- Secondary data analysis grant for the blood
- increase homeostatic mechanisms of satiation (meal termination)
- alter neural, behavioral and perceived hedonic drivers of eating behavior, both contributing to a decrease in palatable food intake in those at high risk for T2DM.
- We expect bromocriptine to modify endocrine-mediated satiation signaling via suppressed prolactin, augmented adiponectin, amylin, glucagon like peptide-1 (GLP1), and decrease postprandial plasma glucose and insulin.
- We expect that, it will contribute to decreased ad lib palatable food intake, as well as promote healthy blood sugar. We also expect that bromocriptine will increase BOLD response during palatable food intake in dopaminergic brain regions thought to encode reward, decrease food specific impulsivity, and increase perceptual hedonic food ratings.
- Test whether the DRD2 TaqIA A1 allele, which is associated with reduced dopamine-D2 receptor density and dopamine signaling, moderates the impact of bromocriptine on homeostatic and hedonic drivers of food intake. This will provide critical information whether individual genetic predisposition alters the effectiveness of this medication, and may provide a foundation for individualized T2DM treatment.
- For Jan 16 11:30am
- Draft prereg
- Mock up of the model
- Git repo github
- Datalad repo creation
- Yana renci account
- Access to NIBL projects on the OneDrive
- Data audit
- Pull together dataset
- Target journal
- Diabetes Care
- Diabetes
- Nutrients
- Model
- Two way interaction: gene x drug
- Control variables
- Correlation matrix
- Preference
- Nausea
- Hunger
- Wanting
- Thirst
- Sex
- Age
- Change in nausea (change on drug vs change off drug)
- BMI
- What ever comes out of the correlation matrix into model
- BOLD response in task contrasts
- Straight taste outcome <- run first
- Milkshake vs. Water
- PE outcome (event is when they don't get what they think they are getting) <- need first level
