The maintenance of blood sugar is very tightly regulated; with a healthy person’s blood glucose being kept in the range from 3.3-5.5 mmol/L (60-100 mg/dl) between meals, however a new study indicates that it may be newer variant of a gene that determines how well (or not) we are able to maintain these levels.
After eating, the higher levels of blood glucose that comes from the broken-down carbohydrate-based food triggers the release of insulin by the pancreas, which in turn causes the release of a special transporter called GLUT4. The GLUT4 transporter acts like a taxi to remove excess glucose from the blood, taking it into muscle and fat tissue.
Newer Variant of an Older Gene
Between meals and with the help of a special protein (CHC22) produced by the CLTCL1 gene, the GLUT4 glucose transporter remains inside muscle and fat, so that some blood sugar will continue to circulate.
A newly published study [1] by research specialists in population genetics, evolutionary biology, ancient DNA and cell biology analyzed the human genomes to understand how the gene producing CHC22 has changed over human history [2].
By examining the genomes of 2,504 people from the global 1000 Genomes Project compared to the genomes of ancient humans, researchers found that almost half of the people in various ethnic groups have a variant of CHC22 protein that is produced by a new variant of the CLTCL1 gene that became more common as humans moved away from being hunter-gathers and began farming and raising crops. Researchers postulate that the increased consumption of carbohydrates may have been the selective force driving this genetic adaptation.
Researchers found that the newer CHC22 variant of the gene is less effective at keeping the GLUT4 glucose transporter inside muscle and fat tissue between meals, which means that the transporter can more readily clear glucose out of the blood.*
As a result, people with the newer variant of the gene will have lower blood sugar than those with the older variant of the gene.
“The older version of this genetic variant likely would have been helpful to our ancestors as it would have helped maintain higher levels of blood sugar during periods of fasting, in times when we didn’t have such easy access to carbohydrates, and this would have helped us evolve our large brains”[2] — lead author Dr Matteo Fumagalli
*Note: It’s important to keep in mind that only GLUT4 transporters are insulin dependent. There are other glucose transporters that allow glucose into the cell that don’t involve insulin, such as the GLUT1 transporter that works on a concentration gradient. That is, the effect of this gene is not on all glucose regulation, but only glucose regulation in adipose and muscle cells that use GLUT4 transporters.
The higher carbohydrate diets that came as a result of the advent of agricultural meant that this newer variant of the gene could be advantageous, as it moves the excess blood sugar from the blood into the muscle and fat tissue and having the older variant of the gene may make people more likely to develop Diabetes and may also make worse the insulin resistance that underlies the process of developing Diabetes.
“People with the older variant (of the gene) may need to be more careful of their carb intake, but more research is needed to understand how the genetic variant we found can impact our physiology”[2] — co-author Dr. Frances Brodsky
Along with the 2015 study from Israel[3] that demonstrated substantial differences in blood glucose response between both healthy individuals and those with Diabetes predictable by their gut microbiome, this new research adds to the knowledge that multiple factors are involved with determining whether people can tolerate specific dietary carbohydrate loads.
Nutritional guidelines for maintaining healthy blood glucose levels are portrayed as universally applicable, however this new study and the 2015 Israeli study demonstrates that blood glucose varies significantly between individuals based on genetics as well as on gut microbiota composition, which necessitates the need for personalized nutrition in managing blood glucose levels.
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Copyright ©2019 The Low Carb Healthy Fat Dietitian (a division of BetterByDesign Nutrition Ltd.)
LEGAL NOTICE: The contents of this blog, including text, images and cited statistics as well as all other material contained here (the ”content”) are for information purposes only. The content is not intended to be a substitute for professional advice, medical diagnosis and/or treatment and is not suitable for self-administration without the knowledge of your physician and regular monitoring by your physician. Do not disregard medical advice and always consult your physician with any questions you may have regarding a medical condition or before implementing anything you have read or heard in our content.
References
- Matteo Fumagalli, Stephane M Camus, Yoan Diekmann, Alice Burke, Marine D Camus, Paul J Norman, Agnel Joseph, Laurent Abi-Rached, Andrea Benazzo, Rita Rasteiro, Iain Mathieson, Maya Topf, Peter Parham, Mark G Thomas, Frances M Brodsky. Genetic diversity of CHC22 clathrin impacts its function in glucose metabolism. eLife, 2019; 8 DOI: 10.7554/eLife.41517
- University College London. “Gene mutation evolved to cope with modern high-sugar diets.” ScienceDaily. ScienceDaily, 4 June 2019, https://www.sciencedaily.com/releases/2019/06/190604084857.htm
- Zeevi D, et al. Personalized nutrition by prediction of glycemic responses. Cell. 2015;163:1079—1094.
- Noecker C, Borenstein E. Getting Personal About Nutrition. Trends Mol Med. 2016;22(2):83—85. doi:10.1016/j.molmed.2015.12.010
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