Several in vitro studies in murine hepatocytes showed that pharmacological concentrations of oestrogen reduced ketogenesis a product of fatty acid oxidation and increased fatty acid incorporation into triglycerides [ 9 , 35 ]. Similar findings were reported in human subjects, where oral oestrogen therapy administered to hypogonadal and postmenopausal women reduced postprandial fatty oxidation and increased triglyceride levels [ 29 , 36 — 38 ].
This indicates that exogenous oestrogen directs intrahepatic fatty acids away from oxidative pathways and into lipogenic pathways. In contrast, the effects of endogenous oestrogens are much harder to elucidate. Studies comparing women in follicular and luteal phases of the menstrual cycle detected no difference in energy metabolism, possibly because the change in oestrogen levels varies and there is also the influence of progesterone [ 24 , 39 ].
Studies correlating oestrogen concentration and postprandial fatty acid oxidation in pregnant and non-pregnant subjects have looked at whole body metabolism of fat rather than isolating the effects on the liver.
In addition, progesterone, which has been shown to have a synergistic and antagonistic effect, depending on the organ system, with oestrogen has not been studied in this context [ 8 ]. Oestrogen, progesterone and androgen receptors are present in adipose tissues [ 26 ]. As Table 2 shows, the expression of these receptors varies by depot and gender [ 40 , 41 ].
Oestrogen receptors are higher in subcutaneous deposits in women, which may explain why women have greater subcutaneous gluteal and femoral deposits of fat [ 40 , 41 ]. Genetic males with androgen insensitivity have a female body habitus [ 42 ], while women given exogenous androgens or suffering from virilising disorders will develop a male body habitus [ 40 , 43 — 45 ]. Postmenopausal women experience an increase in waist to hip ratio and the amount of the visceral adipose tissue depot [ 32 , 46 , 47 ], which is partially reversed by oestrogen administration [ 48 ].
All this evidence indicates that the binding of sex hormones to their adipose tissue receptorspossibly promotes adipogenesis in some regions of the body.
Although, it is known that many genes inadipocytes are transcriptionally regulated by sex hormones [ 26 ], the precise cellular mechanisms have not been fully elucidated.
Leptin is an adipose tissue-derived hormone that inhibits fat gain by promoting hypophagia and hypermetabolism [ 49 ].
Thus, leptin has an important role in helping FM to remain relatively constant during adulthood. There is a gender difference in leptin levels which develops at puberty and is believed to be induced by sex hormones. Leptin concentrations are higher per kilogram body weight in women than men. This difference is eliminated after adjusting for circulating concentrations of sex hormones [ 50 ]. Studies have found that leptin production was inhibited by androgens and promoted by oestrogens [ 26 , 50 ].
Oestrogen has direct effects on FM as it upregulates leptin expression in adipocytes [ 51 ]. Central effects may also be present as oestrogen receptors have been detected in the hypothalamic nuclei controlling energy homeostasis. Circulating oestrogens are proposed to bind to these receptors and alter hypothalamic sensitivity to leptin-mediated signals, thus influencing secretion of leptin and possibly influencing metabolism and even fertility [ 52 — 54 ].
However, the relationship between leptin, oestrogen, and body composition is complex, as there is no change in leptin with menopause or with oestrogen replacement therapy [ 26 ]. Weight loss is associated with reduced leptin levels and hypogonadism [ 55 ].
In addition, the hyperandrogenism and diminished oestrogen surge in polycystic ovaries disease do not affect leptin levels [ 56 , 57 ]. Therefore, the role of leptin in regulating FM is potentially influenced by oestrogen however, the mechanism of action is not completely clear. Female reproduction requires increased amounts of energy.
Yet, throughout history, women have carried their conceptus to term under a wide range of nutritional conditions. This suggests the presence of powerful metabolic adaptations [ 3 ]. During gestation, energy is required to grow the tissues of conception and reproduction, to maintain these tissues, and to prepare for lactation. Butte and King [ 58 ] found that an average weight gain of This variability points to the presence of metabolic adaptations for sustaining pregnancy under different nutritional conditions.
In contrast to expectations, numerous prospective and cross-sectional studies found that the first half of pregnancy is associated with little or no increase in energy intake [ 6 , 60 — 62 ]. One study followed women prospectively through pregnancy and reported that energy intake in the first trimester of pregnancy is identical to pre-pregnancy [ 63 ].
Instead of reducing energy expenditure increased progressively during gestation [ 4 , 64 , 65 ]. Similarly, changes in diet-induced thermogenesis during pregnancy have not been consistently reported and therefore a reduction in diet-induced thermogenesis may not account for the positive energy balance [ 4 , 33 , 66 — 70 ]. These above observations raise the possibility that the energy costs of pregnancy are met by reductions in total energy expenditure. However, conclusive evidence fails to show that significant increases in energy intake or decreases in energy expenditure are the major contributors to the increase in FM in the first half of pregnancy.
It is also important to note that pregnancy is a very plastic metabolic state, because even undernourished women can maintain FM [ 59 ]. Therefore, the cause of gestational fat gain may be mainly due to changes in metabolic pathways regulating the oxidation or storage of specific fuels especially fat.
Throughout their reproductive life, women maintain a higher proportion of body fat compared to men, and this difference is accentuated during the hyperoestrogenic state of pregnancy. However, studies have failed to demonstrate an energy surplus on all accounts.
It is possible that women underestimate their food intake; however, some studies have reported that men underestimate their food intake compared with women [ 71 ]. The differences in physical activity between the sexes also need to be considered. Women do have a greater percent body fat, and it is possible that ovarian hormones, particularly oestrogen, may account for these observations by promoting postprandial conversion of dietary energy into fat.
This theory needs to be supported by larger prospective studies and studies during natural hyper-oestrogenic states such as pregnancy. Further studies are needed to elucidate how these hormonal pathways interact and influence their targets. Goals that take into account gender rather than just body weight or energy intake need to be utilised. Considering the high prevalence of obesity in modern society, it is important to understand the factors that regulate energy homeostasis and subsequently contribute to excess body fat.
In the future, this understanding may culminate in strategies to control or reverse fat gain that do not only emphasise energy restriction. Wu and Anthony J. This is an open access article distributed under the Creative Commons Attribution License , which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
Article of the Year Award: Outstanding research contributions of , as selected by our Chief Editors. Read the winning articles. Journal overview. Special Issues. Wu 1 and Anthony J. O'Sullivan 1,2 1 St. Academic Editor: Andrea Buchholz. Received 01 Mar Accepted 03 May Published 28 Jun Abstract Women have a higher proportion of body fat compared to men.
Introduction Fat gain is always considered to be a result of long-term positive energy balance, whereby daily energy intake exceeds expenditure. Table 1. Percentage FM in healthy non-Hispanic white men and women. Figure 1. Percentage fat mass FM in males and females showing the divergence that occurs at puberty and persists through the pre-menopausal years.
Combined data from Chumlea et al. Table 2. Expression of sex hormone receptors in adipose tissues. Adapted from Mayes, [ 26 ]. References A. Kant and B. View at: Google Scholar M. Kopp-Hoolihan, M. Van Loan, W. Wong, and J. View at: Google Scholar J. Durnin, F. McKillop, S. Grant, and G. Van Raaij, S. Vermaat-Miedema, C. Schonk, M. Peek, and J. Mayes, J. McCann, T.
Ownbey, and G. View at: Google Scholar I. Weinstein, C. Soler-Argilaga, H. Werner, and M. View at: Google Scholar W. Chumlea, S. Gio, R. Kuczmarski et al. Pietrobelli, D. Allison, S. Beginning to implement healthy eating, routine physical activity, and better sleeping has been shown to drastically decrease adiposity and create a healthier lifestyle and overall well being. The differences between male and female metabolism are direct correlations with body composition and hormones see infographic below for a brief summary.
Although females have more difficulty losing weight, both male and female metabolisms change with age, and both slowing metabolisms can yield weight gain if not taking preventative actions to stop or slow the weight gain that can accompany age. Metabolism is the term used to describe all of the chemical and physical body processes that use energy.
True b. Which of the following factors play into metabolism incline? An increase in age b. A decline in physical activity c. An increase in muscle mass d. Hormonal changes. Which of the following does NOT prevent metabolism decline and weight gain? Healthy eating b. Routine physical activity c. Getting better and more consistent sleep d. Having a sedentary office job. American Pregnancy Organization.
Body Image during pregnancy. Castle, J. Fearless feeding: How to raise healthy eaters from high chair to high school.
Jefferson Regional Medical Center. Gender differences in metabolism. Factors That Influence Body Weight. Lundsgaard, A. Gender differences in skeletal muscle substrate metabolism. Menopause Weight Gain. Stop the middle-age spread. Tamborlane, W. Effects of puberty on metabolism and body composition. Our experts answer common questions regarding why metabolism differs for men, how it can change over the years, and what types of foods or workouts either slow or boost metabolism as a whole.
Men naturally have greater amounts of testosterone in their bodies, so that fact combined with less body fat and more muscle, in general, leads to a better metabolism—at least one that burns more calories. In contrast, female bodies are genetically predisposed to store energy for certain activities, such as pregnancy and breastfeeding, says Hollingsworth.
According to Scarlata, testosterone levels decrease with age. This makes men less metabolically active and leads to reduced muscle mass and a slower rate of burning calories. Unfortunately, our metabolism drops a few times as we age, and we commonly see the first major drop in our mid-thirties. As a result, our energy levels drop, too. We tend to utilize less of our caloric intake as energy and store more of it as fat.
Our lean muscle mass decreases, as does our strength and speed. The bad news: Dietary and lifestyle choices, such as eating too many calories and being inactive, also contribute to a slowdown in metabolism and a potential increase in weight gain. The good news?
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