Social stress and recovery: implications for body weight and body composition

Tamashiro, Kellie L.K.; Nguyen, Mary M.N.; Ostrander, Michelle M.; Gardner, Stacy R.; Li, Yun; Woods, Stephen C.; Sakai, Randall R.

doi:10.1152/ajpregu.00371.2007

Cited by 105 publications

(104 citation statements)

References 54 publications

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“…The application of CVS to male mice resulted in lower plasma triacylglycerol levels, body weight, lean mass and SPA, consistent with previous reports regarding several different stressors [2,35,36]. The decrease in body weight in male mice seems to be mainly related to a parallel decrease in lean mass.…”

Section: Discussionsupporting

confidence: 90%

“…The decrease in body weight in male mice seems to be mainly related to a parallel decrease in lean mass. This muscle wasting could be a consequence of the higher levels of corticosterone caused by the application of the stress, as documented in Cushing's disease and in rodents undergoing different stressors [2,[37][38][39]; however, we did not find sustained differences in plasma corticosterone levels weeks, or even after the sustained stress exposure phase. This finding is consistent with our hypothesis that a metabolic impairment associated with PTSD is a late-onset consequence of re-programming rather than a direct and immediate result of higher HPAaxis activity.…”

Section: Discussioncontrasting

confidence: 40%

“…Of the myriad factors thought to be responsible for these metabolic disorders in our society, chronic stress is among the most prevalent [1]. Stress-induced hypercortisolism, upregulation of the hypothalamic-pituitary-adrenal (HPA) axis and downregulation of the sympathetic nervous system have each been proposed to contribute to the prevalence of these pathologies [2,3], although the mechanism(s) by which stress leads to obesity and insulin resistance has yet to be determined.…”

Section: Introductionmentioning

confidence: 99%

“…whereas the correlation between PTSD and obesity/type 2 diabetes is clear, the mechanisms underlying this association are not. That said, it is reasonable to hypothesise that neuroendocrinological changes induced by stress exposure, specifically activation of the HPA axis and/or the sympathetic nervous system, may contribute to the prevalence of reduced insulin sensitivity [2,3] and type 2 diabetes [18,19].…”

Section: Introductionmentioning

confidence: 99%

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Decreased glucose tolerance and plasma adiponectin:resistin ratio in a mouse model of post-traumatic stress disorder

et al. 2010

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Aims/hypothesis Obesity and type 2 diabetes are among the most serious health pathologies worldwide. Stress has been proposed as a factor contributing to the development of these health risk factors; however, the underlying mechanisms that link stress to obesity and diabetes need to be further clarified. Here, we study in mice how chronic stress affects dietary consumption and how that relationship contributes to obesity and diabetes. Methods C57BL/6J mice were subjected to chronic variable stress (CVS) for 15 days and subsequently fed with a standard chow or high-fat diet. Food intake, body weight, respiratory quotient, energy expenditure and spontaneous physical activity were measured with a customised calorimetric system and body composition was measured with nuclear magnetic resonance. A glucose tolerance test was also applied and blood glucose levels were measured with a glucometer. Plasma levels of adiponectin and resistin were measured using Lincoplex kits. Results Mice under CVS and fed with a high-fat diet showed impaired glucose tolerance associated with low plasma adiponectin:resistin ratios. Conclusions/interpretation This study demonstrates, in a novel mouse model, how post-traumatic stress disorder enhances vulnerability for impaired glucose metabolism in an energy-rich environment and proposes a potential adipokine-based mechanism.

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Section: Discussionsupporting

confidence: 90%

Section: Discussioncontrasting

confidence: 40%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Decreased glucose tolerance and plasma adiponectin:resistin ratio in a mouse model of post-traumatic stress disorder

et al. 2010

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“…Reduced weight gain over time is a cardinal feature of chronic stress that endures long after stress termination (29,30). This is seen with both physical (29,30) and social stressors (31) and is sufficiently sensitive to serve as an endpoint of chronic mild stress (32). This is in contrast to hyperthermia, which does not consistently occur with certain chronic physical stressors (33) and habituates with repeated stress, while reduced weight loss is maintained (30).…”

Section: Discussionmentioning

confidence: 99%

Impact of overactive bladder on the brain: Central sequelae of a visceral pathology

Rickenbacher¹,

Baez²,

Hale³

et al. 2008

Proc. Natl. Acad. Sci. U.S.A.

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Neural circuits that allow for reciprocal communication between the brain and viscera are critical for coordinating behavior with visceral activity. At the same time, these circuits are positioned to convey signals from pathologic events occurring in viscera to the brain, thereby providing a structural basis for comorbid central and peripheral symptoms. In the pons, Barrington's nucleus and the norepinephrine (NE) nucleus, locus coeruleus (LC), are integral to a circuit that links the pelvic viscera with the forebrain and coordinates pelvic visceral activity with arousal and behavior. Here, we demonstrate that a prevalent bladder dysfunction, produced by partial obstruction in rat, has an enduring disruptive impact on cortical activity through this circuit. Within 2 weeks of partial bladder obstruction, the activity of LC neurons was tonically elevated. LC hyperactivity was associated with cortical electroencephalographic activation that was characterized by decreased low-frequency (1-3 Hz) activity and prominent theta oscillations (6 -8 Hz) that persisted for 4 weeks. Selective lesion of the LC-NE system significantly attenuated the cortical effects. The findings underscore the potential for significant neurobehavioral consequences of bladder disorders, including hyperarousal, sleep disturbances, and disruption of sensorimotor integration, as a result of central noradrenergic hyperactivity. The results further imply that pharmacological manipulation of central NE function may alleviate central sequelae of these visceral disorders.Barrington's nucleus ͉ bladder obstruction ͉ electroencephalographic activity ͉ locus coeruleus O veractive bladder is a prevalent disorder, affecting 17% of the population and negatively impacting quality of life (1). Partial bladder obstruction is a common cause of overactive bladder in males and is used to model overactive bladder in laboratory animals (2). Whereas the structural and functional changes induced in bladder by partial obstruction are well studied (3, 4), the impact on brain function has been neglected. The potential for central consequences of bladder dysfunctions exists because neural circuits are present that communicate pelvic visceral status to the brain so that behavior can be coordinated with visceral functions. Barrington's nucleus (the pontine micturition center) and the locus coeruleus (LC) are integral components of a circuit that performs this task (5). Barrington's nucleus neurons project to spinal preganglionic parasympathetic neurons, where they regulate activity of the bladder and other pelvic viscera (6). These projections form the efferent limb of the micturition reflex, in which Barrington's nucleus neurons are activated by bladder distention and in response, initiate bladder contraction (7). The same Barrington's nucleus neurons project to the LC, a major norepinephrine (NE)-containing nucleus with divergent efferent projections that densely innervate the forebrain (8, 9). Among its functions, the LC regulates arousal, shifts in attention, and involv...

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