Betaine recovers hypothalamic neural injury by inhibiting astrogliosis and inflammation in fructose‐fed rats

Li, Jianmei; Ge, Chenxu; Xu, Minxuan; Wang, Wei; Rao, Yu; Fan, Chenyu; Kong, Ling-Dong

doi:10.1002/mnfr.201400307

Cited by 78 publications

(39 citation statements)

References 63 publications

(80 reference statements)

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“…Data on stress-related perturbations in the hypothalamic inflammatory status are rather conflicting, as the expression of proinflammatory cytokines has been reported to be elevated [27] or unchanged [28] in male rats after chronic stress. As for nutrients, a high-fat diet has been predominantly described to induce obesity-related hypothalamic inflammation [50], though fructose overconsumption also has a potential to activate the NFκB signaling pathway [2, 26]. However, most in vivo studies describing fructose-related neuroinflammation, also reported increased fat mass and a disturbed lipid status in the form of elevated plasma triglycerides and free fatty acids.…”

Section: Discussionmentioning

confidence: 99%

“…It is postulated that the proinflammatory cytokines IL-1β [24] and TNFα [25] can induce inhibitory phosphorylation of insulin receptor substrate 1 (IRS1) on the Ser 307 residue (pIRS1-Ser 307 ), inhibiting kinase activity of the insulin receptor. High fructose consumption has a potential to activate the nuclear factor-κB (NFκB) signaling pathway in the hypothalamus elevating proinflammatory cytokines [2, 26]. On the other hand, data on stress-related perturbations in the hypothalamic inflammatory status are rather conflicting.…”

Section: Introductionmentioning

confidence: 99%

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Chronic Stress Combined with a Fructose Diet Reduces Hypothalamic Insulin Signaling and Antioxidative Defense in Female Rats

et al. 2018

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Background: Increased fructose consumption and chronic exposure to stress have been associated with the development of obesity and insulin resistance. In the hypothalamus, a crossroad of stress responses and energy balance, insulin and glucocorticoids regulate the expression of orexigenic neuropeptides, neuropeptide Y (NPY) and agouti-related protein (AgRP), and anorexigenic neuropeptides, proopiomelanocortin (POMC) and cocaine- and amphetamine-regulated transcript (CART). Objectives: We investigated whether chronic stress and fructose diet disrupt these hormonal signaling pathways and appetite control in the hypothalamus, contributing to the development of insulin resistance and obesity. Potential roles of hypothalamic inflammation and oxidative stress in the development of insulin resistance were also analyzed. Methods: Insulin, glucocorticoid, and leptin signaling, expression of orexigenic and anorexigenic neuropeptides, and antioxidative and inflammatory statuses in the whole hypothalamus of fructose-fed female rats exposed to unpredictable stress for 9 weeks were analyzed using quantitative PCR and Western blotting. Results: Chronic stress combined with a fructose-enriched diet reduced protein content and stimulatory phosphorylation of Akt kinase, and elevated 11β-hydroxysteroid dehydrogenase 1 and glucocorticoid receptor expression, while alterations in appetite regulation (NPY, AgRP, POMC, CART, leptin receptor, and SOCS3 expression) were not observed. The expression of antioxidative defense enzymes (mitochondrial manganese superoxide dismutase 2, glutathione reductase, and catalase) and proinflammatory cytokines (IL-1β, IL-6, and TNFα) was reduced. Conclusions: Our results underline the combination of long-term stress exposure and fructose overconsumption as more detrimental for hypothalamic function than for either of the factors separately, as it enhanced glucocorticoid and impaired insulin signaling, antioxidative defense, and inflammatory responses of this homeostasis- regulating center.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Chronic Stress Combined with a Fructose Diet Reduces Hypothalamic Insulin Signaling and Antioxidative Defense in Female Rats

et al. 2018

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“…Fructose induces hypothalamic astrogliosis both in vivo and in vitro (Li et al 2014). On the contrary, although high sucrose intake induces hypothalamic inflammation, this was not found to be associated with astrogliosis (FuenteMartin et al 2013).…”

Section: R62mentioning

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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“…All the histological protocols were in accordance with the standard procedures demonstrated previously. 34 . The sequences used in this study are shown in Table 1.…”

Section: Histological Analysismentioning

confidence: 99%

Gold-quercetin nanoparticles prevent metabolic endotoxemia-induced kidney injury by regulating TLR4/NF-kB signaling and Nrf2 pathway in high fat diet fed mice

Xu¹,

Wang²,

Yang³

2017

IJN

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Betaine recovers hypothalamic neural injury by inhibiting astrogliosis and inflammation in fructose‐fed rats

Cited by 78 publications

References 63 publications

Chronic Stress Combined with a Fructose Diet Reduces Hypothalamic Insulin Signaling and Antioxidative Defense in Female Rats

Chronic Stress Combined with a Fructose Diet Reduces Hypothalamic Insulin Signaling and Antioxidative Defense in Female Rats

Glial cells and energy balance

Gold-quercetin nanoparticles prevent metabolic endotoxemia-induced kidney injury by regulating TLR4/NF-kB signaling and Nrf2 pathway in high fat diet fed mice

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