Nicotine Addiction Linked to Diabetes in Animal Models
Researchers have discovered a mechanism in rats that links cigarette smoking and the risk of developing type 2 diabetes. Scientists found a crucial role for a diabetes-associated gene, called transcription factor 7-like 2 (Tcf7l2), in regulating the response to nicotine in the brain.
Tcf7l2, which regulates the expression of genes in the pancreas and liver that determine blood glucose levels, also regulates the response of cells in the habenula, an area of the brain that controls reward and aversion behaviors, to nicotine. Variation in Tcf7l2 increases the risk of developing type 2 diabetes, but little has been known about its function in the brain. The study discovered that Tcf7l2 controls a pathway linking the habenula, which controls nicotine intake, to the pancreas, with this circuit responsible for nicotine-induced increases in blood glucose.
To investigate the association between Tcf7l2, nicotine addiction and blood glucose regulation, researchers genetically deleted Tcf7l2 in rats. The mutant rats consumed much greater quantities of nicotine at each dose. Unexpectedly, while the loss of Tcf7l2 function in the habenula increased nicotine consumption in rats, this change also reduced nicotine-driven blood glucose increases and protected against the emergence of diabetes-associated abnormalities in blood glucose levels.
“This unanticipated finding suggests a link between nicotine use and the onset of type 2 diabetes, with implications for future prevention and treatment strategies for both diseases,” said NIDA director Dr. Nora Volkow. “Although addiction is a brain disease, this discovery underscores how the body’s complex functions are exquisitely interconnected, revealing the need for integrated and innovative research.”