Why Men and Women Store and Burn Fat Differently
It is well established that women tend to have a higher % of body fat than men. Men and women also differ where their body fat is stored. Differences in hormones, hormone receptors, and enzymes play a contributing role in this process. Before going on to discuss the different types of hormones, the question of how fat is metabolized in both genders must be addressed.
Fat Metabolism and Fat Mobilization
Fat mobilization is a process of releasing fats from storage sites within the body. ‘Fat metabolism’ is the method of how the body breaks down the fats so that they can be used as a fuel source. Hormone-sensitive lipase (HSL) and lipoprotein lipase (LPL) are the two hormones that the body uses to regulate the mobilization of free fatty acids.
Hormone-sensitive lipase is located within the actual fat cells and it releases fat due to the signaling of cyclic AMP (cyclic adenosine monophosphate is a second messenger that is used for intracellular signaling, and it helps to transfer hormones that couldn’t pass through the cell membrane). This is impacted by the activity hormone receptors in the fat cells called the ‘adrenergic receptors’. When HSL is secreted it helps to breakdown triglycerides in the adipose tissue into 3 free fatty acids and one glycerol. This mechanism of breaking down the triglycerides into fatty acids and glycerol is called ‘lipolysis’.
When the free fatty acids are in the bloodstream, they attach themselves to ‘albumin’ which is the main vehicle that the FFAs use to travel. Once the free fatty acids arrive at the muscle cells, they are transported into the cells via the following 3 transporters:
- Fatty acid-binding proteins
- Fatty acid translocase
- Fatty acid transport proteins
The 3 protein transporters then carry the FFAs across the muscle cells membrane and into the mitochondria to be oxidized. The additional glycerol molecule that is created during lipolysis is either oxidized in the liver and/or used in the breakdown of glucose and/or to create more triglycerides.
Lipoprotein lipase is located in the blood vessel walls of the circulatory system in adipose tissue and within the liver. Fundamentally, lipoprotein lipase acts upon the triglycerides within the lipoproteins in the blood, and these lipoproteins are vehicles that carry cholesterol and triglycerides for fat storage. Triglycerides are then broken down into free fatty acids and used as fuel or stored in the liver as resynthesized triglycerides. Lipoprotein lipase controls the amount of fat that is stored in sites around the body.
The catecholamines which are secreted by the SNS are the primary catalysts for lipolysis. They bind to the adipocytes and muscle cells and can either block or activate hormone-sensitive lipase.
Catecholamines have 2 main types of receptors and often these receptors can be found in the same cells:
- Alpha receptors – these inhibit lipolysis (A = anti burn) and they decrease blood flow to a specific area.
- Beta receptors – these help to active lipolysis (B= burn) and they increase blood flow to a specific area.
The receptor available and its sensitivity or resistance to the catecholamine will determine the overall response of hormone-sensitive lipase within the cells. In addition, the higher the amount of alpha or beta receptors within the cells will determine the response of the hormone-sensitive lipase.
For example, abdominal adipocytes are more sensitive to beta-receptor stimulation by the catecholamine compared to the hip/thigh in both genders. Therefore, abdominal fat is easier to mobilize than hip/thigh fat in women, as they have an increased number of alpha receptors in the thigh/hip area.
This is the main rationale why women tend to store fat in the fat/thigh area (pre-menopausal); combined with differences in the type and number of fat cells in the lower body region. Hence, this could be a leading factor in the fat distribution differences between both sexes. Another mechanism associated with fat distribution differences between both genders is the amount of lipoprotein lipase in various cells. Women tend to have increased levels of lipoprotein lipase within the hip/thigh area in comparison to the abdominal region. In addition, women’s lower body subcutaneous fat has a higher amount of estrogen receptors which makes it very stubborn to burn.
In terms of the fat-burning hierarchy, the thyroid and adrenal catecholamine are much higher than estrogen and progesterone. Wilmore and Costill(2010) postulated that women have 10 times more alpha receptor cells than men, and the hormone estrogen increases the number and activity of the alpha receptor cells. In addition, a female’s subcutaneous fat has more alpha cells when compared to males, and this may be a key rationale why it’s difficult to shift the fat in the hip, thigh regions, and lower belly regions for women compared to men. Men do, however, have a higher saturation of alpha cells in the belly area compared to women.
Nevertheless, from the research gathered, there are some generalities that can be made in terms of body shape, gender, and fat distribution. They are as follows:
- Increased insulin and cortisol seem to correlate with fat storage around the middle of the body.
- Fat storage in the lower body may be linked to lower levels of insulin and cortisol, accompanied by higher levels of estrogen and progesterone.
- Subcutaneous fat at the back of the arms and legs could signal a reduction in HGH and/or testosterone and an increase in estrogen.
- Subcutaneous fat storage in the hips and breasts may be influenced by estrogen and/or progesterone.
Although it is not as cut and dry as described above; hormones not only inform the body how to use the fuel but behave differently depending on their ratios with other hormones. A good example of this is the ratio of insulin to catecholamine which is a major factor in fat storage. In addition, if insulin and catecholamine are both high, fat storage is reduced. The rise in insulin is unopposed by the catecholamine and fat storage is increased because insulin increases LPL activity and suppresses HSL activity. Insulin impairs the normal function of beta receptors, which is another form of blocking HSL.
With the fat-burning potential of the catecholamine being absent, the fat storage of insulin is increased. In addition, the catecholamine can speed up fat release when they bind to the beta receptors which would increase the HSL activity. On the other hand, they can slow down fat metabolism when they combine with the alpha receptors. This is one of the main reasons that stubborn fat, which has a higher number of alpha receptors, is harder to shift. Another key point to remember is that the alpha receptors reduce blood flow to the areas that are holding onto the subcutaneous fat. This will reduce the body’s fat mobilization potential.
Also, GLUT4 is an important hormone transporter. GLUT4 is found in muscle and adipose tissue. It is transported to the plasma membrane as a result of the increased levels of insulin. This helps to move the glucose into the cells, readying them to be broken down and used as a prime energy source. Prolonged levels of insulin and cortisol inhibit GLUT 4 gene transcription and this can result in the reduction of glucose entering into the muscle. Subsequently, the blood glucose in the body is then stored as fat; which is not very good news for an athlete. Although, labeling points on the body with a particular hormone may not the wisest approach.
For example, testosterone reduces levels of belly fat in men and when too high, can increase belly fat in women. In addition, when female bodybuilders take anabolic steroids, their breasts become pectoral muscles and their arms and legs get more muscle mass. This has to do with testosterone’s relationship with estrogen and progesterone and not just testosterone as an independent factor. Insulin and cortisol, however, have a far greater impact on fat metabolism than estrogen and progesterone.
Some simple advice for controlling estrogen levels and weight loss:
- Control carb intake, as a high carb diet, will wash away any benefits of estrogen.
- Time the eating and training cycle with the client’s menstrual cycle.
- Monitor the amount of animal and plant-based estrogen that is being consumed (e.g. dairy, fatty meats, etc.).
- Watch the body’s exposure to environmental estrogen through plastic, pesticides, cosmetics, and caffeine
Do Not Forget about Testosterone
Fat cells are richly saturated with androgen receptors. Adipose tissue is the key target for testosterone. One of the main roles of testosterone is to augment the density of the beta receptors, and as mentioned previously, they are controlled by catecholamine. If testosterone binds to the adipose cells, it will indirectly burn fat. If the beta receptors are boosted, it takes less catecholamine to burn the fat via lipolysis.
In biochemical terms, the androstenedione enhances fat sensitivity during lipolysis and some of the androstenedione in the bloodstream is converted into testosterone within the adipose tissue. The sensitizing makeup of testosterone is backed up by the presence of the growth hormone. There is a very clear pathway and the relationship between the catecholamine and HGH in upregulating the beta receptors.
Testosterone can be a catalyst for the release of HGH, and both hormones have the same metabolic reactions in creating muscle anabolism. Also, testosterone can block fat uptake in the adipose cells. This mechanism can stop fat storage and the catecholamine can only prevent fat release by blocking the fat from entering the cells.
The mitochondria in the cells have testosterone binding sites and these increase the speed at which the fat enters the cells. Again this is controlled by the catecholamine and the rate of entry will determine the amount of fat that is burnt. The higher the increased rate of entry into the mitochondria, the higher the fat-burning potential. The enhanced rate of fat oxidation caused by the catecholamine is very useful, especially during the cutting phase of pre-competition. This is the main rationale why competitors use androgenic fat burners – they are steroid-free.
The Thyroid and Fat Metabolism
The thyroid gland is the only endocrine gland that stores its secretory product in large quantities. The thyroid hormones are called thyroxine T4 and triiodothyronine T3. The difference between the two hormones is the number of iodine modules that each has (i.e. T3= 3 iodine molecules and T4=4 iodine molecules). In essence, T3 and T4 are synthesized by attaching iodines to the amino acid tyrosine which is stored and then secreted into the blood. This is stimulated by the presence of TSH and T4 is normally secreted in greater quantities than T3. It should be noted that T3 is several times more powerful than T4 and when T3 circulates in the bloodstream and enters the cells, much of the T4 is converted into T3 by removing one molecule of iodine. T3 is definitely the more active between the two hormones.
The thyroid hormones increase BMR by stimulating the cellular use of ATP. They play a vital role in thermoregulation of the body and in the following metabolic processes:
- They stimulate protein synthesis.
- They increase lipolysis.
- They enhance cholesterol excretion in the bile.
- They improve the use of glucose for ATP production.
- They enhance the actions of the catecholamine because they regulate the beta receptors and block the activity of the alpha receptors.
The activity and size of the thyroid are controlled in two ways:
- By the level of iodine in the thyroid gland.
- By a negative feedback loop that involves the hypothalamus and the anterior pituitary.
High levels of iodine can suppress the thyroid gland in females have a larger thyroid glands than males; as high levels of estrogen can hinder thyroid function. Low levels of T3 stimulate the hypothalamus to secrete TRH and the anterior pituitary to secrete TSH. TRH also informs the anterior pituitary to secrete TSH. At this point, TSH stimulates all of the thyroid gland activity. The thyroid gland releases T3 and T4 until the metabolic rate returns to normal. It is this negative feedback loop that increases fat metabolism by increasing the use of ATP and energy demand. In addition, the thyroid hormones increase beta-receptor activity and work in opposition to estrogen, making subcutaneous fat less stubborn to burn.
Other factors that affect thyroid function:
- Cortisol is required to sensitize the thyroid receptors. However, too much or too little cortisol reduces thyroid activity.
- Too much or too little iodine can affect thyroid function.
- Progesterone aids thyroid function by helping the receptors and having the active conversion of the thyroid hormones.
- Excessive caffeine can cause issues with the thyroid, due to its increase in cortisol levels.
- Vitamin D deficiency can cause issues with the thyroid.
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