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KCNJ11

A Genetic Link Between Potassium Passageways and Low Blood Sugar (KCN)

Written by Shany Lahan, MS (Neuroscience) on October 13th, 2020
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KCN genes code for proteins that comprise parts of passageways. These passageways allow potassium ions to exit pancreatic cells, ultimately leading to the release or suppression of a hormone that regulates blood sugar levels. Variants of these genes have been associated with low blood sugar levels. Read more to learn about this association, and to learn about recommendations you may follow to mitigate the negative effects of these variants. 

Summary

KCN genes code for parts of passageways that are involved in the release of the blood sugar-regulating hormone, insulin. Variants of these genes may play a role in low blood sugar by reducing the production or activity of potassium passageways, leading to excess release of insulin. Supplement modifications may counteract the effects of these variants by increasing production of parts of these potassium passageways.

KCN and Blood Sugar

Insulin is a hormone that promotes the storage of blood sugar in muscle, fat, and the liver, thereby lowering levels of this sugar in the blood. Insulin is usually released from cells of the pancreas in response to elevated blood sugar levels; for example, after consumption of a meal [R].

The release of substances from cells of the body often depends on a change in electrical charge across cell surfaces. In the case of insulin release from a pancreatic cell, the charge on the inner surface of the cell must be more positive than the outer surface [R, R]. 

The KCNJ11 and KCNQ1 genes are involved in the formation of distinct passageways (channels) that are found on the surface of pancreatic cells. These passageways allow positively-charged potassium ions to pass from the inside of pancreatic cells to the outside, thus leaving a negative charge on the inner surface of the cells [R, R, R]. 

Potassium channels containing the protein encoded by KCNJ11 (Kir6.2) maintain pancreatic cells in negatively-charged and inactive states by remaining open until blood sugar levels rise. When this occurs, Kir6.2-containing channels become blocked, and positively-charged potassium ions build up within pancreatic cells. This results in a more positive charge on the inner surface of these cells than the outer surface, which can stimulate insulin release [R, R]. 

A positive inner charge can also open potassium channels containing the protein encoded by KCNQ1 (KvLQT1). This allows potassium ions to slowly exit, and pancreatic cells to eventually return to their negatively-charged and inactive states [R].

Variants of KCNJ11 and KCNQ1 have been associated with low blood sugar levels. These variants may decrease the production or activity of potassium channels, leading to overactivity of pancreatic cells [R, R, R].

Overactivity of pancreatic cells can result in excess release of insulin and low blood sugar levels. High insulin levels experienced over a prolonged period of time can also result in decreased insulin receptor sensitivity, which may increase the risk of type 2 diabetes [R].

Your KCN Results for Blood Sugar

SNP Table

 

 

Primary SNP

KCNJ11 rs5215

  • ‘C’ = Increased risk of low blood sugar
  • ‘T’ = Not associated with low blood sugar

Other Important SNPs

KCNJ11 rs5219

  • ‘T’ = Increased risk of low blood sugar 
  • ‘C’ = Not associated with low blood sugar

KCNQ1 rs2237892

  • ‘C’ = Increased risk of low blood sugar
  • ‘T’ = Not associated with low blood sugar

KCNQ1 rs2237897

  • ‘C’ = Increased risk of low blood sugar
  • ‘T’ = Not associated with low blood sugar

 

 

Recommendations

Supplements

Zinc

Zinc is a mineral that can mimic the actions of insulin, as well as prevent the release of insulin from pancreatic cells [R, R].

Low blood zinc levels have been associated with diabetes and prediabetes. Conversely, greater intake of this mineral may protect against type 2 diabetes [R, R, R].

Several meta-analyses have found that zinc supplementation may regulate blood glucose and insulin resistance in people with obesity, type 1 and type 2 diabetes, and metabolic syndrome [R, R, R].

Zinc was shown to increase the production of KvLQT1 in cell-based experiments [R].

Zinc supplements may regulate blood sugar by increasing production of KvLQT1.

Resveratrol

Resveratrol is an antioxidant mainly found in grapes and red wine. It is also available as a supplement. 

A meta-analysis of 11 small studies found that resveratrol may improve blood glucose control and insulin sensitivity in people with type 2 diabetes, but not in healthy individuals. However, another meta-analysis found this evidence to be insufficient [R, R].

In individuals with metabolic syndrome, supplementation with at least 500 mg resveratrol for over 10 weeks was shown to regulate blood sugar levels [R].

In a mouse study, treatment with resveratrol increased production of Kir6.2 [R].

Resveratrol may regulate blood sugar levels by increasing production of Kir6.2.

Author photo
Shany Lahan
MS (Neuroscience)

Shany received her MSc in Neuroscience from Western University.

Prior to joining SelfDecode, Shany conducted research related to Alzheimer’s disease, and taught science to undergraduate students. She believes that research should be accessible to everyone, regardless of scientific background. Shany joined SelfDecode with a mission to help others optimize their health and wellbeing – as well as help them understand the science behind it all.

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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