Sensory Science and Metabolism; Molecular and Neuronal Mechanisms

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The Section of Sensory Science and Metabolism (SenSMet) laboratory at NINR/NIAAA conducts translation and clinical inpatient and outpatient studies. Active collaborations to investigate areas of common interest in nutrition, taste, and obesity have been undertaken. Specifically, double-blind clinical protocols for which sensory phenotyping measures have been implemented in collaboration with Dr. Gibbons (NIHGRI) and Dr. Hall (NIDDK). In addition, new collaborations develop to investigate neuronal mechanisms in obesity. Sensory Systems and Chronic Disorders. Excessive alcohol consumption is associated with poor diet. There are mixed reports in the literature, so far, and it is imperative to obtain a more detailed understanding of the relationships between diet composition and binge drinking at different thresholds (i.e., number of drinks). Drs. Khushbu Agarwal and Paule Joseph investigated the association between different alcohol consumption thresholds, macronutrient composition, caloric intake, and anthropometric measures from a publicly available dataset. Results showed that higher frequency drinkers consumed a lower percentage of their energy from carbohydrates (42.11%, 41.68%, and 41.94%) compared to never/infrequent drinkers. Participants who drank 12+ drinks/episode consumed significantly fewer grams of dietary fiber (12.81g) compared to never/infrequent drinkers (16.67g). High alcohol intake is associated with differences in eating habits and body composition. We published a manuscript showing that decision-making deficits in obesity and alcohol use disorder (AUD) may contribute to the choice of immediate rewards despite their long-term deleterious consequences. Results from this study led by Dr. Khushbu Agarwal, showed that interaction between BMI and alcohol drinking was seen in brain regions of the default mode network (DMN) and those implicated in self-related processing, memory, and salience attribution. Obesity high risk (obesityHR) relative to obesity low risk (obesityLR) individuals also recruited DMN along with primary motor cortex and regions implicated in inattention, negative perception, and uncertain choices, which might facilitate impulsive choices in obesityHR. Furthermore, obesityHR compared to leanHR/leanLR individuals also demonstrated heightened activation in DMN and regions implicated in uncertain decisions (Agarwal, et al., 2021). Dr. Agarwal and collaborators Dr. Kim Steele and Susan Carnell carried out a project entitled: Neuro-Endo-Microbio-Ome Study: A Pilot Study of Neurobiological Alterations Pre- Versus Post-Bariatric Surgery. We observed more widespread fALFF differences post-bariatric surgery versus post-MWL. Decreased post-prandial fALFF was seen in food reward regions post-RYGB. The highest number of microbial taxa that increased post-intervention occurred in the RYGB group, followed by VSG and MWL groups. The combined hormone, microbiome, and MRI dataset most accurately clustered samples into pre- versus post-VSG phenotypes followed by RYGB subjects. The data suggest surgical weight loss (VSG and RYGB) has a bigger impact on brain and gut function versus MWL and leads to lesser post-prandial activation of food-related neural circuits. VSG subjects had the greatest phenotype differences in interactions of microbiome, rsfMRI, and gut hormone features, followed by RYGB and MWL. These results will inform future prospective research studying gut-brain changes post-bariatric surgery. In collaboration with Dr. Lorenzo leggio, we contributed to a manuscript examining Gut microbiome and metabolome in a non-human primate model of chronic excessive alcohol drinking. Overall, this study showed that changes in the fecal microbiome and metabolome occur after significant long-term excessive drinking and are only partially affected by acute forced abstinence from alcohol. These results provide novel information on the relationship between the fecal microbiome and metabolome in a controlled experimental setting and using a unique non-human primate model of chronic excessive alcohol drinking.