**1. Introduction**

Menopause is a special period for women, which is the end of menstrual cycle and fertility and also the start of a series of changes, such as hot flashes and mood changes. Energy metabolism also changes during menopausal transition, which is important and yet does not receive enough attention. Clinical surveys observed a trend of weight gain, increased food intake, intra-abdominal fat accumulation, increased low-density lipoprotein cholesterol and triglycerides, insulin resistance, and reduced energy expedition [1, 2]. All of these changes in energy metabolism add to the risk of diabetes and cardiovascular diseases (CVDs).

The characteristic and fundamental differences in postmenopausal women are the changes in ovarian hormones. Estrogen and progesterone decreased while androgen, follicular stimulating hormone (FSH), and luteinizing hormone (LH) increased [3]. Among them, the effect of the declination of estrogen level is most studied. Estrogen receptors are expressed in various tissues, such as brain, adipose tissue, liver, and intestinal mucosa, of which all regulate energy expenditure [4]. Apart from ovarian hormones, leptin, growth hormone, and others also affect energy homeostasis and will be discussed in the text.

In this chapter, we summarize the evidence from clinical and animal studies and target to explain how hormonal changes in menopause lead to alterations in lipid

#### **Figure 1.**

*Graphical overview on the contents of this chapter.*

#### **Figure 2.**

*Schematic illustration of possible pathophysiology underlying the ovarian hormone changes related to energy metabolism and obesity in menopause women.*

**99**

*Ovarian Hormonal Change-Related Energy Metabolism and Obesity in Menopausal Women*

**2. Adipose distribution, metabolic consequences at menopause, and** 

**2.1 The influence of menopause on adipose distribution and menopausal** 

The body adipose tissue distribution is different between males and females. The figure of men is pear shaped, since the adipose tissue tends to accumulate on the subcutaneous and intra-abdominal part. Whereas women's figure is apple shaped, since women's fat is more likely to accumulate on gluteal and femoral part [5]. However, mounting evidence indicated that postmenopausal women underwent deleterious changes of body adipose tissue distribution, from noncentral adiposity

A number of factors contribute to the altered body adipose tissue distribution in postmenopausal women, including age, menopause, appetite, physical activity, and emotional changes, while age and menopause are the main reasons. A prospective study carried by Ho et al. concerning Chinese women aged 44–55 showed that the body fat percentage and central adiposity were higher among perimenopausal and postmenopausal women than that in premenopausal women [6]. Another study followed up by Caucasus and black women for 4 years and found that menopause was related to total fat increase and visceral fat increase [7]. A meta-analysis revealed that the decrease in total leg fat percentage and increase in measures of central fat were related to menopause, while increasing age was a predominant contributor [8]. This epidemiological and clinical evidence suggests that ovarian hormone may play

Since 1990s, accumulating evidence suggests that androgen receptor (AR), estrogen receptor (ER), and progesterone receptor (PR) are present in adipose tissues [5]. Ovarian hormones enter the cell and bind to their specific receptors, and then the complex regulates the transcription of targeted genes. Lipoprotein lipase (LPL) is one of the most important proteins that are involved in lipid deposition. LPL is the key enzyme hydrolyzing the circulating triglycerides into glycerol and free fatty acids, which accumulate in the adipose tissues. The hormonal regulation of LPL in adipose tissues is complicated. Generally, growth hormone and estrogen inhibit lipid accumulation by suppressing the activity of LPL, while cortisol and

Iverius et al. found that fasting plasma LPL activity was inversely correlated with plasma estradiol levels and positively correlated with plasma-free testosterone in obese women [9]. One study observed that when 17β-estradiol patch was placed transdermally in the gluteal region of postmenopausal women, LPL in adipose tissue from beneath was significantly decreased compared to placebo group [10]. It is also found that compared to premenopausal women, postmenopausal women have lower LPL activity in femoral adipose tissue, whereas abdominal LPL activity is comparable [11]. Palin et al. found that estrogen regulates LPL activity in a dose-

reduced LPL expression relative to control, while the lower concentration significantly increased LPL expression relative to control [12]. However, whether estrogen

mol/L significantly

and how it influences fat redistribution and metabolism (**Figure 1**).

to central adiposity, which leads to an increased risk of CVD [6–8].

a major role in the regulation of adipose tissue distribution.

dependent manner, the highest concentration of estrogen 10<sup>−</sup><sup>7</sup>

insulin appear to exert opposite function [5].

and glucose metabolism, fat distribution, and food intake (**Figures 1** and **2**). We are also interested in the latest progress of the menopausal hormone therapy (MHT)

*DOI: http://dx.doi.org/10.5772/intechopen.89336*

**menopausal hormone therapy**

*2.1.1 Adipose distribution at menopause*

**hormone therapy**

*Ovarian Hormonal Change-Related Energy Metabolism and Obesity in Menopausal Women DOI: http://dx.doi.org/10.5772/intechopen.89336*

and glucose metabolism, fat distribution, and food intake (**Figures 1** and **2**). We are also interested in the latest progress of the menopausal hormone therapy (MHT) and how it influences fat redistribution and metabolism (**Figure 1**).
