]. For this reason, male mice are more susceptible to diet-induced obesity than female mice.…”

Section: Discussionmentioning

confidence: 99%

IL-7 receptor deletion ameliorates diet-induced obesity and insulin resistance in mice

et al. 2015

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Aim/hypothesis Obesity-induced inflammation plays an important role in the development of insulin resistance and type 2 diabetes. Recent studies have demonstrated that adiposity can be improved by ablating certain inflammatory signalling pathways. Although the IL-7 receptor (IL-7R) is mostly known as a key regulator of T lymphocyte development and homeostasis, its role in obesity and metabolic diseases is unknown. Because IL-7 is markedly increased in the serum of obese individuals and IL-7R (also known as IL7R) is overexpressed in white adipose tissue (WAT) in obesity, we studied the metabolic consequences of genetic Il-7r ablation in mice. Methods Age-matched Il-7r-deficient (Il-7r KO) and wildtype (WT) littermates were fed a standard chow or high-fat diet (HFD) for 14 weeks. Their serum metabolic variables were measured. The expression of genes and proteins related to insulin resistance and inflammation was evaluated in WAT. Results We demonstrated that Il-7r KO mice exhibited significantly reduced body weight gain and visceral adiposity compared with WT controls on both chow and HFD. The expression of signalling molecules involved in adipogenesis was reduced in the WAT of Il-7r KO mice. We also found that Il-7r KO mice had significantly enhanced glucose homeostasis and insulin sensitivity. Consistent with an improved metabolic phenotype, proinflammatory cytokine production and macrophage infiltration was attenuated in the WAT of Il-7r KO mice. Conclusions/interpretation The IL-7R plays an important role in the induction of HFD-induced adipogenesis and insulin resistance in mice.

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Estrogens Protect against High-Fat Diet-Induced Insulin Resistance and Glucose Intolerance in Mice

Cited by 67 publications

References 0 publications

Vascular Smooth Muscle Cell Alterations Triggered by Mice Adipocytes: Role of High-Fat Diet

Vascular Smooth Muscle Cell Alterations Triggered by Mice Adipocytes: Role of High-Fat Diet

17β-Estradiol protects against the effects of a high fat diet on cardiac glucose, lipid and nitric oxide metabolism in rats

IL-7 receptor deletion ameliorates diet-induced obesity and insulin resistance in mice

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