Distinguishing the Time-Dependent Effects of High-Fat Diet Exposure
Lauren T. Seabrook, Colleen S. Peterson, Duncan Noble, Marissa Sobey, Temoor Tayyab, et al.
(see pages 8582–8595)
The World Obesity Atlas 2022 estimates that 1 billion individuals globally will be living with obesity by 2030. This is concerning because obesity has major health consequences, including heart disease, diabetes, high blood pressure and cholesterol, liver disease, sleep apnea, and several kinds of cancer. While genetic and environmental factors contribute to obesity, the ease of access to calorically dense foods high in sugars and fats may contribute as well. The orbitofrontal cortex (OFC) guides food-related decisions and is associated with diet-induced obesity. In rodent models of obesity, high-fat diets (HFDs) drive morphological and electrophysiological changes in the lateral OFC (lOFC), but the time course of these effects is unknown. Seabrook et al. fed male mice an HFD for either a short or long duration. Both time courses increased excitability of lOFC neurons, but GABAergic signaling was altered in discrete ways. Short exposure to an HFD diminished tonic GABAergic signaling and long-term exposure changed phasic signaling. The effects of short-term exposure were transient and could be restored when the diet was removed, but this was not the case following long-term HFD. Lastly, mice were unable to use satiety to update their subjective food valuations early on during HFD exposure, suggesting that behavioral changes may occur prior to obesity. These findings advance our understanding of how lOFC functioning is altered by HFD time course and suggest that the ease of access to foods high in fats may serve as a risk factor for obesity, though future work may address this more directly.
A whole-brain union-intersected test on the change in cortical orientation dispersion index (ODI) revealed a training-induced increase in ODI and a correlation between ODI change and dynamic balancing task learning rate. See Figure 4A for more information.
Human Study Validates Neural Mechanisms of Motor Learning Detected by Animal Research
Nico Lehmann, Norman Aye, Jörn Kaufmann, Hans-Jochen Heinze, Emrah Düzel, et al.
(see pages 8637–8648)
Learning and acquiring motor skills is fundamental to autonomous survival, but the neural underpinnings of these processes in humans are unknown. Animal research suggests that motor learning directly rearranges the structure of synaptic connections in the brain. However, this finding has not been replicated in humans. In this issue, Lehmann et al. imaged dendritic and axonal processes in humans as they learned and performed a difficult dynamic balancing task for 4 consecutive weeks. The imaging technique they used, diffusion magnetic resonance imaging, provided signals that could be fitted with a theory-driven biophysical model of diffusion. During the motor-learning task, microstructural changes occurred. More specifically, neurite orientation dispersion was increased in primary sensorimotor, prefrontal, premotor, supplementary motor, and cingulate motor areas. Notably, microstructural cortical changes that occurred while learning were predictive of behavioral changes. These findings support prior animal studies by demonstrating that structural alterations of neurites may underly complex motor learning. Future work may explore whether these structures are aberrantly modulated and therapeutically targetable in disease states where motor learning is impaired.
Footnotes
This Week in The Journal was written by Paige McKeon
