blood sugar control
TSPAN3

How Does This Cell Growth Gene Affect Blood Sugar? (TSPAN3)

Written by Jasmine Foster, BSc, BEd on October 19th, 2020
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TSPAN3 encodes tetraspanin-3, which regulates cell growth and movement. How might it be connected to blood sugar? Read on to learn more.

Summary

TSPAN3 encodes tetraspanin-3. Variants of TSPAN3 may play a role in diabetes either through impaired insulin signalling or autoimmune reactions. Lifestyle, diet, and supplement modifications may counteract the effects of these variants by preventing insulin resistance and reducing autoimmune inflammation.

TSPAN3 and Blood Sugar

TSPAN3 encodes tetraspanin-3, a protein that plays a role in cell growth, development, and migration through the body into the appropriate tissues. Because of these functions, it is best studied for its potential role in cancers such as acute myelogenous leukemia, a deadly blood cancer [R, R, R].

Association studies have found that certain TSPAN3 variants are more common in people with diabetes, but the reason for this link is unclear [R, R].

Tetraspanin-3 might have an indirect interaction with insulin. Tetraspanin-3 regulates the expression of a protein called ADAM10 in the nervous system, and ADAM10 needs insulin to break apart the longevity protein klotho. However, researchers don’t know whether this interaction has any effect on insulin’s blood sugar functions [R, R].

Researchers have found a couple of other clues about how tetraspanin-3 might affect blood sugar. In type 1 diabetes, people sometimes develop autoimmune antibodies against a similar tetraspanin protein, tetraspanin-7. It could be that a similar reaction exists for tetraspanin-3, but this option has not yet been explored [R].

TSPAN3 or PEAK1?

The variants in the SNP table below have been associated with multiple genes, namely TSPAN3 and PEAK1. Researchers aren’t quite sure which one they “really” belong to; they’re physically close enough to both genes that they could affect either one… or both of them [R, R].

Both TSPAN3 and PEAK1 are genes involved in cell growth, development, and migration around the body. So, even if it turns out that one or both of these variants actually only affects PEAK1, the mechanism by which they affect blood sugar may be similar [R, R].

TSPAN3 encodes tetraspanin-3, which plays a role in the growth, development, and migration of cells. Its connection to blood sugar is poorly studied, but it may have something to do with insulin signalling or autoimmune inflammation.

Your TSPAN3 Results for Blood Sugar

SNP Table

variant genotype frequency risk allele
rs7177055
rs7178572

 

TSPAN3 rs7177055

  • ‘G’ = Not associated with blood sugar levels
  • ‘A’ = Associated with relatively high blood sugar [R]

TSPAN3 rs7178572

  • ‘G’ = Associated with relatively higher blood sugar levels
  • ‘A’ = Possibly protective against high blood sugar [R]

 

Recommendations

Avoid Cigarettes & Air Pollution

Exposure to cigarette smoke and other forms of air pollution have been associated with both insulin resistance and autoimmune disease [R, R, R].

Air pollution (particularly traffic pollution, nitrogen dioxide, tobacco smoke, and particulate matter) is a leading cause of insulin resistance and type 2 diabetes mellitus [R, R, R, R, R].

Intermediate- and long-term exposure to pollution increases fasting glucose, glycated hemoglobin, blood fat levels, and the risk of heart disease and stroke, especially in people with type 2 diabetes [R, R, R, R].

Smoking has been clearly associated with higher glycated hemoglobin, a marker of long-term exposure to glucose that indicates poor blood glucose control and predicts risk of type 2 diabetes [R, R].

Similarly, women with gestational diabetes who smoked at the beginning of their pregnancy showed higher glycated hemoglobin levels and blood sugar spikes after an oral glucose tolerance test [R].

Air pollutants, including cigarette smoke, are associated with both insulin resistance and autoimmune disease. Those with detrimental TSPAN3 variants should be especially careful to avoid such pollutants.

Magnesium

Magnesium deficiency is associated with autoimmune and inflammatory diseases [R].

Low magnesium levels play a role in the development of insulin resistance, type 2 diabetes, and metabolic syndrome, while high intake of magnesium-rich foods such as whole grains, beans, nuts, and green leafy vegetables has been associated with a lower incidence of type 2 diabetes [R, R, R, R].

Dietary magnesium improved insulin sensitivity and reduced fasting glucose levels in a clinical trial [R].

Major food sources containing magnesium are leafy green vegetables, fruits, legumes (especially soy), nuts (almonds, cashews), whole grains, red meat, and seafood. Magnesium supplements are also readily available [R, R].

Magnesium deficiency may play a role in the development of insulin resistance and autoimmunity. Magnesium-rich foods contain enough to ward off deficiency in most people, but supplements are also available.

Zinc

Zinc is a vital mineral for correct immune function, and zinc deficiency is common in both autoimmunity and insulin resistance [R].

Several meta-analyses have found that zinc supplementation may reduce blood glucose, insulin resistance, and glycated hemoglobin levels in people with obesity, diabetes (both type 1 and 2) and metabolic syndrome [R, R, R].

Zinc may also decrease the severity of diabetic neuropathy (nerve pain), oxidative stress, and cholesterol/triglyceride levels in type 2 diabetic patients [R, R, R, R].

Zinc is absolutely essential for the correct function of the immune system and has also been linked to insulin resistance. Zinc supplementation is an easy way to prevent deficiency.

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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