Astrogliosis in the brain of obese Zucker rat: A model of metabolic syndrome

Tomassoni, Daniele; Nwankwo, Innocent Ejike; Gabrielli, María Gabriella; Bhatt, Siddhartha; Muhammad, Abdul Bari; Lokhandwala, Mustafa F.; Tayebati, Seyed Khosrow; Amenta, Francesco

doi:10.1016/j.neulet.2013.03.025

Cited by 46 publications

(39 citation statements)

References 27 publications

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“…Subsequently, an inflammatory process in the brain might still be present, even though the correlation between the proinflammatory biomarker and the quantitative parameters was undetected by this study. For example, other researchers have reported a significant increase in the glial fibrillary acidic protein (GFAP)‐immunoreactive astrocytes, a sign of inflammation, in the parietal and frontal cortices and in the hippocampus of obese Zucker rats . Interestingly, our results show an increased T 1 in these GM regions.…”

Section: Discussionmentioning

confidence: 99%

Increasing body mass index in an elderly cohort: Effects on the quantitative MR parameters of the brain

Schall¹,

Iordanishvili²,

Mauler³

et al. 2019

Magnetic Resonance Imaging

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Background Body mass index (BMI) is increasing in a large number of elderly persons. This increase in BMI is known to put one at risk for many "diseases of aging," although less is known about how a change in BMI may affect the brains of the elderly. Purpose To investigate the relationship between BMI and quantitative water content, T1, T2*, and the semi‐quantitative magnetization transfer ratio (MTR) of various structures in elderly brains. Study Type Cross‐sectional. Subjects Forty‐two adults (BMI range: 19.1–33.5 kg/m2, age range: 58–80 years). Field Strength 3T MRI (two multi‐echo gradient echoes, actual flip angle imaging, magnetization prepared rapid gradient echo, fluid attenuated inversion recovery). Assessment The 3D two‐point method was used to derive (semi‐)quantitative parameters in global white (WM) and gray matter (GM) and their regions as defined by the Johns Hopkins University and the Montreal Neurological Institute atlases. Statistical Tests Multivariate linear regression with BMI as principal regressor, corrected for the additional regressors age, gender, and glycated hemoglobin. Spearman correlation between quantitative parameters of the regions showing significant changes and the lipid spectra / C‐reactive protein (CRP). Voxel‐based morphometry and analysis of covariance (ANCOVA) to explore changes in the GM volume. Results T1 increased significantly (P < 0.05) in the frontal, temporal, and parietal cortices, while the bilateral corona radiata, right superior longitudinal fasciculus, as well as the corpus callosum showed significant changes in the WM regions. T2* increased significantly in the global WM and left corona radiata. Changes in MTR and the free water content did not reach significance. No significant correlation between any quantitative parameter and the lipid spectra or CRP could be identified. Data Conclusion These results suggest that an elevated BMI predominantly affects T1 in WM as well as GM structures in the elderly human brain. Level of Evidence: 3 Technical Efficacy: Stage 3 J. Magn. Reson. Imaging 2020;51:514–523.

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Section: Discussionmentioning

confidence: 99%

Increasing body mass index in an elderly cohort: Effects on the quantitative MR parameters of the brain

Schall¹,

Iordanishvili²,

Mauler³

et al. 2019

Magnetic Resonance Imaging

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“…Recently, it has been reported that hyperglycemic rats intoxicated with streptozocin showed an exacerbated reactive astrogliosis. Likewise, Zucker rats, a model of obesity and 2‐type diabetes, showed an increase in GFAP expression in different brain regions, including the Hp and cerebral cortex (Tomassoni et al, ). All this evidence supports our findings and suggests that the consumption of an HCD triggers a reactive astrogliosis in the temporal cortex and hippocampus of the rat.…”

Section: Discussionmentioning

confidence: 99%

“…Studies in hyperglycemic rats indicate that the increment of pro‐inflammatory cytokines such as IL‐1β and TNF‐α in the brain, increase in response to blood glucose levels (Hotamisligil, ; Tomassoni et al, ). In this sense, a condition of over‐nutrition is to induce the activation of astrocytes and promote the release of IL‐1β and TNF‐α, which may exacerbate inflammation (Freeman et al, ).…”

Section: Discussionmentioning

confidence: 99%

A high calorie diet causes memory loss, metabolic syndrome and oxidative stress into hippocampus and temporal cortex of rats

Treviño

Aguilar-Alonso

Hernández

et al. 2015

Synapse

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A high calorie intake can induce the appearance of the metabolic syndrome (MS), which is a serious public health problem because it affects glucose levels and triglycerides in the blood. Recently, it has been suggested that MS can cause complications in the brain, since chronic hyperglycemia and insulin resistance are risk factors for triggering neuronal death by inducing a state of oxidative stress and inflammatory response that affect cognitive processes. This process, however, is not clear. In this study, we evaluated the effect of the consumption of a high-calorie diet (HCD) on both neurodegeneration and spatial memory impairment in rats. Our results demonstrated that HCD (90 day consumption) induces an alteration of the main energy metabolism markers, indicating the development of MS in rats. Moreover, an impairment of spatial memory was observed. Subsequently, the brains of these animals showed activation of an inflammatory response (increase in reactive astrocytes and interleukin1-β as well as tumor necrosis factor-α) and oxidative stress (reactive oxygen species and lipid peroxidation), causing a reduction in the number of neurons in the temporal cortex and hippocampus. Altogether, these results suggest that a HCD promotes the development of MS and contributes to the development of a neurodegenerative process and cognitive failure. In this regard, it is important to understand the relationship between MS and neuronal damage in order to prevent the onset of neurodegenerative disorders.

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“…Moreover, changes in the configuration and/or tortuosity of the extracellular space itself (e.g. as a consequence of astrogliosis, a common finding in numerous diseases, including heart failure, obesity and the metabolic syndrome ), is also likely to affect the diffusion capacity and strength of a volume‐transmitted signal, such as dendritically‐released VP. Thus, it will be important for future studies to determine whether an altered peptidergic dendritic release process and/or structural remodeling of the extracellular space constitute novel, alternative mechanisms contributing to exacerbated neurohumoral activation in disease conditions.…”

Section: Summary and Perspectivesmentioning

confidence: 99%

Neuroendocrine‐Autonomic Integration in the Paraventricular Nucleus: Novel Roles for Dendritically Released Neuropeptides

Stern

2015

J Neuroendocrinology

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Communication between pairs of neurones in the central nervous system typically involves classical ‘hard-wired’ synaptic transmission, characterised by high temporal and spatial precision. Over the last two decades, however, knowledge regarding the repertoire of communication modalities used in the brain has notably expanded to include less conventional forms, characterised by a diffuse and less temporally precise transfer of information. These forms are best suited to mediate communication among entire neuronal populations, now recognised to be a fundamental process in the brain for the generation of complex behaviours. In response to an osmotic stressor, the hypothalamic paraventricular nucleus (PVN) generates a multimodal homeostatic response that involves orchestrated neuroendocrine (i.e. systemic release of vasopressin) and autonomic (i.e. sympathetic outflow to the kidneys) components. The precise mechanisms that underlie interpopulation cross-talk between these two distinct neuronal populations, however, remain largely unknown. The present review summarises and discusses a series of recent studies that have identified the dendritic release of neuropeptides as a novel interpopulation signalling modality in the PVN. A current working model is described in which it is proposed that the activity-dependent dendritic release of vasopressin from neurosecretory neurones in the PVN acts in a diffusible manner to increase the activity of distant presympathetic neurones, resulting in an integrated sympathoexcitatory population response, particularly within the context of a hyperosmotic challenge. The cellular mechanism underlying this novel form of intercellular communication, as well as its physiological and pathophysiological implications, is discussed.

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Astrogliosis in the brain of obese Zucker rat: A model of metabolic syndrome

Cited by 46 publications

References 27 publications

Increasing body mass index in an elderly cohort: Effects on the quantitative MR parameters of the brain

Increasing body mass index in an elderly cohort: Effects on the quantitative MR parameters of the brain

A high calorie diet causes memory loss, metabolic syndrome and oxidative stress into hippocampus and temporal cortex of rats

Neuroendocrine‐Autonomic Integration in the Paraventricular Nucleus: Novel Roles for Dendritically Released Neuropeptides

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