The role of the cerebellum in obesity-associated feeding behavior
Active Project Grant Awarded Last action
- Award ID
- F31DK142443
- Recipient
-
The University Of Texas Southwestern Medical Center UEI YZJ6DKPM4W63
- Awarding agency
-
National Institute of Diabetes and Digestive and Kidney Diseases
National Institutes of Health, Department of Health and Human Services
- Obligated
- $82,896
Award facts
- Assistance listing
- 93.847 Diabetes, Digestive, and Kidney Diseases Extramural Research
- Completion date 0% complete
- Originally
- Place of performance
- Dallas, TX 75390, USA
Award details come from USAspending.gov.
Description
- Abstract
- A common factor in the development of obesity involves maladaptive eating behaviors that lead to health- concerning increases in weight. In an effort to better understand feeding-regulating brain circuits, the hypothalamus has been a primary focus in studying satiety mechanisms, as IT plays an important role in energy homeostasis and has a high expression of leptin receptors, a well-known satiety hormone. However, IT has been shown that global deletion of leptin receptor (LEPR) in mice leads to more severe obesity phenotypes than hypothalamic-specific deletions. These data suggest that leptin signaling in other brain regions may play important roles in feeding regulation. Interestingly, several mrna studies in rodents and humans have reported substantial expression of LEPR in the cerebellum. Yet, the specific contributions of cerebellar leptin signaling in feeding behavior remain unknown. Additionally, my preliminary data show that inhibition of purkinje cells (PCS) in a cerebellar lobule, crus I, might be sufficient to decrease feeding, and potentially body weight, in LEPR-null mice. This points to the potential roles for the cerebellum in feeding regulation, which could prove beneficial in activating satiation circuits in the context of hyperphagia and obesity. Based on these data, I hypothesize that important feeding behavior functions reside in the cerebellum, and that understanding the circuits and molecules critical for these functions could offer potential therapeutic opportunities in the treatment of obesity. To test these hypotheses, I propose the following specific aims. Aim 1: delineate the efficacy of crus I-mediated decreased feeding in models of obesity. Aim 2: define the involvement of PC leptin signaling in feeding behavior. Understanding of the extra-hypothalamic contribution to feeding behavior remains limited despite mounting evidence for a role of brain regions beyond the hypothalamus. Successful completion of these aims can create a more complete understanding of satiety circuits by revealing the mechanisms of cerebellar-induced decreased food intake in obesity and the role of cerebellar leptin signaling. Therefore, this project can ultimately aid in identifying new targets to develop more effective treatments or prevention strategies for obesity.
Transactions
| Action | Obligated | Date |
|---|---|---|
| Amendment | $41,448 | |
| Amendment | $41,448 | |
| Original award | $0 |
Quick answers
Who received award F31DK142443?
F31DK142443 was awarded to The University Of Texas Southwestern Medical Center by National Institute of Diabetes and Digestive and Kidney Diseases (National Institutes of Health) on December 20, 2026.
How much is award F31DK142443 worth?
$82,896 has been obligated on F31DK142443.
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