Appetite Regulation of TLR4-Induced Inflammatory Signaling

Li, Yongxiang; Jiang, Qingyan; Wang, Lina

doi:10.3389/fendo.2021.777997

Cited by 20 publications

(8 citation statements)

References 138 publications

(145 reference statements)

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“…The balance of α-MSH with other orexigenic peptides has also been investigated, and the serum α-MSH level might be a good biomarker for hypothalamic obesity, as well as for the detection of patients with PCSK1, POMC, and LEPR deficiencies, which may be another breakthrough for the treatment of obesity [[99], [254]]. Additionally, high-fat diet-induced obesity is associated with low-grade inflammation (including IL-1, IL-6, and TNF-α), which changes the levels of neuropeptides, potentially increasing appetite, and weight [[255]]. By downregulating inflammatory factors and changing cell response mechanisms, α-MSH is also an anti-inflammatory hormone that has the potential to treat obesity [[256]].…”

Section: Discussionmentioning

confidence: 99%

Alpha-Melanocyte-Stimulating Hormone-Mediated Appetite Regulation in the Central Nervous System

Wu¹,

Jing-mei²,

Hua³

et al. 2023

Neuroendocrinology

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Understanding the complex action mechanism of appetite regulation peptides can significantly impact therapeutic options in the treatment of obesity and other metabolic diseases. Hypothalamic α-melanocyte-stimulating hormone (α-MSH) is an anorexigenic peptide, closely related to the occurrence of obesity, playing a central role in food intake and energy expenditure. In the central nervous system (CNS), α-MSH is cleaved from proopiomelanocortin (POMC) and then released into different hypothalamic regions to act on melanocortin 3/4 receptor (MC3/4R)-expressing neurons, lowering food intake and raising energy expenditure via appetite suppression and sympathetic nervous system. Furthermore, it can increase the transmission of some anorexigenic hormones (e.g., dopamine) and interact with other orexigenic factors (e.g., agouti-related protein, neuropeptide Y) to influence food reward rather than merely feeding behavior. Therefore, α-MSH is a critical node of the hypothalamus in transmitting appetite suppression signals and is a key component of the central appetite-regulating circuits. Herein, we describe the role of α-MSH in appetite suppression in terms of specific receptors, effector neurons, sites of action, and the interaction with other appetite-relative peptides, respectively. We focus on the role of α-MSH in obesity. The status of research on α-MSH-related drugs is also discussed. With the intention of illuminating a new approach for targeting α-MSH in the hypothalamus as a strategy to manage obesity, we hope to further understand the direct or indirect mechanisms by which α-MSH exerts its appetite-regulating effects.

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Section: Discussionmentioning

confidence: 99%

Alpha-Melanocyte-Stimulating Hormone-Mediated Appetite Regulation in the Central Nervous System

Wu¹,

Jing-mei²,

Hua³

et al. 2023

Neuroendocrinology

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“…Toll-like receptor 4, a member of the toll-like receptor family, plays an important role in cellular immunity [55]. Studies have shown that TLR4 is abundantly expressed in microglia and is associated with pathogenesis of neuroinflammation [56].…”

Section: Discussionmentioning

confidence: 99%

Aucubin promoted neuron functional recovery by suppressing inflammation and neuronal apoptosis in a spinal cord injury model

Xiao

Zhong

Yang

et al. 2022

Preprint

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Spinal cord injury (SCI) can cause severe motor impairment. Post-SCI treatment has focused primarily on secondary injury, with neuroinflammation and neuronal apoptosis as the primary therapeutic targets. Aucubin (Au), a Chinese herbal medicine, exerts anti-inflammatory and neuroprotective effects. The therapeutic effects of Au in SCI have not been reported. We showed that Au can promote functional recovery after SCI. Recovery may occur through the toll-like receptor 4 (TLR4)/nuclear factor kappa B (NF-κB) pathway to promote M2/M1 polarization in microglia and inhibit mitochondrial dysfunction to reduce neuronal apoptosis. These biochemical changes result in reduced secondary injury and facilitate axon regeneration. Therefore, Au may be a promising post-SCI therapeutic medication.

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“…On the other hand, experimental research shows that melatonin upregulates sirtuins, with a consequent downregulation of transcription for pro-inflammatory proteins and kappa-light-chain-enhancer of activated B cells (NF-κB) by suppressing the activation of toll-like receptor 4 (TLR4) and NLRP3 inflammasome [4,69]. TLR4 activation leads to pro-inflammatory signaling (i.e., NF-κB) and synthesis of proinflammatory cytokines [70,71]. NLRP3 inflammasome is a protein complex that assembles in response to cellular stress, promoting inflammation; its chronic aberrant activation is part of the etiopathogenesis of numerous diseases characterized by lowgrade inflammation [72].…”

Section: Cardiovascular Diseasesmentioning

confidence: 99%

Sirtuins and Melatonin: Linking Chronobiology to Inflammation and Aging

Ungurianu,

Manuela Drăgoi,

Crenguța Nicolae

et al. 2024

Advances in Geriatrics and Gerontology - Challenges of the New Millennium

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In recent years, the intricate interplay between sirtuins and melatonin has emerged as a fascinating area of research, with profound implications on various aspects of human health. This comprehensive chapter delves into the complex relationship between sirtuins and melatonin, as well as their essential roles in the regulation of circadian rhythms, inflammation, and aging. The attention is primarily directed to their impact on a range of critical health focal points, including cardiovascular diseases, central nervous system disorders, metabolic imbalances, musculoskeletal disorders, neoplasms, and the overarching process of aging, detailing all the complex biochemical mechanisms and physiological pathways that validate the intimately tailored functional relationship between the indoleamine hormone synthesized in the pinealocytes and the NAD+-dependent histone deacetylases. These two components interact in complex ways, influencing processes such as cellular homeostasis, oxidative stress, and inflammatory cascade regulation. Age-related reductions in SIRT1 expression, influenced by melatonin levels, can deeply impact cellular functions. By elucidating the complex connections between sirtuins, melatonin, and chronobiological processes, we contribute to a deeper understanding of the fundamental mechanisms that trigger inflammation and aging-related diseases, and in the meantime underscore the promising avenues for future research and clinical interventions aimed at enhancing human health and extending the quality of life.

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Appetite Regulation of TLR4-Induced Inflammatory Signaling

Cited by 20 publications

References 138 publications

Alpha-Melanocyte-Stimulating Hormone-Mediated Appetite Regulation in the Central Nervous System

Alpha-Melanocyte-Stimulating Hormone-Mediated Appetite Regulation in the Central Nervous System

Aucubin promoted neuron functional recovery by suppressing inflammation and neuronal apoptosis in a spinal cord injury model

Sirtuins and Melatonin: Linking Chronobiology to Inflammation and Aging

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