Leptin as a Neuroprotector and a Central Nervous System Functional Stability Factor

Teryaeva, N. B.

doi:10.1007/s11055-015-0120-x

Cited by 5 publications

(2 citation statements)

References 85 publications

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“…Leptin receptors are widespread in the brain (e.g., throughout the cortex and the hippocampus) and their activation is implicated in memory processes (15). Leptin has also been shown to exert neuroprotective functions by inhibiting apoptosis and improving cell survival through regulation of apoptotic enzymes and activation of neurotrophic factors such as the brain-derived neurotrophic factor (BDNF) (16). However, it is still unknown whether bariatric surgery can impact on one of the fundamental properties of the brain: the ability to modify its connection or rewire in response to experience, a phenomenon known as neural plasticity (17).…”

Section: Introductionmentioning

confidence: 99%

Bariatric surgery restores visual cortical plasticity in nondiabetic subjects with obesity

et al. 2021

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HAL is a multi-disciplinary open access archive for the deposit and dissemination of scientific research documents, whether they are published or not. The documents may come from teaching and research institutions in France or abroad, or from public or private research centers. L'archive ouverte pluridisciplinaire HAL, est destinée au dépôt et à la diffusion de documents scientifiques de niveau recherche, publiés ou non, émanant des établissements d'enseignement et de recherche français ou étrangers, des laboratoires publics ou privés.

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Section: Introductionmentioning

confidence: 99%

Bariatric surgery restores visual cortical plasticity in nondiabetic subjects with obesity

et al. 2021

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“…At the molecular level, leptin stimulates neurogenesis, axon growth, synaptogenesis, and dendritic morphology, both pre- and postnatal life [ 48 ]. Leptin also has neuroprotective actions, by inhibiting apoptotic cell death and improving cell survival through the regulation of apoptotic enzymes (by inhibiting the expression of Bcl-xL, caspases and TRAIL ligand, and activating the synthesis of neurotrophic factors such as BDNF), protecting against glutamatergic cytotoxicity, protecting against oxidative stress via expression of the membrane antioxidant MnSOD and stabilization of mitochondrial membranes, and promoting the proliferation of hippocampal progenitor cells [ 49 – 52 ]. Leptin regulates the synapse morphology of hippocampal neurons, enhancing the motility and density of dendritic filopodia [ 53 ].…”

Section: Physiology Of Leptin In the Brainmentioning

confidence: 99%

The Effects of Leptin Replacement on Neural Plasticity

Paz-Filho

2016

Neural Plasticity

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Leptin, an adipokine synthesized and secreted mainly by the adipose tissue, has multiple effects on the regulation of food intake, energy expenditure, and metabolism. Its recently-approved analogue, metreleptin, has been evaluated in clinical trials for the treatment of patients with leptin deficiency due to mutations in the leptin gene, lipodystrophy syndromes, and hypothalamic amenorrhea. In such patients, leptin replacement therapy has led to changes in brain structure and function in intra- and extrahypothalamic areas, including the hippocampus. Furthermore, in one of those patients, improvements in neurocognitive development have been observed. In addition to this evidence linking leptin to neural plasticity and function, observational studies evaluating leptin-sufficient humans have also demonstrated direct correlation between blood leptin levels and brain volume and inverse associations between circulating leptin and risk for the development of dementia. This review summarizes the evidence in the literature on the role of leptin in neural plasticity (in leptin-deficient and in leptin-sufficient individuals) and its effects on synaptic activity, glutamate receptor trafficking, neuronal morphology, neuronal development and survival, and microglial function.

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Leptin reduces LPS‐induced A1 reactive astrocyte activation and inflammation via inhibiting p38‐MAPK signaling pathway

Sun,

Song,

et al. 2024

Glia

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Neurotoxic A1 reactive astrocytes are induced by inflammatory stimuli. Leptin has been confirmed to have neuroprotective properties. However, its effect on the activation of A1 astrocytes in infectious inflammation is unclear. In the current study, astrocytes cultured from postnatal day 1 Sprague–Dawley rats were stimulated with lipopolysaccharide (LPS) to induce an acute in vitro inflammatory response. Leptin was applied 6 h later to observe its protective effects. The viability of the astrocytes was assessed. A1 astrocyte activation was determined by analyzing the gene expression of C3, H2‐D1, H2‐T23, and Serping 1 and secretion of pro‐inflammatory cytokines IL‐6 and TNF‐α. The levels of phospho‐p38 (pp38) and nuclear factor‐κB (NF‐κB) phosphor‐p65 (pp65) were measured to explore the possible signaling pathways. Additionally, an LPS‐induced inflammatory animal model was established to investigate the in vivo effects of leptin on A1 astrocytic activation. Results showed that in the in vitro culture system, LPS stimulation caused elevated expression of A1 astrocyte‐specific genes and the secretion of pro‐inflammatory cytokines, indicating the activation of A1 astrocytes. Leptin treatment significantly reversed the LPS induced upregulation in a dose‐dependent manner. Similarly, LPS upregulated pp38, NF‐κB pp65 protein and inflammatory cytokines were successfully reduced by leptin. In the LPS‐induced animal model, the amelioratory effect of leptin on A1 astrocyte activation and inflammation was further confirmed, showed by the reduced sickness behaviors, A1 astrocyte genesis and inflammatory cytokines in vivo. Our results demonstrate that leptin efficiently inhibits LPS‐induced neurotoxic activation of A1 astrocytes and neuroinflammation by suppressing p38‐MAPK signaling pathway.

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Leptin as a Neuroprotector and a Central Nervous System Functional Stability Factor

Cited by 5 publications

References 85 publications

Bariatric surgery restores visual cortical plasticity in nondiabetic subjects with obesity

Bariatric surgery restores visual cortical plasticity in nondiabetic subjects with obesity

The Effects of Leptin Replacement on Neural Plasticity

Leptin reduces LPS‐induced A1 reactive astrocyte activation and inflammation via inhibiting p38‐MAPK signaling pathway

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