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In 1902, Ralph Larrabee provided intriguing evidence suggesting parallels between the changes in white blood cell counts observed in Boston Marathon runners and those seen in specific disease states. Notably he also noted a considerable leukocytosis of the inflammatory type, suggesting a potential link between extreme exercise and inflammatory responses. This early observation laid the groundwork for further investigations into the complex relationship between exercise intensity, immune system activation, and health outcomes, igniting an ongoing debate about the impact of exercise on the immune system.
Today we know exercise shows quantifiable and observable benefits to human health across multiple scales, but the specific genetic and biological processes and pathways underlying these benefits remain unclear. This is primarily caused by individuals exhibiting significant physiological variations in their response to exercise training, coupled with the diverse methods, subjects and timelines used in studying this phenomenon, which impacts the potential for clear and reproducible analysis. A deeper grasp of the metabolic and cellular impacts of exercise could lead to more targeted exercise approaches. Additionally, unraveling the molecular shifts induced by various exercise methods may hasten the identification of pharmaceutical targets for improving metabolic well-being. To combat the global pandemic of physical inactivity and its associated toll of 5.3 million deaths annually, we must gain a better understanding of the fundamental principles governing physical activity’s benefits.
Current Issue
Hunger signalling in the olfactory bulb primes exploration, food-seeking and peripheral metabolism
Hunger signalling in the olfactory bulb primes exploration, food-seeking and peripheral metabolism
Objective
Although the metabolic state of an organism affects olfactory function, the precise mechanisms and their impact on behavior and metabolism remain unknown. Here, we assess whether ghrelin receptors (GHSRs) in the olfactory bulb (OB) increase olfactory function and influence foraging behaviors and metabolism.
Methods
We performed a detailed behavioural and metabolic analysis in mice lacking GHSRs in the OB (OBGHSR deletion). We also analsyed OB scRNA-seq and spatial transcriptomic datasets to assess GHSR+ cells in the main and accessory olfactory bulbs, as well as the anterior olfactory nucleus.
Results
OBGHSR deletion affected olfactory discrimination and habituation to both food and non-food odors. Anxiety-like and depression-like behaviors were significantly greater after OBGHSR deletion, whereas exploratory behavior was reduced, with the greatest effect under fasted conditions. OBGHSR deletion impacted feeding behavior as evidenced by altered bout number and duration, as well as buried food-seeking. OBGHSR deletion increased body weight and fat mass, spared fat utilisation on a chow diet and impaired glucose metabolism indicating metabolic dysfunction. Cross referenced analysis of OB scRNA-seq and spatial transcriptomic datasets revealed GHSR+ glutamate neurons in the main and accessory olfactory bulbs, as well as the anterior olfactory nucleus. Ablation of glutamate neurons in the OB reduced ghrelin-induced food finding and phenocopied results seen after OBGHSR deletion.
Conclusions
OBGHSRs help to maintain olfactory function, particularly during hunger, and facilitate behavioral adaptations that optimise food-seeking in anxiogenic environments, priming metabolic pathways in preparation for food consumption.
Articles in Press
Hunger signalling in the olfactory bulb primes exploration, food-seeking and peripheral metabolism
Hunger signalling in the olfactory bulb primes exploration, food-seeking and peripheral metabolism
Objective
Although the metabolic state of an organism affects olfactory function, the precise mechanisms and their impact on behavior and metabolism remain unknown. Here, we assess whether ghrelin receptors (GHSRs) in the olfactory bulb (OB) increase olfactory function and influence foraging behaviors and metabolism.
Methods
We performed a detailed behavioural and metabolic analysis in mice lacking GHSRs in the OB (OBGHSR deletion). We also analsyed OB scRNA-seq and spatial transcriptomic datasets to assess GHSR+ cells in the main and accessory olfactory bulbs, as well as the anterior olfactory nucleus.
Results
OBGHSR deletion affected olfactory discrimination and habituation to both food and non-food odors. Anxiety-like and depression-like behaviors were significantly greater after OBGHSR deletion, whereas exploratory behavior was reduced, with the greatest effect under fasted conditions. OBGHSR deletion impacted feeding behavior as evidenced by altered bout number and duration, as well as buried food-seeking. OBGHSR deletion increased body weight and fat mass, spared fat utilisation on a chow diet and impaired glucose metabolism indicating metabolic dysfunction. Cross referenced analysis of OB scRNA-seq and spatial transcriptomic datasets revealed GHSR+ glutamate neurons in the main and accessory olfactory bulbs, as well as the anterior olfactory nucleus. Ablation of glutamate neurons in the OB reduced ghrelin-induced food finding and phenocopied results seen after OBGHSR deletion.
Conclusions
OBGHSRs help to maintain olfactory function, particularly during hunger, and facilitate behavioral adaptations that optimise food-seeking in anxiogenic environments, priming metabolic pathways in preparation for food consumption.
You are what you eat
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