weight & body fat
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MTCH2

Could This Gene Help You Spend More Energy & Gain Less Weight? (MTCH2)

Written by Jasmine Foster, BSc, BEd on July 13th, 2020
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MTCH2 promotes energy conservation and the buildup of fat tissue. Can diet control the detrimental effects of this gene? Read on to learn more?

What is MTCH2?

MTCH2 encodes mitochondrial carrier homolog 2, a protein that sits on the membrane of the mitochondria alongside a Bcl-2 type protein involved in cell death [R].

The function of MTCH2 is not completely understood; it is believed to be multifaceted and complex, heavily dependent on which tissue is being discussed. In the brain, MTCH2 is believed to play a role in maintaining cognitive function; in the liver, it is essential for normal cell death cycles. MTCH2 has also been implicated in the progression of some types of cancers [R, R, R].

MTCH2 might be best studied in the context of fat metabolism, however; it appears to signal the body to conserve energy and produce fat tissue [R].

How Does MTCH2 Affect Fat Metabolism & Weight Gain?

One study found that mice without MTCH2 spent more energy and were able to exercise for longer than mice with normal MTCH2. The MTCH2-deficient mice, unlike the normal mice, also did not get obese when they were fed a high-fat diet [R].

MTCH2 is believed to be essential for a process called fat homeostasis: that is, your body uses MTCH2 to maintain the same weight and healthy amount of fat tissue. However, the specific role of MCTH2 may be to promote fat deposition and prevent the body from spending too much energy—you can probably see how that might be harmful in excess [R].

MTCH2 participates in programmed cell death and regulates how much energy is burned by the body. High MTCH2 may decrease energy expenditure and promote weight gain.

MTCH2 Variants in Obesity

At least three MTCH2 variants have been associated with obesity. The best-studied of these is rs10838738, at which the uncommon ‘G’ allele has been associated with slightly increased BMI in multiple studies. Some of these studies have also found a link between the ‘G’ allele and obesity, weight, and waist to height ratio (intended to measure abdominal fat) [R, R, R, R, R].

The other two variants that have been associated with obesity are rs3817334-T and rs4752856-A. The first (rs3817334-T) has been linked to BMI, while the second (rs4752856-A) has been linked to obesity rates and abdominal fat mass [R, R, R].

Your MTCH2 Results for Obesity

SNP Table

 

SNP Summary and Table

MTCH2 rs10838738

  • ‘A’ = Associated with relatively lower BMI
  • ‘G’ = Associated with relatively higher BMI
  • About 43% of all people worldwide have at least one copy of the ‘G’ allele.
  • The ‘G’ allele is more common in people of American descent (64%) and much less common in people of African descent (9%).

MTCH2 rs3817334

  • ‘C’ = Associated with relatively lower BMI
  • ‘T’ = Associated with relatively higher BMI
  • About 53% of all people worldwide have at least one copy of the ‘T’ allele.
  • The ‘T’ allele is more common in people of European descent (65%) and less common in people of African descent (38%).

MTCH2 rs4752856

  • ‘G’ = Not associated with obesity or abdominal fat mass
  • ‘A’ = Associated with obesity & increased abdominal fat mass
  • About 42% of all people worldwide have at least one copy of the ‘A’ allele.
  • The ‘A’ allele is more common in people of American descent (67%) and much less common in people of African descent (9%).

 

Recommendations

Diet

MTCH2 strongly affects how the body responds to energy intake; much of the research on this gene’s interactions with outside factors have to do with diet-induced obesity. As such, there are a few dietary strategies with some promise for counteracting the negative effects of overactive MTCH2 [R].

Low Energy Density Foods

Animals with high MTCH2 burn fewer calories, especially between meals. The most important step to prevent weight gain may therefore be to simply consume fewer calories, and the most sustainable way to do that (without risking nutritional deficiency!) is to choose foods that are less energy-dense [R, R].

Some human research suggests that eating the exact same food, except made in a soup instead of as solid food, makes people feel more satiated and eat significantly fewer calories [R, R].

The idea is that soup has a very low energy density; that is, you would have to eat much more soup by weight than other foods to get the same number of calories. In several human studies, dieters who ate less energy dense foods lost more weight than those who ate foods with a high energy density [R, R, R].

In one study, women who ate low energy density soup lost 50% more weight than women who ate an energy-dense snack [R].

Because people with high MTCH2 may burn less energy, they may benefit most from reducing the energy density of their foods.

Reduce Dietary Carbohydrates

Animals with low MTCH2 burn more energy from carbohydrates than animals with high MTCH2; high MTCH2 may make someone more susceptible to weight gain from carbs. If you have detrimental MTCH2 variants, it may be worth experimenting with low-carb diets [R].

In a clinical trial on 119 overweight people, a low-carbohydrate ketogenic diet was as effective as a low-fat diet for weight loss but had the advantages that it reduced appetite and negative affect. A meta-analysis of 13 studies and over 1,500 people concluded that low-carbohydrate ketogenic diets are more effective than low-fat diets for losing weight [R, R].

Insulin is one of the big four fattening hormones. High glycemic index carbs will cause insulin spikes and insulin resistance, ultimately increasing your risk of obesity. However, they also increase satiation in the short term [R].

MTCH2 reduces the amount of energy burned from carbohydrates; people with detrimental mutations may benefit from a low carb diet.

Intermittent Fasting

Animals with high MTCH2 conserve more energy in between meals and store more fat after they eat; while this may be a beneficial adaptation to periods of scarcity, it can make it difficult to lose weight because the body is always trying to store energy as fat. Extending the time period between meals may help force the body to use those fat stores and shed some weight [R].

Intermittent fasting describes any diet in which a person eats their required caloric intake during predetermined periods of time and fasts during the remaining time. Some people choose to eat only during specific times of day (for example, between 10am and 6pm), while others choose to fast for one or two entire days per week.

Results of one study of intermittent fasting in humans showed that fasting every other day for 12 weeks caused 32 people to lose an average of 12 pounds more than those who followed a daily program of calorie restriction. These people ate 25% of their calories every other day [R].

In a clinical trial on 52 women, caloric intake after 8:00 PM increased the risk of obesity, independent of sleep timing and duration [R].

Time-restricted feeding, a strategy in which a person only eats during a specific window of time each day, has also produced good results for weight loss. However, time-restricted feeding was not as effective as other forms of intermittent fasting, according to a meta-analysis of the practice [R, R, R].

Extending the time period between meals may encourage the body to store less and burn more fat.

Author photo
Jasmine Foster
BSc, BEd

Jasmine received her BS from McGill University and her BEd from Vancouver Island University.

Jasmine loves helping people understand their brains and bodies, a passion that grew out of her dual background in biology and education. From the chem lab to the classroom, everyone has the right to learn and make informed decisions about their health.

Disclaimer

The information on this website has not been evaluated by the Food & Drug Administration or any other official medical body. This information is presented for educational purposes only, and may not be used to diagnose or treat any illness or disease.

Also keep in mind that the “Risk Score” presented in this post is based only on a select number of SNPs, and therefore only represents a small portion of your total risk as an individual. Furthermore, these analyses are based primarily on associational studies, which do not necessarily imply causation. Finally, many other (non-genetic) factors can also play a significant role in the development of a disease or health condition — therefore, carrying any of the risk-associated genotypes discussed in this post does not necessarily mean you are at increased risk of developing a major health condition.

Always consult your doctor before acting on any information or recommendations discussed in this post — especially if you are pregnant, nursing, taking medication, or have been officially diagnosed with a medical condition.

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