Nutritional genomics is broadly defined as the science behind gene and nutrient interactions. While still in its infancy, the field is fast-moving and potentially lays the groundwork for a more highly “personalized nutrition” approach. A common question a lot of people have is if type-2 diabetes is genetic. The answer is there is a connection. In this article, I dove into the molecular function to help understand this connection.
“Let us understand what our own selfish genes are up to because we may then at least have the chance to upset their designs.” - Richard Dawkins
Passed down from our parents, our genetic makeup is outside our control. And with genetic testing having become commonplace, we now have easy access to incredible information detailing variations to thousands of individual genes (“SNPs” or single nucleotide polymorphisms). First of all, it’s essential to understand that our genetics are not our destinies; possessing certain disease-associated genes does not preordain us to poor health. Since we’re stuck with our genetics, the key question becomes: Why is it important to concern ourselves with genetic information, and do we enjoy any leeway in managing how our genetics – SNPs and all - impact both our general health and disease progression?
Fortunately, the high-level answer is we have a lot of room to work with. For starters, there are associations between many gene variations (SNPs) and disease, though it matters whether individual genes are “expressed.” “Gene expression” is the observable physical manifestation of a gene or genes by gene transcription and translation processes. Simplistically, it’s the instructions – the on and off switches - our DNA communicates with our cells. Even though we can’t modify our genes, the great news is that epigenetic factors such as diet and lifestyle play critical roles in gene expression (turn the switches "on" or “off”). This means nutrigenomic science has exciting potential as a tool for enhancing gene expression/nutrient interactions – giving each of us the power to reduce disease risk and take charge of our health prospects.
For example, I’ll highlight the gene-nutrient-disease connections by noting the SLC30A8 gene, zinc status, and glucose metabolism relationship. While challenging to comprehend the complex mechanisms involved, I hope this discussion at least sheds a little light on an aspect of type 2 diabetes (T2D) development.
Most people understand that the liver and pancreas are critical organ systems in maintaining glucose homeostasis. The pancreas’s ability to produce insulin is especially crucial. When it comes to insulin secretion, it’s essential to look at the underlying molecular mechanisms involving the SLC30A8 gene and its associated nutrient, zinc. Many appreciate that zinc plays a vital role in immune function and energy metabolism. What is not commonly known is that zinc deficiency is also a risk factor for obesity and T2D. The SLC30A8 (rs11558471) gene encodes a protein called zinc transporter 8 (ZnT8). It supports the movement of zinc within cells. ZnT8 is mainly expressed in the pancreas, playing a role in insulin secretion from pancreatic beta cells.
The breakthrough scientific discovery identified that the common polymorphism in SLC30A8 and ZnT8 may increase susceptibility to T2D, and an altered ZnT8 function may be involved in the pathogenesis of T2D. This provided novel insight into the role of zinc in T2D and that the regulation of zinc homeostasis can be a tangible therapeutic target for preventing or treating obesity, T2D, and metabolic syndrome.
Another 2020 study conducted on 128 Iranian subjects with T2D revealed that the risk allele carriers (A allele) of the SLC30A8 gene have higher blood IL-17 concentration, fasting glucose, and HOMA-IR levels. For the first time, it demonstrated the genetic association of SLC30A8 (rs11558471) with IL-17 and glycemic traits in patients with T2D. More studies that looked at the gene and diet interactions suggest that A allele carriers of the SLC30A8 gene may benefit from higher zinc intakes to help maintain glucose homeostasis.
With constantly evolving technologies and sciences, we now have greater tools available for us to take charge of our health proactively. Learning about our genetic information is an excellent place to start. If you’d like to learn more about your genetics and their associations with your nutrient status, please follow the following steps:
Take the 23&Me or Ancestry genetic test.
Download your raw data from your account at 23&Me.com or Ancestry.com.
Purchase a 60-minute "Nutritional Genomic Consultation" session at https://www.jennynoland.com/by-appointment-consultations.
Head over to the Book Consults page to schedule a consultation by choosing the "Standard Follow-up" option.
Jenny Noland, MS, CNS, CNGS, CKNS, LDN, MBA
Functional Nutritionist in Eugene, Oregon
Board-Certified Nutrition Specialist
Board-Certified Nutritional Genomics Specialist
Board-Certified Ketogenic Nutrition Specialist
Certified Oncology Nutrition Specialist
Personalized Nutrition Therapy for Metabolic Dysfunction and Cancer Care
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Gene Expression. Accessed February 20, 2022. https://www.ncbi.nlm.nih.gov/probe/docs/applexpression/
Fukunaka A, Fujitani Y. Role of Zinc Homeostasis in the Pathogenesis of Diabetes and Obesity. Int J Mol Sci. 2018;19(2). doi:10.3390/IJMS19020476
Ahmadi M, Mahrooz A, Abediankenari S, Roodbari NH. Association of rs11558471 in SLC30A8 gene with interleukin 17 serum levels and insulin resistance in iranian patients with type 2 diabetes. Iran J Immunol. 2020;17(3):215-225. doi:10.22034/IJI.2020.85513.1715