Neonatal LPS injection alters the body weight regulation systems of rats under non‐stress and immune stress conditions

Iwasa, Takeshi; Matsuzaki, Takashi; Kinouchi, Riyo; Fujisawa, S.; Murakami, Masahirô; Kiyokawa, Machiko; Kuwahara, Akira; Irahara, Minoru

doi:10.1016/j.ijdevneu.2009.08.015

Cited by 32 publications

(24 citation statements)

References 43 publications

(70 reference statements)

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“…Conversely, P14 is a point in development where HPA axis responsiveness to stress begins to acquire an adult-like profile (50), potentially a vulnerable stage in the development of HPA axis function. In this regard, we have also observed, under some housing conditions, changes in adult body weight after an LPS challenge at P7 (82,83), an observation that has been replicated in rats treated at P10 (42). The hypothalamic pathways regulating body weight and metabolism are known to mature, in the rodent, between P6 and P12 (2, 13), making this a particularly sensitive time for these pathways.…”

Section: Unresolved Issuessupporting

confidence: 60%

Neonatal programming of innate immune function

Spencer

Galic

Pittman

2011

American Journal of Physiology-Endocrinology and Metabolism

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The early life environment can be crucial in influencing the development of an animal's long-term physiology. There is now much evidence to suggest that perinatal challenges to an animal's immune system will result in changes in adult rat behavior, physiology, and molecular pathways following a single inflammatory event during development caused by the bacterial endotoxin lipopolysaccharide (LPS). In particular, it is now apparent that neonatal LPS administration can influence the adult neuroimmune response to a second LPS challenge through hypothalamic-pituitary-adrenal axis modifications, some of which are caused by alterations in peripheral prostaglandin synthesis. These pronounced changes are accompanied by a variety of alterations in a number of disparate aspects of endocrine physiology, with significant implications for the health and well-being of the adult animal. In this review, we discuss the newly elucidated mechanisms by which neonatal immune challenge can permanently alter an animal's endocrine and metabolic physiology and the implications this has for various disease states.lipopolysaccharide; fever; hypothalamic-pituitary-adrenal axis Early Life Events Program Physiology Long TermEARLY LIFE EVENTS can have significant long-term effects on an animal's physiology. In humans, an adverse early life experience such as emotional neglect can lead to an increased likelihood of the individual developing anxiety, depression, chronic illness, even drug addiction, in later life (15,32,39,54). Similar findings have been demonstrated in primate models, with parental or social deprivation during the neonatal period producing socially maladjusted, timid, depressed adults that have alterations in neuroimmune and hypothalamic-pituitary-adrenal (HPA) axis function (32,75). In rodents, too, an experience as subtle as a brief period of handling or withdrawal of maternal attention can have pronounced effects on physiology and behavior throughout the life of the animal. For instance, seminal work by Meaney and colleagues has revealed that parenting style, categorized by high-vs. low-intensity nursing and grooming, can program anxiety levels and responsiveness of the HPA axis in the offspring. Thus, rats nursed by dams that impart low-intensity nursing/grooming have exacerbated HPA axis responses to stress (19, 53). They also have alterations in other functions, ranging from their ability to perform cognitive tasks (52) to sexual behavior (17).Early life events other than social and maternal contact can also have an impact upon the animal's physiology long term. For instance, neonatal overfeeding can lead to obesity in adulthood coupled with changes to anxiety and HPA axis responses to stress (84). Also, a painful inflammatory event experienced at critical time points during development alters perception of a painful stimulus in later life (4). Clearly, the early postnatal developmental period is important in programming adult physiology.One of the more common types of physical stimulus encountered during childhood is an...

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Section: Unresolved Issuessupporting

confidence: 60%

Neonatal programming of innate immune function

Spencer

Galic

Pittman

2011

American Journal of Physiology-Endocrinology and Metabolism

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“…Restraint stress experienced in rats in mid-late gestation produces long-term changes in the body weights of offspring of stress-sensitive dams, whereas early gestation restraint stress does not (Mueller and Bale 2006). Similarly, the physical stressor of an immune challenge with LPS experienced at either post-natal days 3, 7 or 14 does not affect long-term growth or adiposity in the pair-housed rat (Spencer et al 2007), whereas a similar challenge presented at day 10 does appear to mildly increase adult body weight (Iwasa et al 2010). Interestingly, it appears that the programming effects of stress may not be confined to the perinatal period.…”

Section: Stress Obesity and Neonatal Programmingmentioning

confidence: 93%

The glucocorticoid contribution to obesity

Spencer¹,

Tilbrook²

2011

Stress

117

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Obesity is fast becoming the scourge of our time. It is one of the biggest causes of death and disease in the industrialized world, and affects as many as 32% of adults and 17% of children in the USA, considered one of the world's fattest nations. It can also cost countries billions of dollars per annum in direct and indirect care, latest estimates putting the USA bill for obesity-related costs at $147 billion in 2008. It is becoming clear that the pathophysiology of obesity is vastly more complicated than the simple equation of energy in minus energy out. A combination of genetics, sex, perinatal environment and life-style factors can influence diet and energy metabolism. In this regard, psychological stress can have significant long-term impact upon the propensity to gain and maintain weight. In this review, we will discuss the ability of psychological stress and ultimately glucocorticoids (GCs) to alter appetite regulation and metabolism. We will specifically focus on (i) GC regulation of appetite and adiposity, (ii) the apparent sexual dimorphism in stress effects on obesity and (iii) the ability of early life stress to programme obesity in the long term.

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“…1), corresponding to the observed decrease in food-intake [15,83,84]. More importantly, administration of NPY or blocking the induced inflammatory response in these animal models prevents the development of anorexia [15,85].…”

Section: Hypothalamic Inflammation: Orexigenic Signallingmentioning

confidence: 92%