Sociality, Hierarchy, Health Comparative Biodemography: A Collection of Papers (2014) / Chapter Skim
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11 Stress and Metabolic Disease--Karen K. Ryan
11 Stress and Metabolic Disease--Karen K. Ryan
Pages 247-268
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From page 247... ...
This paper explores the role of stress-induced activation of the sympathoadrenomedullary system and the hypothalamic-pituitary-adrenocortical axis as key mechanisms linking chronic stress exposure to metabolic health and disease. PHYSIOLOGICAL RESPONSES TO STRESS Stress can be defined as a real or perceived threat to homeostasis or well-being, and it can be either psychological or physical in nature.
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From page 248... ...
. Together, this increased SAM activity facilitates the mobilization of stored energy, increases heart rate and blood pressure, and redirects blood flow away from reproductive and digestive processes.
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. Consistent with this possibility, chronic stress alters feeding behavior and promotes obesity, and is thought to be an important risk factor for a number of metabolic diseases, including cardiovascular disease (CVD)
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. Unfortunately, however, such fat redistribution may also have long-term pathophysiological consequences, since increased visceral adiposity is also thought to contribute to various metabolic diseases, by promoting ectopic fat storage in liver and vascular tissues.
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For example, stress-induced vascular pathology in male cynomolgus monkeys can be abolished by concurrent treatment with the β-adrenergic antagonist propranolol, supporting that elevated SAM tone is a contributing mechanism (Kaplan et al., 1987)
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Fetal exposure to high concentrations of maternal glucocorticoids retards intrauterine growth in humans (Goedhart et al., 2010; Reinisch et al., 1978) , nonhuman primates, and laboratory rodents, whereas low birth weight is associated with increased risk of developing cardiometabolic disease during adulthood (Edwards et al., 1993; Barker, 1995; Seckl and Meaney, 2004; Gluckman et al., 2008)
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. The molecular and physiological mechanisms linking early life stress to cardiometabolic disease have not been clearly elucidated, but may be the consequence of organizational changes to the developing HPA axis, which eventually result in altered basal and stress-evoked SAM and HPA tone during adulthood.
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From page 254... ...
Importantly, a growing body of evidence implicates chronic low-grade activation of the innate immune response in the pathogenesis of various metabolic diseases including CVD, obesity, and T2DM. It is well known, for example, that inflammation plays a key role in the development of atherosclerosis (Cole et al., 2013)
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The innate immune system responds to conserved molecular structures that are essential for the lifecycle of various microbial species -- both pathogenic and commensal. In this way, commensal gut microbiota may affect host physiology by modulating inflammatory signaling pathways (Caesar et al., 2010; Chu and Mazmanian, 2013)
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From page 256... ...
HPA and/or SAM activity may contribute to the etiology of metabolic disease either directly, or by eliciting mild, persistent activation of the innate immune system. Finally, stress is known to alter the composition of gut microbial communities, whereas differences in gut microbial ecology has likewise been linked to both inflammation and the risk of metabolic disease.
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From page 257... ...
. Thus, one interesting possibility is that activation of the SAM and HPA axis by psychosocial stress facilitates chronic metabolic disease by altering the gut microbiota, thereby activating the innate immune system, although this possibility has not yet been tested.
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From page 258... ...
In addition to directly blunting activation of the SAM system and HPA axis, social interactions may alter stress system function and/or risk of metabolic disease by facilitating the inter-individual transmission of commensal microbes (Lombardo, 2007; Archie and Theis, 2011)
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From page 259... ...
A better understanding of how maternal stress affects maternal gut microbial communities, and downstream physiological consequences for both mother and offspring, will be informative. Importantly, this may represent a critical period for therapeutic interventions aimed at disrupting the connections among maternal stress, low birth weight, and metabolic disease of adult offspring.
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. Effects of gut microbiota on obesity and athero sclerosis via modulation of inflammation and lipid metabolism.
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. Differential adaptation of human gut microbiota to bariatric surgery-induced weight loss: Links with metabolic and low-grade inflamma tion markers.
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. Metagenomic sequencing of the human gut microbiome before and after bariatric surgery in obese patients with type 2 diabetes: Correlation with inflammatory and metabolic parameters.
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. Early-life stress and the development of obesity and insulin resistance in juvenile bonnet macaques.
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. Conserved shifts in the gut microbiota due to gastric bypass reduce host weight and adiposity.
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. Social deprivation and coronary artery atherosclerosis in female cynomolgus monkeys.
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. Functional interactions between the gut microbiota and host metabolism.
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From page 267... ...
. Psychosocial stress and atherosclerosis: Family and work stress accelerate progression of coronary disease in women.
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