Class
Article
College
College of Science
Department
English Department
Faculty Mentor
Mirella Meyer-Ficca
Presentation Type
Poster Presentation
Abstract
Niacin (NAD+) is a a vital molecule in human metabolism. NAD+ decline with age is well documented and low NAD+ levels may cause aging symptoms, however the molecular cause of NAD+ decline is poorly understood. Few pathways in the human metabolism fully consume NAD+ as it is usually recycled to NADH. One protein found on immune cells, called CD38, does fully consume NAD+ in its reaction, and so it may contribute to niacin deficiency by depleting the NAD+ in the body over time. To determine CD38’s role in causing niacin deficiency and aging, we knocked out the CD38 gene in mice and observed their NAD+ levels over time on a niacin deficient diet. If CD38 is a primary driver of NAD+ loss, then mice without the gene would have a higher NAD+ level than those with the gene. Results showed that CD38 knock-out mice on a niacin deficient diet had a similar progression of NAD+ deficiency as control mice on a deficient diet, but with slightly higher NAD+ content. According to these results, CD38 is not a significant contributor to NAD+ consumption and niacin deficiency, but may play some role.
Location
Logan, UT
Start Date
4-8-2022 12:00 AM
Included in
Transgenic Mice Demonstrate the Level of Contribution of Protein CD38 to NAD+ Decline Seen in Human Aging
Logan, UT
Niacin (NAD+) is a a vital molecule in human metabolism. NAD+ decline with age is well documented and low NAD+ levels may cause aging symptoms, however the molecular cause of NAD+ decline is poorly understood. Few pathways in the human metabolism fully consume NAD+ as it is usually recycled to NADH. One protein found on immune cells, called CD38, does fully consume NAD+ in its reaction, and so it may contribute to niacin deficiency by depleting the NAD+ in the body over time. To determine CD38’s role in causing niacin deficiency and aging, we knocked out the CD38 gene in mice and observed their NAD+ levels over time on a niacin deficient diet. If CD38 is a primary driver of NAD+ loss, then mice without the gene would have a higher NAD+ level than those with the gene. Results showed that CD38 knock-out mice on a niacin deficient diet had a similar progression of NAD+ deficiency as control mice on a deficient diet, but with slightly higher NAD+ content. According to these results, CD38 is not a significant contributor to NAD+ consumption and niacin deficiency, but may play some role.