Exercise is a key component to health and wellness and is thought to play an important role in brain activity. Changes in brain activity after exercise have been observed through various neuroimaging techniques, such as functional magnetic resonance imaging (fMRI) and positron emission tomography (PET). The precise impact of exercise on brain glucose metabolism (BGluM) is still unclear; however, results from PET studies seem to indicate an increase in regional metabolism in areas related to cognition and memory, direction, drive, motor functions, perception, and somatosensory areas in humans. Using PET and the glucose analog [18F]-Fluorodeoxyglucose (18F-FDG), we assessed the changes in BGluM between sedentary and chronic exercise in rats. Chronic treadmill exercise treatment demonstrated a significant increase in BGluM activity in the following brain regions: the caudate putamen (striatum), external capsule, internal capsule, deep cerebellar white matter, primary auditory cortex, forceps major of the corpus callosum, postsubiculum, subiculum transition area, and the central nucleus of the inferior colliculus. These brain regions are functionally associated with auditory processing, memory, motor function, and motivated behavior. Therefore, chronic daily treadmill running in rats stimulates BGluM in distinct brain regions. This identified functional circuit provides a map of brain regions for future molecular assessment which will help us understand the biomarkers involved in specific brain regions following exercise training, as this is critical in exploring the therapeutic potential of exercise in the treatment of neurodegenerative disease, traumatic brain injury, and addiction.
Exercise, a proven method of boosting health and wellness, is thought to act as a protective factor against many neurological and psychological diseases. Recent studies on exercise and drug exposure have pinpointed some of the neurological mechanisms that may characterize this protective factor. Using positron emission tomography (PET) imaging techniques and the glucose analog [18F]-Fluorodeoxyglucose (18F-FDG), our team sought to identify how chronic aerobic exercise modulates brain glucose metabolism (BGluM) after drug-naïve rats were exposed to an acute dose of cocaine. Using sedentary rats as a control group, we observed significant differences in regional BGluM. Chronic treadmill exercise treatment coupled with acute cocaine exposure induced responses in BGluM activity in the following brain regions: postsubiculum (Post), parasubiculum (PaS), granular and dysgranular insular cortex (GI and DI, respectively), substantia nigra reticular (SNR) and compact part dorsal tier (SNCD), temporal association cortex (TeA), entopenduncular nucleus (EP), and crus 1 of the ansiform lobule (crus 1). Inhibition, characterized by decreased responses due to our exercise, was found in the ventral endopiriform nucleus (VEn). These areas are associated with memory and various motor functions. They also include and share connections with densely dopaminergic areas of the mesolimbic system. In conclusion, these findings suggest that treadmill exercise in rats mediates brain glucose response to an acute dose of cocaine differently as compared to sedentary rats. The modulated brain glucose utilization occurs in brain regions responsible for memory and association, spatial navigation, and motor control as well as corticomesolimbic regions related to reward, emotion, and movement.
It is predicted that by 2030, globally, an estimated 2.16 billion adults will be overweight, and 1.12 billion will be obese. This study examined genetic data regarding Reward Deficiency Syndrome (RDS) to evaluate their usefulness in counselling patients undergoing bariatric surgery and gathered preliminary data on the potential use in predicting short term (6-month) weight loss outcomes. Methods: Patients undergoing bariatric surgery (n = 34) were examined for Genetic Addiction Risk Severity (GARS) [measures the presence of risk alleles associated with RDS]; as well as their psychosocial traits (questionnaires). BMI changes and sociodemographic data were abstracted from Electronic Health Records. Results: Subjects showed ∆BMI (M = 10.0 ± 1.05 kg/m2) and a mean % excess weight loss (56 ± 13.8%). In addition, 76% of subjects had GARS scores above seven. The homozygote risk alleles for MAO (rs768062321) and DRD1 (rs4532) showed a 38% and 47% prevalence among the subjects. Of the 11 risk alleles identified by GARS, the DRD4 risk allele (rs1800955), was significantly correlated with change in weight and BMI six months post-surgery. We identified correlations with individual risk alleles and psychosocial trait scores. The COMT risk allele (rs4680) showed a negative correlation with EEI scores (r = −0.4983, p < 0.05) and PSQI scores (r = −0.5482, p < 0.05). The GABRB3 risk allele (rs764926719) correlated positively with EEI (r = 0.6161, p < 0.01) and FCQ scores (r = 0.6373, p < 0.01). The OPRM1 risk allele showed a positive correlation with the DERS score (r = 0.5228, p < 0.05). We also identified correlations between DERS and BMI change (r = 0.61; p < 0.01). Conclusions: These data support the potential benefit of a personalized medicinal approach inclusive of genetic testing and psychosocial trait questionnaires when counselling patients with obesity considering bariatric surgery. Future research will explore epigenetic factors that contribute to outcomes of bariatric surgery.
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