Estrogen Deficiency and the Origin of Obesity during Menopause (original) (raw)
Related papers
Metabolic impact of sex hormones on obesity
Brain Research, 2010
Obesity and its associated health disorders and costs are increasing. Men and postmenopausal women have greater risk of developing complications of obesity than younger women. Within the brain, the hypothalamus is an important regulator of energy homeostasis. Two of its sub-areas, the ventrolateral portion of the ventral medial nucleus (VL VMN) and the arcuate (ARC) respond to hormones and other signals to control energy intake and expenditure. When large lesions are made in the hypothalamus which includes both the VL VMN and the ARC, animals eat more, have reduced energy expenditure, and become obese. The ARC and the VL VMN, in addition to other regions in the hypothalamus, have been demonstrated to contain estrogen receptors. There are two estrogen receptors, estrogen receptor alpha (ERα) and estrogen receptor beta (ERβ). We and others have previously demonstrated that activation of ERα by estrogens reduces food intake and increases body weight. This review focuses on the relative contribution of activation of ERα by estrogens in the ARC and the VL VMN in the regulation of food intake and body weight. Additionally, estrogen receptors have been found in many peripheral tissues including adipose tissue. Estrogens are thought to have direct effects on adipose tissue and estrogens may provide anti-inflammatory properties both in the periphery and the in the central nervous system (CNS) which may protect women from diseases associated with inflammation. Understanding the mechanisms by which estrogens regulate body weight and inflammation will assist in determining potential therapeutic agents for menopausal women to decrease the propensity of diseases associated with obesity.
Association of obesity with serum estrogen level in postmenopausal women
Bangladesh Medical Journal, 2016
Incidence of obesity among postmenopausal women is increasing throughout the world, leading to life threatening medical problem like cardiovascular diseases, type 2 diabetes mellitus. Estrogen deficiency that develops during menopause is likely the etiological factors for development of abdominal obesity. Increased incidence of cardiovascular diseases in postmenopausal women may be due to abdominal obesity caused by lower level of estrogen hormone. The study was carried out to observe the association of obesity with serum estrogen level in postmenopausal women. This cross sectional study was conducted in the Department of Physiology, Dhaka Medical College, Dhaka, during the period of January 2011 to December 2011. A total number of 90 female subjects were selected from different areas of Dhaka city. Among them, 60 postmenopausal women with age ranging from 50 to 60 years were taken as study group and 30 apparently healthy premenopausal women with age ranging from 20 to 30 years were...
The Emergence of the Metabolic Syndrome with Menopause
2003
Women with the metabolic syndrome (central obesity, insulin resistance, and dyslipidemia) are known to be at especially high risk for cardiovascular disease (CVD). The prevalence of the metabolic syndrome increases with menopause and may partially explain the apparent acceleration in CVD after menopause. The transition from pre-to postmenopause is associated with the emergence of many features of the metabolic syndrome, including 1) increased central (intraabdominal) body fat; 2) a shift toward a more atherogenic lipid profile, with increased low density lipoprotein and triglycerides levels, reduced high density lipoprotein, and small, dense low density lipoprotein particles; 3) and increased glucose and insulin levels. The emergence of these risk factors may be a direct result of ovarian failure or, alternatively, an indirect result of the metabolic consequences of central fat redistribution with estrogen deficiency. It is unclear whether the transition to menopause increases CVD risk in all women or only those who develop features of the metabolic syndrome. This article will review the features of the metabolic syndrome that emerge with estrogen deficiency. A better understanding of these metabolic changes with menopause will aid in the recognition and treatment of women at risk for future CVD, leading to appropriate interventions. (J Clin Endocrinol
Impaired estrogen receptor action in the pathogenesis of the metabolic syndrome
Molecular and Cellular Endocrinology, 2015
Considering the current trends in life expectancy, women in the modern era are challenged with facing menopausal symptoms as well as heightened disease risk associated with increasing adiposity and metabolic dysfunction for up to three decades of life. Treatment strategies to combat metabolic dysfunction and associated pathologies have been hampered by our lack of understanding regarding the biological underpinnings of these clinical conditions and our incomplete understanding of the effects of estrogens and the tissue-specific functions and molecular actions of its receptors. In this review we provide evidence supporting a critical and protective role for the estrogen receptor α specific form in the maintenance of metabolic homeostasis and insulin sensitivity. Studies identifying the ER-regulated pathways required for disease prevention will lay the important foundation for the rational design of targeted therapeutics to improve women's health while limiting complications that have plagued traditional hormone replacement interventions.
International journal of health sciences
This narrative review paper aims at highlighting the menopausal obesity-related health problems in women, their effects on physical and mental health, the mechanism of its development and its impact on the functionality of the female hormones. Furthermore, we also try to understand the lifestyle behaviour patterns that cause deleterious health consequences, thus disrupting the production of estrogen and increasing hyperandrogenaemia (high levels of androgens) in postmenopausal females. Also, we have addressed some healthier lifestyle alternatives and the use of hormonal substitution treatment, if applicable. Menopause is characterized by a change in the hormonal structure in women, wherein, there is a rapid decline in estrogen levels, which is a major contributor to the central abdominal fat accumulation, reduction in subcutaneous fat and increase in total adiposity. Women after menopause are thus thrice as likely as premenopausal women to develop obesity and metabolic syndrome. The...
The Role of Estrogens in Control of Energy Balance and Glucose Homeostasis
Endocrine Reviews, 2013
Estrogens play a fundamental role in the physiology of the reproductive, cardiovascular, skeletal, and central nervous systems. In this report, we review the literature in both rodents and humans on the role of estrogens and their receptors in the control of energy homeostasis and glucose metabolism in health and metabolic diseases. Estrogen actions in hypothalamic nuclei differentially control food intake, energy expenditure, and white adipose tissue distribution. Estrogen actions in skeletal muscle, liver, adipose tissue, and immune cells are involved in insulin sensitivity as well as prevention of lipid accumulation and inflammation. Estrogen actions in pancreatic islet -cells also regulate insulin secretion, nutrient homeostasis, and survival. Estrogen deficiency promotes metabolic dysfunction predisposing to obesity, the metabolic syndrome, and type 2 diabetes. We also discuss the effect of selective estrogen receptor modulators on metabolic disorders. regulatory elementbinding protein 1c; STAT3, signal transducer and activator of transcription 3; STZ, streptozotocin; TSEC, tissue-selective estrogen complex; VMH, ventromedial hypothalamus; VMN, ventromedial nucleus; WAT, white adipose tissue.
The role of estrogens in the adipose tissue milieu
Annals of the New York Academy of Sciences, 2019
One of the leading causes for the development of adverse metabolic effects, including type 2 diabetes, dyslipidemia, and cardiovascular diseases, is the accumulation of excess body weight, often measured by body mass index (BMI). Although BMI, calculated using weight and height, is the standard measure used to determine body adiposity in clinical and public health guidelines, an inherent limitation is that BMI does not distinguish where in the body adiposity is deposited. Central obesity, characterized by greater accumulation of adiposity in the abdominal region, has been associated with a higher risk of mortality, independent of BMI. Importantly, one of the determinants of body fat distribution is sex hormones. Both estrogens and androgens appear to directly and indirectly influence body fat distribution. Our review will focus specifically on the role of estrogens and their influence in determining body fat distribution and overall health of adipose tissues, and the role of epigenetic mechanisms in regulating the production and function of estrogens.
Maturitas, 2012
Menopause is associated with changes in bone, muscle and fat mass. The importance of postmenopausal estrogen metabolism in bone health has been established. However, its relationship to body composition in postmenopausal women remains undetermined. The objective of this study is to determine the association between estrogen metabolism and body composition in postmenopausal women. This is a cross sectional study of 97 postmenopausal Caucasian women, 49-80 y.o., ≥1 year from the last normal menstrual period or those who have had oophorectomy. Inactive [2-hydroxyestrone (2OHE 1 )] and active [16␣-hydroxyestrone (16␣-OHE 1 )] urinary metabolites of estrogen were measured by ELISA. The whole and regional body composition was measured by DXA.
Estrogen regulation of adipose tissue functions: Involvement of estrogen receptor isoforms
Infectious Disorders - Drug Targets, 2008
Adipose tissue has recently been described as one of the major endocrine gland that plays a role in energy homeostasis, lipid metabolism, immune response, and reproduction. An excess of white adipose tissue, caused by a complex interaction between genetic, hormonal, behavioral, and environmental factors, results in obesity: a heterogeneous disorder that predisposes humans to a variety of diseases. Among several hormones, estrogens promote, maintain, and control the typical distribution of body fat and adipose tissue metabolism through still unknown mechanisms. These steroids are known to regulate fat mass, adipose deposition and differentiation, and adipocyte metabolism. Moreover, estrogen deficiency results in increases in adipose tissue, preferentially in visceral fat, which would link obesity to the susceptibility of related disorders. In this review the role of estrogens in adipose tissue differentiation and in the protection against the onset of obesity will be discussed with particular attention being drawn to the underlying molecular mechanisms mediated by estrogen receptor isoforms ER and ER .
Steroids, 2006
There is scarce information about the factors associated with estrogen receptors (ER) at menopause. In 113 volunteers pre-and post-menopausal healthy women, grouped as with and without obesity, estrogen receptors-␣ and-, and progesterone receptor (PR) were measured by immunohistochemistry in skin punch biopsies obtained from the external gluteal area. In pre-menopausal women, biopsies and a blood sample were performed between days 7 and 14 of the cycle. Serum hormone levels were measured by immunoradiometric assay or radioimmunoassay. After menopause, ER and PR amounts decreased significantly. At pre-menopause, obese women had lower PR levels than non obese (P < .006). In the postmenopausal group, obese women showed higher ER-␣ (P < .03) and ER- (P < .02) levels than the non obese group. In the analysis of factors associated with the amount of steroid receptors for the total group, log[ER-␣], log[ER-], and log[PR] were associated with age