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PEMT

A Surprising Player in Obesity and Diabetes (PEMT)

Written by Aleksa Ristic, MS (Pharmacy) on September 26th, 2019
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PEMT is an overlooked player in fat and glucose metabolism. Specific variants correlate with obesity and diabetes, but they also have a positive side. Read on to check your PEMT gene and learn how it impacts metabolic health.

The Role of PEMT in Metabolism

Source: Wikimedia Commons 

The PEMT gene encodes an enzyme that makes phosphatidylcholine (PC) in the liver. It makes sure you don’t run out of PC and choline, even if you don’t get them from food [R, R].

Choline and PC play central roles in fat transport and metabolism. Recent studies underline the importance of phospholipids in weight control, insulin functions, and metabolic health [R, R, R].

When scientists put PEMT-deficient mice on a high-fat diet, they [R]:

PEMT encourages the body to burn fat for energy; this is beneficial to some extent and shields the liver from disease, but it can lead to obesity and insulin resistance when fat intake is higher. Lower PEMT activity forces the body to use glucose and boosts insulin sensitivity, but excessive fat accumulates in the liver [R]. 

As always, the answer lies in the right balance—this post will help you find it.

PEMT produces phosphatidylcholine and choline, which are essential for fat metabolism. High PEMT activity protects the liver but plays a role in obesity and insulin resistance.

Do PEMT Variants Correlate with Obesity and Diabetes?

A clinical trial of 257 adults confirmed the above findings: obesity was more common in people with the “CC” genotype on rs7946 (higher PEMT), but this same group had lower rates of fatty liver [R].

A 2015 review included over 200,000 people and examined the association between different gene variants and obesity or fat distribution. One PEMT variant, rs4646404-G, correlated with the waist-to-hip ratio (WHR). High WHR (larger waist circumference relative to hip size) indicates a buildup of abdominal fat (central or abdominal obesity), and it’s a significant risk factor for heart disease and metabolic disorders [R, R, R].

Two more variants, rs4646343-G and rs7946-C, show a weaker correlation with WHR [R].

In over 370 individuals, people with at least one “G” allele on rs12325817 (lower PEMT) had two times lower rates of diabetes compared with those with the “CC” genotype [R].

Variants that increase PEMT activity are associated with weight gain and abdominal obesity; decreased PEMT activity correlates with lower rates of diabetes. 

How It Works

Scientists noticed that PEMT-deficient mice were more likely to gain weight and become insulin-resistant when supplemented with choline. Thus, higher PEMT may play a role in obesity and diabetes by making excessive choline [R, R].

Following this observation, they set out to determine how choline induced these metabolic changes and discovered the following [R, R]:

  1. It stimulated fat transport out of the liver and increased blood lipids
  2. It suppressed PPAR-gamma receptors in the liver
  3. It boosted glucagon levels and impaired glucose metabolism

Additionally, increased PEMT expression in fat tissue may contribute to abdominal fat buildup [R, R, R].

According to animal trials, excess choline from high PEMT activity may contribute to obesity and diabetes by increasing blood lipids, suppressing PPAR-gamma receptors, and impairing glucose metabolism.

Your PEMT Results for Obesity and Diabetes

 

Primary SNPs: 

PEMT rs7946

  • ‘T’ = Doesn’t correlate with obesity
  • ‘C’ = Correlates with obesity

Population frequency:

  • Around 37% of the general population has the “CC” genotype
  • Around 10% of European descendants have this genotype

PEMT rs12325817

  • ‘G’ = Correlates with lower rates of diabetes
  • ‘C’ = Doesn’t correlate with diabetes

Population frequency:

  • Around 61% of the general population has the “CC” genotype
  • Around 31% of European descendants have this genotype

Other important SNPs:

PEMT rs4646404

  • ‘A’ = Doesn’t correlate with abdominal obesity
  • ‘G’ = Correlates with abdominal obesity

Population frequency:

  • Around 74% of the general population has the “GG” genotype
  • Around 43% of European descendants have this genotype

PEMT rs4646343

  • ‘T’ = Doesn’t correlate with abdominal obesity
  • ‘G’ = Correlates with abdominal obesity

Population frequency:

  • Around 65% of the general population has the “GG” genotype
  • Around 31% of European descendants have this genotype

SNP Table

 

Recommendations

Lifestyle

Stress Reduction

Stress causes the pancreas to release more glucagon, which increases blood glucose and may worsen the effects of overactive PEMT. The stress hormone, cortisol, mediates this effect [R].

Stress plays a crucial role in obesity and insulin resistance, and it’s among the worst enemies in maintaining optimal metabolic health [R, R, R].

Embrace Cold

Cold exposure may lessen the harmful effects of overactive PEMT by boosting PPAR-gamma and adiponectin. As a result, it improved insulin sensitivity and glucose metabolism in a couple of small clinical trials [R, R, R, R].

Short-term cold exposure may also help burn calories. One study even suggested it “may contribute to counteracting the current obesity epidemic.” [R, R].

You can practice cold exposure wherever you are by taking cold showers. From Joe’s personal experience: “they are perfect for balancing blood sugar and insulin.”

Diet

Limit the Intake of Saturated Fat

The negative effects of overactive PEMT in mice appeared only on a high-fat diet. Although clinical trials haven’t confirmed this, dietary fats may play an important role in humans, too.

You want to be particularly careful with saturated fat, as many human studies link its higher intake with obesity and insulin resistance [R, R, R].

Try to limit the intake of foods rich in saturated fat, such as [R, R]:

  • Lard
  • Palm oil
  • Butter
  • Cheese
  • Coconut oil

Should you eat more carbs instead? Not necessarily. Other types of fat, especially polyunsaturated fatty acids such as omega-3, may be the best swap when it comes to metabolic health [R, R, R].

High intake of saturated fats from lard, dairy, and palm oil may worsen the negative effects of PEMT on weight gain and blood sugar. Consume more polyunsaturated fatty acids instead.

Cinnamon

Cinnamon may improve insulin resistance and lower blood sugar and cholesterol by activating PPAR-gamma receptors [R, R].

Try to consume this delicious spice on a daily basis.

Supplements

The studies on mice blame excessive choline for weight gain and insulin resistance. If your variants boost PEMT activity, try not to make things worse by consuming too much choline in the form of supplements.

That said, choline is vital for the liver, heart, brain, and more. It’s best not to go below the recommended daily amount: 500 mg for men and 425 mg for women [R].

Some studies have linked higher choline intake with obesity and insulin resistance, while others found the opposite effects [R, R, R, R].

The following supplements may balance overactive PEMT by boosting PPAR-gamma:

They can have beneficial effects on obesity and diabetes by improving insulin sensitivity and reducing blood lipids [R, R, R, R, R].

PPAR-gamma activation benefits glucose metabolism and inflammation, but its impact on weight loss is mixed and depends on other factors [R, R, R, R, R].

You can check out a more complete list of PPAR-gamma activators over on SelfHacked.

That said, most supplements are still in the investigational phase and haven’t been approved by the FDA.

Author photo
Aleksa Ristic
MS (Pharmacy)

Aleksa received his MS in Pharmacy from the University of Belgrade, his master thesis focusing on protein sources in plant-based diets.  

Aleksa is passionate about herbal pharmacy, nutrition, and functional medicine. He found a way to merge his two biggest passions—writing and health—and use them for noble purposes. His mission is to bridge the gap between science and everyday life, helping readers improve their health and feel better.

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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