Estrogens, inflammation and obesity: an overview

doi:10.1007/s11515-011-1174-y

Front Biol

2012, Vol. 7

Issue (1) : 40-47 https://doi.org/10.1007/s11515-011-1174-y

REVIEW

Estrogens, inflammation and obesity: an overview

Colette N. MILLER¹, Lynda M. BROWN², Srujana RAYALAM³, Mary Anne DELLA-FERA³, Clifton A. BAILE^1,3(

)

1. Department of Foods and Nutrition, University of Georgia, Athens, GA 30602, USA; 2. Department of Nutrition, University of North Carolina at Greensboro, Greensboro, NC 27401, USA; 3. Department of Animal and Dairy Science, University of Georgia, Athens, GA 30602, USA

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Abstract

Emerging research has suggested that inflammatory stress may play a role in the development of obesity. Both the leptin and insulin receptor are sensitive to intracellular inflammatory signaling that can be stimulated through toll-like receptor 4 activation by saturated fat. Pharmacological intervention within this cascade often protects animals from becoming obese, thus highlighting inflammatory pathways as a possible site of study in the prevention of pathologic weight gain. It has been well established in animal models that females display a marked reduction in the susceptibility to weight gain on high-fat diets compared to males. In addition, it has been widely accepted that females are partially protected from inflammatory-related diseases. At the molecular level, this reduction in disease susceptibility has been suggested to be due to the anti-inflammatory properties of 17 β-estradiol. Through direct free radical scavenging, transcriptional regulation, and protein interactions, chronic exposure to estradiol can reduce systemic inflammatory stress. As the knowledge base continues to grow on the etiology of obesity, further research is needed on the precise molecular pathways that can be inhibited by estradiol. Understanding of such pathways may provide a basis for the future use of estrogen and its related compounds (daidzein, genistein, resveratrol) to prevent weight gain in peri- and post-menopausal females.

Keywords inflammation obesity sex differences estrogen high fat diets phytoestrogens

Corresponding Author(s): A. BAILE Clifton,Email:cbaile@uga.edu

Issue Date: 01 February 2012

Cite this article:

Colette N. MILLER,Lynda M. BROWN,Srujana RAYALAM, et al. Estrogens, inflammation and obesity: an overview[J]. Front Biol, 2012, 7(1): 40-47.

URL:

https://academic.hep.com.cn/fib/EN/10.1007/s11515-011-1174-y
https://academic.hep.com.cn/fib/EN/Y2012/V7/I1/40

Fig.1 Chronic inflammation disrupts hypothalamic leptin and insulin signaling. Leptin receptor results in SOCS3 gene expression (1), resulting in inhibition of JAK-STAT signaling (2). Leptin receptor is also inhibited through saturated fat-induced activation of NFκB, and downstream increases in SOCS3 (3). Insulin receptor is sensitive to SOCS3 (4), as well as JNK (5), both a consequence of saturated fat-induced NFκB activation. Abbreviations: toll-like receptor (TLR), inhibitor of nuclear factor kappa-B kinase subunit beta (IKKβ), nuclear factor kappa B (NFκB), c-jun N-terminal kinase (JNK), insulin receptor substrate 1 (IRS 1), insulin receptor (IR), suppressor of cytokine signaling 3 (SOCS3), leptin receptor (ObR), janus kinase (JAK), signal transducers and activators of transcription (STAT), tumor necrosis factor alpha (TNFα), interleukin 6 (IL6)

Fig.2 Anti-inflammatory effects of estrogens and phytoestrogens. Estrogens are capable of reducing ROS concentrations through direct free radical scavenging and ERα-mediated increases in other scavenger proteins (1). Intracellular reductions of ROS would reduce cellular stress and subsequent inflammatory signaling. ERα also mediates NFκB activity through increasing the inhibitory subunit IκBα (2) and direct protein on protein interactions with the NFκB complex (3). It is also important to mention that the anti-obesity effects of estrogens are in part due to ERα-mediated suppression of adipogenic genes (4). Abbreviations: estrogen receptor alpha (ERα), reactive oxygen species (ROS), nuclear factor kappa B (NFκB), tumor necrosis factor alpha (TNFα), interleukin 6 (IL6), nuclear factor of kappa light polypeptide gene enhancer in B cells inhibitor, alpha (IkBα), peroxisome proliferator-activated receptor gamma (PPARγ), CCAAT-enhancer binding proteins (C/EBPs)

Fig.3 Molecular structure of estrogen and common phytoestrogens. Anti-inflammatory properties of the estrogens are in part due to the free-radical scavenging capabilities of the hydroxyl (-OH) groups in their structures. Reduction in free radicals and reactive oxygen species result in reduced cellular stress and inflammatory signaling.

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