Neonatal overfeeding alters hypothalamic microglial profiles and central responses to immune challenge long-term

Ziko, Ilvana; Luca, Simone N. De; Dinan, T.G.; Barwood, J.M.; Sominsky, Luba; Cai, Guohui; Kenny, Rachel; Stokes, Leanne; Jenkins, Trisha A.; Spencer, Sarah J.

doi:10.1016/j.bbi.2014.06.014

Cited by 66 publications

(103 citation statements)

References 62 publications

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“…Rodent models of postnatal overnutrition and accelerated growth by manipulation of litter size show that a HFD may not be required to trigger inflammation and generate lifelong effects on metabolic dysfunction (58)(59)(60). Postnatal overfeeding (PNOF) in rats is sufficient to induce hypothalamic inflammation and gliosis as early as postnatal day 14 and leads to a persistent increase in hypothalamic NF-κB activity in adulthood (61,62). PNOF can enhance microglial activation in response to HFD in adults, which suggests that the inflammatory set point in the brain is permanently modified with accelerated early life growth (63,64).…”

Section: What Are the Initiators Of Metainflammation?mentioning

confidence: 99%

The initiation of metabolic inflammation in childhood obesity

Singer

Lumeng

2017

Journal of Clinical Investigation

136

115

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Section: What Are the Initiators Of Metainflammation?mentioning

confidence: 99%

The initiation of metabolic inflammation in childhood obesity

Singer

Lumeng

2017

Journal of Clinical Investigation

136

115

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“…Likewise, rodents born to mothers ingesting a HFD during gestation have increased microglial activation in the hippocampus at birth, as well as increased hippocampal microglial density in adulthood . Overnutrition during lactation results in microglial activation in the hypothalamus and other brain areas when these animals reach adulthood, in addition to having increased expression of inflammatory cytokines in the hypothalamus (Tapia-González et al 2011, Tu et al 2011, Ziko et al 2014.…”

Section: Microglia In Metabolic Controlmentioning

confidence: 99%

Glial cells and energy balance

Argente-Arizón

Guerra-Cantera

Garcia-Segura

et al. 2017

Journal of Molecular Endocrinology

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The search for new strategies and drugs to abate the current obesity epidemic has led to the intensification of research aimed at understanding the neuroendocrine control of appetite and energy expenditure. This intensified investigation of metabolic control has also included the study of how glial cells participate in this process. Glia, the most abundant cell type in the central nervous system, perform a wide spectrum of functions and are vital for the correct functioning of neurons and neuronal circuits. Current evidence indicates that hypothalamic glia, in particular astrocytes, tanycytes and microglia, are involved in both physiological and pathophysiological mechanisms of appetite and metabolic control, at least in part by regulating the signals reaching metabolic neuronal circuits. Glia transport nutrients, hormones and neurotransmitters; they secrete growth factors, hormones, cytokines and gliotransmitters and are a source of neuroprogenitor cells. These functions are regulated, as glia also respond to numerous hormones and nutrients, with the lack of specific hormonal signaling in hypothalamic astrocytes disrupting metabolic homeostasis. Here, we review some of the more recent advances in the role of glial cells in metabolic control, with a special emphasis on the differences between glial cell responses in males and females.

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“…Both obese rats and patients with increased risk for stroke exhibited increased microglial cell activation. Finally, evidence of microgliosis in feeding-regulatory brain regions (e.g., paraventricular nucleus and arcuate nucleus) has been reported in rats overfed in the neonatal period (Ziko et al, 2014) and in adult mice given a high-fat diet (Gao et al, 2014). In adult rats that were overfed in the neonatal period, microglia were hypersensitive to peripheral immune stimulation with LPS (Ziko et al, 2014).…”

Section: Effects Of Diet On Microglia: Feeding the Beastmentioning

confidence: 99%

“…Finally, evidence of microgliosis in feeding-regulatory brain regions (e.g., paraventricular nucleus and arcuate nucleus) has been reported in rats overfed in the neonatal period (Ziko et al, 2014) and in adult mice given a high-fat diet (Gao et al, 2014). In adult rats that were overfed in the neonatal period, microglia were hypersensitive to peripheral immune stimulation with LPS (Ziko et al, 2014). The potential for overweight and obesity to be associated with altered development of microglia adds another layer of concern regarding maternal obesity during pregnancy and childhood obesity.…”

Section: Effects Of Diet On Microglia: Feeding the Beastmentioning

confidence: 99%

Feeding the beast: Can microglia in the senescent brain be regulated by diet?

Johnson

2015

Brain, Behavior, and Immunity

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Microglial cells, resident macrophages in the central nervous system (CNS), are relatively quiescent but can respond to signals from the peripheral immune system and induce neuroinflammation. In aging, microglia tend to transition to the M1 pro-inflammatory state and become hypersensitive to messages emerging from immune-to-brain signaling pathways. Thus, whereas in younger individuals where microglia respond to signals from the peripheral immune system and induce a well-controlled neuroinflammatory response that is adaptive (e.g., when well controlled, fever and sickness behavior facilitate recovery from infection), in older individuals with an infection, microglia overreact and produce excessive levels of inflammatory cytokines causing behavioral pathology including cognitive dysfunction. Importantly, recent studies indicate a number of naturally occurring bioactive compounds present in certain foods have anti-inflammatory properties and are capable of mitigating brain microglial cells. These include, e.g., flavonoid and non-flavonoid compounds in fruits and vegetables, and n-3 polyunsaturated fatty acids (PUFA) in oily fish. Thus, dietary bioactives have potential to restore the population of microglial cells in the senescent brain to a more quiescent state. The pragmatic concept to constrain microglia through dietary intervention is significant because neuroinflammation and cognitive deficits are co-morbid factors in many chronic inflammatory diseases. Controlling microglial cell reactivity has important consequences for preserving adult neurogenesis, neuronal structure and function, and cognition.

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Neonatal overfeeding alters hypothalamic microglial profiles and central responses to immune challenge long-term

Cited by 66 publications

References 62 publications

The initiation of metabolic inflammation in childhood obesity

The initiation of metabolic inflammation in childhood obesity

Glial cells and energy balance

Feeding the beast: Can microglia in the senescent brain be regulated by diet?

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