Cannabinoid CB1R Receptor Mediates Metabolic Syndrome in Models of Circadian and Glucocorticoid Dysregulation
type: CreativeWork
description: The most recent projections in the growing obesity rates across the nation show an increase to 60% by the year 2030. These growing rates of obesity are paralleled by an increased rates of depressive conditions, anxiety, and sleep loss, often with environmental factors at the root of the cause. Stress and the stress response is a dynamic system that reflects one's ability to cope with events, behaviorally or physiologically, as stressors occur over a lifetime. While many key players mediate the effects of stress exposure on disease outcomes including the sympathetic nervous system, parasympathetic, inflammatory cytokines and metabolic hormones, this dissertation focuses on glucocorticoids because of the extensive regulatory role they play in mounting the adaptative response to stress. Additionally, glucocorticoids act to regulate feeding and energy balance, and when not properly regulated, they can lead to increased weight gain, particularly the development of abdominal visceral fat. Independent from their role in the stress response, glucocorticoids are also secreted in a diurnal fashion as regulated by the master circadian (daily) clock in the suprachiasmatic nuclei ( SCN). Signaling in this regard is at least partially responsible for entraining circadian clocks outside of the SCN. Just as shifts in glucocorticoid exposure are associated with metabolic disturbances, disruption of circadian rhythms has also been linked to the development of obesity. However, it remains unclear how the two systems independently and/or collectively regulate energy balance. The first aim of this dissertation was to determine how disruptions in the environmental photoperiod impacts clock gene expression and if this environmental exposure affects circulating glucocorticoid levels. The second aim was to determine if increased exposure to a rhythmic corticosterone (CORT) disrupted circadian rhythms. Given that CORT imbalances result in circadian disruption and weight gain in both models, …
abstract: The most recent projections in the growing obesity rates across the nation show an increase to 60% by the year 2030. These growing rates of obesity are paralleled by an increased rates of depressive conditions, anxiety, and sleep loss, often with environmental factors at the root of the cause. Stress and the stress response is a dynamic system that reflects one's ability to cope with events, behaviorally or physiologically, as stressors occur over a lifetime. While many key players mediate the effects of stress exposure on disease outcomes including the sympathetic nervous system, parasympathetic, inflammatory cytokines and metabolic hormones, this dissertation focuses on glucocorticoids because of the extensive regulatory role they play in mounting the adaptative response to stress. Additionally, glucocorticoids act to regulate feeding and energy balance, and when not properly regulated, they can lead to increased weight gain, particularly the development of abdominal visceral fat. Independent from their role in the stress response, glucocorticoids are also secreted in a diurnal fashion as regulated by the master circadian (daily) clock in the suprachiasmatic nuclei ( SCN). Signaling in this regard is at least partially responsible for entraining circadian clocks outside of the SCN. Just as shifts in glucocorticoid exposure are associated with metabolic disturbances, disruption of circadian rhythms has also been linked to the development of obesity. However, it remains unclear how the two systems independently and/or collectively regulate energy balance. The first aim of this dissertation was to determine how disruptions in the environmental photoperiod impacts clock gene expression and if this environmental exposure affects circulating glucocorticoid levels. The second aim was to determine if increased exposure to a rhythmic corticosterone (CORT) disrupted circadian rhythms. Given that CORT imbalances result in circadian disruption and weight gain in both models, …
author: Bowles, Nicole
keywords: obesity, glucocorticoids, circadian rhythm, endocannabinoids, metabolism, stress, Life Sciences
date published: 2013-01-01T08:00:00Z
date modified: 2026-07-24T04:11:51Z
provider: Rockefeller
publisher: Networked Digital Library of Theses and Dissertations
type: WebPage
source organization: Rockefeller