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1
Sikiric, Predrag, Slaven Gojkovic, Ivan Krezic, Ivan Maria Smoday, Luka Kalogjera, Helena Zizek, Katarina Oroz, et al. "Stable Gastric Pentadecapeptide BPC 157 May Recover Brain–Gut Axis and Gut–Brain Axis Function." Pharmaceuticals 16, no. 5 (April 30, 2023): 676. http://dx.doi.org/10.3390/ph16050676.
Повний текст джерелаАнотація:
Conceptually, a wide beneficial effect, both peripherally and centrally, might have been essential for the harmony of brain–gut and gut–brain axes’ function. Seen from the original viewpoint of the gut peptides’ significance and brain relation, the favorable stable gastric pentadecapeptide BPC 157 evidence in the brain–gut and gut–brain axes’ function might have been presented as a particular interconnected network. These were the behavioral findings (interaction with main systems, anxiolytic, anticonvulsive, antidepressant effect, counteracted catalepsy, and positive and negative schizophrenia symptoms models). Muscle healing and function recovery appeared as the therapeutic effects of BPC 157 on the various muscle disabilities of a multitude of causes, both peripheral and central. Heart failure was counteracted (including arrhythmias and thrombosis), and smooth muscle function recovered. These existed as a multimodal muscle axis impact on muscle function and healing as a function of the brain–gut axis and gut–brain axis as whole. Finally, encephalopathies, acting simultaneously in both the periphery and central nervous system, BPC 157 counteracted stomach and liver lesions and various encephalopathies in NSAIDs and insulin rats. BPC 157 therapy by rapidly activated collateral pathways counteracted the vascular and multiorgan failure concomitant to major vessel occlusion and, similar to noxious procedures, reversed initiated multicausal noxious circuit of the occlusion/occlusion-like syndrome. Severe intracranial (superior sagittal sinus) hypertension, portal and caval hypertensions, and aortal hypotension were attenuated/eliminated. Counteracted were the severe lesions in the brain, lungs, liver, kidney, and gastrointestinal tract. In particular, progressing thrombosis, both peripherally and centrally, and heart arrhythmias and infarction that would consistently occur were fully counteracted and/or almost annihilated. To conclude, we suggest further BPC 157 therapy applications.
2
Sanjay Kalra, Saurabh Arora, and Nitin Kapoor. "The Mood-Muscle Meta Bridge (Brain Muscle Axis)." Journal of the Pakistan Medical Association 74, no. 4 (February 11, 2024): 589–90. http://dx.doi.org/10.47391/jpma.24-16.
Повний текст джерелаАнотація:
Psychological well-being is essential for the maintenance of good metabolic health. Modern management of most chronic metabolic disorders rightly focusses on improving the health-related quality of life of persons living with disease. In this brief communication we describe the bidirectional association between muscle function and mood (psychological health), explore the various pathways that link these aspects of health, and underscore their clinical implications. This paper emphasizes the importance of maintaining good mental health through exercise and vice a versa.
Keywords: Muscle function, muscle strength, sarcopenia, dysthymia, depression, physical activity.
3
Burtscher, Johannes, Grégoire P. Millet, Nicolas Place, Bengt Kayser, and Nadège Zanou. "The Muscle-Brain Axis and Neurodegenerative Diseases: The Key Role of Mitochondria in Exercise-Induced Neuroprotection." International Journal of Molecular Sciences 22, no. 12 (June 17, 2021): 6479. http://dx.doi.org/10.3390/ijms22126479.
Повний текст джерелаАнотація:
Regular exercise is associated with pronounced health benefits. The molecular processes involved in physiological adaptations to exercise are best understood in skeletal muscle. Enhanced mitochondrial functions in muscle are central to exercise-induced adaptations. However, regular exercise also benefits the brain and is a major protective factor against neurodegenerative diseases, such as the most common age-related form of dementia, Alzheimer’s disease, or the most common neurodegenerative motor disorder, Parkinson’s disease. While there is evidence that exercise induces signalling from skeletal muscle to the brain, the mechanistic understanding of the crosstalk along the muscle–brain axis is incompletely understood. Mitochondria in both organs, however, seem to be central players. Here, we provide an overview on the central role of mitochondria in exercise-induced communication routes from muscle to the brain. These routes include circulating factors, such as myokines, the release of which often depends on mitochondria, and possibly direct mitochondrial transfer. On this basis, we examine the reported effects of different modes of exercise on mitochondrial features and highlight their expected benefits with regard to neurodegeneration prevention or mitigation. In addition, knowledge gaps in our current understanding related to the muscle–brain axis in neurodegenerative diseases are outlined.
4
Arosio, Beatrice, Riccardo Calvani, Evelyn Ferri, Hélio José Coelho-Junior, Angelica Carandina, Federica Campanelli, Veronica Ghiglieri, Emanuele Marzetti, and Anna Picca. "Sarcopenia and Cognitive Decline in Older Adults: Targeting the Muscle–Brain Axis." Nutrients 15, no. 8 (April 12, 2023): 1853. http://dx.doi.org/10.3390/nu15081853.
Повний текст джерелаАнотація:
Declines in physical performance and cognition are commonly observed in older adults. The geroscience paradigm posits that a set of processes and pathways shared among age-associated conditions may also serve as a molecular explanation for the complex pathophysiology of physical frailty, sarcopenia, and cognitive decline. Mitochondrial dysfunction, inflammation, metabolic alterations, declines in cellular stemness, and altered intracellular signaling have been observed in muscle aging. Neurological factors have also been included among the determinants of sarcopenia. Neuromuscular junctions (NMJs) are synapses bridging nervous and skeletal muscle systems with a relevant role in age-related musculoskeletal derangement. Patterns of circulating metabolic and neurotrophic factors have been associated with physical frailty and sarcopenia. These factors are mostly related to disarrangements in protein-to-energy conversion as well as reduced calorie and protein intake to sustain muscle mass. A link between sarcopenia and cognitive decline in older adults has also been described with a possible role for muscle-derived mediators (i.e., myokines) in mediating muscle–brain crosstalk. Herein, we discuss the main molecular mechanisms and factors involved in the muscle–brain axis and their possible implication in cognitive decline in older adults. An overview of current behavioral strategies that allegedly act on the muscle–brain axis is also provided.
5
Przewłócka, Katarzyna, Daria Korewo-Labelle, Paweł Berezka, Mateusz Jakub Karnia, and Jan Jacek Kaczor. "Current Aspects of Selected Factors to Modulate Brain Health and Sports Performance in Athletes." Nutrients 16, no. 12 (June 12, 2024): 1842. http://dx.doi.org/10.3390/nu16121842.
Повний текст джерелаАнотація:
This review offers a comprehensive evaluation of current aspects related to nutritional strategies, brain modulation, and muscle recovery, focusing on their applications and the underlying mechanisms of physiological adaptation for promoting a healthy brain, not only in athletes but also for recreationally active and inactive individuals. We propose that applying the rule, among others, of good sleep, regular exercise, and a properly balanced diet, defined as “SPARKS”, will have a beneficial effect on the function and regeneration processes of the gut–brain–muscle axis. However, adopting the formula, among others, of poor sleep, stress, overtraining, and dysbiosis, defined as “SMOULDER”, will have a detrimental impact on the function of this axis and consequently on human health as well as on athletes. Understanding these dynamics is crucial for optimizing brain health and cognitive function. This review highlights the significance of these factors for overall well-being, suggesting that adopting the “SPARKS” approach may benefit not only athletes but also older adults and individuals with health conditions.
6
Saponaro, Federica, Andrea Bertolini, Riccardo Baragatti, Leonardo Galfo, Grazia Chiellini, Alessandro Saba, and Giuseppina D’Urso. "Myokines and Microbiota: New Perspectives in the Endocrine Muscle–Gut Axis." Nutrients 16, no. 23 (November 25, 2024): 4032. http://dx.doi.org/10.3390/nu16234032.
Повний текст джерелаАнотація:
This review explores the dual role of skeletal muscle as both a mechanical and endocrine organ, highlighting its contributions to overall health and its adaptability to various inputs such as nutrition, hormones, exercise, and injuries. In addition to its role in metabolism and energy conversion, skeletal muscle secretes signalling molecules called myokines (at rest) and exerkines (during/after physical exercise), which communicate with other organs like the brain, the cardiovascular system, and the immune system. Key molecules such as interleukins, irisin, and myostatin are discussed for their roles in mediating muscle health and inter-organ communication. This work also focuses on the muscle–gut axis, emphasising the bidirectional interaction between skeletal muscle and the gut microbiota, a complex ecosystem influencing immune defence, digestion, and metabolism. Muscle activity, particularly exercise, alters the gut microbial composition, promoting beneficial species, while gut-derived metabolites like short-chain fatty acids (SCFAs) impact muscle metabolism, mitochondrial function, and insulin sensitivity. Dysbiosis, or an imbalanced microbiota, can lead to muscle atrophy, inflammation, and metabolic dysfunction. This evidence highlights emerging research into myokines and exerkines as potential therapeutic targets for managing conditions like muscle decline, ageing, and metabolic diseases through muscle–gut interactions.
7
Liu, Tingting, Haojie Wu, Jingwen Li, Chaoyang Zhu, and Jianshe Wei. "Unraveling the Bone–Brain Axis: A New Frontier in Parkinson’s Disease Research." International Journal of Molecular Sciences 25, no. 23 (November 29, 2024): 12842. http://dx.doi.org/10.3390/ijms252312842.
Повний текст джерелаАнотація:
Parkinson’s disease (PD), as a widespread neurodegenerative disorder, significantly impacts patients’ quality of life. Its primary symptoms include motor disturbances, tremor, muscle stiffness, and balance disorders. In recent years, with the advancement of research, the concept of the bone–brain axis has gradually become a focal point in the field of PD research. The bone–brain axis refers to the interactions and connections between the skeletal system and the central nervous system (CNS), playing a crucial role in the pathogenesis and pathological processes of PD. The purpose of this review is to comprehensively and deeply explore the bone–brain axis in PD, covering various aspects such as the complex relationship between bone metabolism and PD, the key roles of neurotransmitters and hormones in the bone–brain axis, the role of inflammation and immunity, microRNA (miRNA) functional regulation, and potential therapeutic strategies. Through a comprehensive analysis and in-depth discussion of numerous research findings, this review aims to provide a solid theoretical foundation for a deeper understanding of the pathogenesis of PD and to offer strong support for the development of new treatment methods.
8
Cutuli, Debora, Davide Decandia, Giacomo Giacovazzo, and Roberto Coccurello. "Physical Exercise as Disease-Modifying Alternative against Alzheimer’s Disease: A Gut–Muscle–Brain Partnership." International Journal of Molecular Sciences 24, no. 19 (September 28, 2023): 14686. http://dx.doi.org/10.3390/ijms241914686.
Повний текст джерелаАнотація:
Alzheimer’s disease (AD) is a common cause of dementia characterized by neurodegenerative dysregulations, cognitive impairments, and neuropsychiatric symptoms. Physical exercise (PE) has emerged as a powerful tool for reducing chronic inflammation, improving overall health, and preventing cognitive decline. The connection between the immune system, gut microbiota (GM), and neuroinflammation highlights the role of the gut–brain axis in maintaining brain health and preventing neurodegenerative diseases. Neglected so far, PE has beneficial effects on microbial composition and diversity, thus providing the potential to alleviate neurological symptoms. There is bidirectional communication between the gut and muscle, with GM diversity modulation and short-chain fatty acid (SCFA) production affecting muscle metabolism and preservation, and muscle activity/exercise in turn inducing significant changes in GM composition, functionality, diversity, and SCFA production. This gut–muscle and muscle–gut interplay can then modulate cognition. For instance, irisin, an exercise-induced myokine, promotes neuroplasticity and cognitive function through BDNF signaling. Irisin and muscle-generated BDNF may mediate the positive effects of physical activity against some aspects of AD pathophysiology through the interaction of exercise with the gut microbial ecosystem, neural plasticity, anti-inflammatory signaling pathways, and neurogenesis. Understanding gut–muscle–brain interconnections hold promise for developing strategies to promote brain health, fight age-associated cognitive decline, and improve muscle health and longevity.
9
Manti, Sara, Federica Xerra, Giulia Spoto, Ambra Butera, Eloisa Gitto, Gabriella Di Rosa, and Antonio Gennaro Nicotera. "Neurotrophins: Expression of Brain–Lung Axis Development." International Journal of Molecular Sciences 24, no. 8 (April 11, 2023): 7089. http://dx.doi.org/10.3390/ijms24087089.
Повний текст джерелаАнотація:
Neurotrophins (NTs) are a group of soluble growth factors with analogous structures and functions, identified initially as critical mediators of neuronal survival during development. Recently, the relevance of NTs has been confirmed by emerging clinical data showing that impaired NTs levels and functions are involved in the onset of neurological and pulmonary diseases. The alteration in NTs expression at the central and peripheral nervous system has been linked to neurodevelopmental disorders with an early onset and severe clinical manifestations, often named "synaptopathies" because of structural and functional synaptic plasticity abnormalities. NTs appear to be also involved in the physiology and pathophysiology of several airway diseases, neonatal lung diseases, allergic and inflammatory diseases, lung fibrosis, and even lung cancer. Moreover, they have also been detected in other peripheral tissues, including immune cells, epithelium, smooth muscle, fibroblasts, and vascular endothelium. This review aims to provide a comprehensive description of the NTs as important physiological and pathophysiological players in brain and lung development.
10
Igual Gil, Carla, Bethany M. Coull, Wenke Jonas, Rachel N. Lippert, Susanne Klaus, and Mario Ost. "Mitochondrial stress-induced GFRAL signaling controls diurnal food intake and anxiety-like behavior." Life Science Alliance 5, no. 11 (September 6, 2022): e202201495. http://dx.doi.org/10.26508/lsa.202201495.
Повний текст джерелаАнотація:
Growth differentiation factor 15 (GDF15) is a mitochondrial stress-induced cytokine that modulates energy balance in an endocrine manner. However, the importance of its brainstem-restricted receptor GDNF family receptor alpha-like (GFRAL) to mediate endocrine GDF15 signaling to the brain upon mitochondrial dysfunction is still unknown. Using a mouse model with muscle-specific mitochondrial dysfunction, we here show that GFRAL is required for activation of systemic energy metabolism via daytime-restricted anorexia but not responsible for muscle wasting. We further find that muscle mitochondrial stress response involves a GFRAL-dependent induction of hypothalamic corticotropin-releasing hormone, without elevated corticosterone levels. Finally, we identify that GFRAL signaling governs an anxiety-like behavior in male mice with muscle mitochondrial dysfunction, with females showing a less robust GFRAL-dependent anxiety-like phenotype. Together, we here provide novel evidence of a mitochondrial stress-induced muscle–brain crosstalk via the GDF15-GFRAL axis to modulate food intake and anxiogenic behavior.
11
Zhong, Ran, Renling Miao, Jiao Meng, Rimao Wu, Yong Zhang, and Dahai Zhu. "Acetoacetate promotes muscle cell proliferation via the miR-133b/SRF axis through the Mek-Erk-MEF2 pathway." Acta Biochimica et Biophysica Sinica 53, no. 8 (June 29, 2021): 1009–16. http://dx.doi.org/10.1093/abbs/gmab079.
Повний текст джерелаАнотація:
Abstract Acetoacetate (AA) is an important ketone body that is used as an oxidative fuel to supply energy for the cellular activities of various tissues, including the brain and skeletal muscle. We recently revealed a new signaling role for AA by showing that it promotes muscle cell proliferation in vitro, enhances muscle regeneration in vivo, and ameliorates the dystrophic muscle phenotype of Mdx mice. In this study, we provide new molecular insight into this function of AA. We show that AA promotes C2C12 cell proliferation by transcriptionally upregulating the expression of muscle-specific miR-133b, which in turn stimulates muscle cell proliferation by targeting serum response factor. Furthermore, we show that the AA-induced upregulation of miR-133b is transcriptionally mediated by MEF2 via the Mek-Erk1/2 signaling pathway. Mechanistically, our findings provide further convincing evidence that AA acts as signaling metabolite to actively regulate various cellular activities in mammalian cells.
12
Iriondo-DeHond, Amaia, José Antonio Uranga, Maria Dolores del Castillo, and Raquel Abalo. "Effects of Coffee and Its Components on the Gastrointestinal Tract and the Brain–Gut Axis." Nutrients 13, no. 1 (December 29, 2020): 88. http://dx.doi.org/10.3390/nu13010088.
Повний текст джерелаАнотація:
Coffee is one of the most popular beverages consumed worldwide. Roasted coffee is a complex mixture of thousands of bioactive compounds, and some of them have numerous potential health-promoting properties that have been extensively studied in the cardiovascular and central nervous systems, with relatively much less attention given to other body systems, such as the gastrointestinal tract and its particular connection with the brain, known as the brain–gut axis. This narrative review provides an overview of the effect of coffee brew; its by-products; and its components on the gastrointestinal mucosa (mainly involved in permeability, secretion, and proliferation), the neural and non-neural components of the gut wall responsible for its motor function, and the brain–gut axis. Despite in vitro, in vivo, and epidemiological studies having shown that coffee may exert multiple effects on the digestive tract, including antioxidant, anti-inflammatory, and antiproliferative effects on the mucosa, and pro-motility effects on the external muscle layers, much is still surprisingly unknown. Further studies are needed to understand the mechanisms of action of certain health-promoting properties of coffee on the gastrointestinal tract and to transfer this knowledge to the industry to develop functional foods to improve the gastrointestinal and brain–gut axis health.
13
Caturano, Alfredo, Raffaele Galiero, Erica Vetrano, Celestino Sardu, Luca Rinaldi, Vincenzo Russo, Marcellino Monda, Raffaele Marfella, and Ferdinando Carlo Sasso. "Insulin–Heart Axis: Bridging Physiology to Insulin Resistance." International Journal of Molecular Sciences 25, no. 15 (July 31, 2024): 8369. http://dx.doi.org/10.3390/ijms25158369.
Повний текст джерелаАнотація:
Insulin signaling is vital for regulating cellular metabolism, growth, and survival pathways, particularly in tissues such as adipose, skeletal muscle, liver, and brain. Its role in the heart, however, is less well-explored. The heart, requiring significant ATP to fuel its contractile machinery, relies on insulin signaling to manage myocardial substrate supply and directly affect cardiac muscle metabolism. This review investigates the insulin–heart axis, focusing on insulin’s multifaceted influence on cardiac function, from metabolic regulation to the development of physiological cardiac hypertrophy. A central theme of this review is the pathophysiology of insulin resistance and its profound implications for cardiac health. We discuss the intricate molecular mechanisms by which insulin signaling modulates glucose and fatty acid metabolism in cardiomyocytes, emphasizing its pivotal role in maintaining cardiac energy homeostasis. Insulin resistance disrupts these processes, leading to significant cardiac metabolic disturbances, autonomic dysfunction, subcellular signaling abnormalities, and activation of the renin–angiotensin–aldosterone system. These factors collectively contribute to the progression of diabetic cardiomyopathy and other cardiovascular diseases. Insulin resistance is linked to hypertrophy, fibrosis, diastolic dysfunction, and systolic heart failure, exacerbating the risk of coronary artery disease and heart failure. Understanding the insulin–heart axis is crucial for developing therapeutic strategies to mitigate the cardiovascular complications associated with insulin resistance and diabetes.
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Zhang, Li, Ruhao Zhang, and Lu Li. "Effects of Probiotic Supplementation on Exercise and the Underlying Mechanisms." Foods 12, no. 9 (April 25, 2023): 1787. http://dx.doi.org/10.3390/foods12091787.
Повний текст джерелаАнотація:
Long-term, high-intensity exercise can trigger stress response pathways in multiple organs, including the heart and lungs, gastrointestinal tract, skeletal muscle, and neuroendocrine system, thus affecting their material and energy metabolism, immunity, oxidative stress, and endocrine function, and reducing exercise function. As a natural, safe, and convenient nutritional supplement, probiotics have been a hot research topic in the field of biomedical health in recent years. Numerous studies have shown that probiotic supplementation improves the health of the body through the gut–brain axis and the gut–muscle axis, and probiotic supplementation may also improve the stress response and motor function of the body. This paper reviews the progress of research on the role of probiotic supplementation in material and energy metabolism, intestinal barrier function, immunity, oxidative stress, neuroendocrine function, and the health status of the body, as well as the underlying mechanisms.
15
Daily, James W., and Sunmin Park. "Sarcopenia Is a Cause and Consequence of Metabolic Dysregulation in Aging Humans: Effects of Gut Dysbiosis, Glucose Dysregulation, Diet and Lifestyle." Cells 11, no. 3 (January 20, 2022): 338. http://dx.doi.org/10.3390/cells11030338.
Повний текст джерелаАнотація:
Skeletal muscle mass plays a critical role in a healthy lifespan by helping to regulate glucose homeostasis. As seen in sarcopenia, decreased skeletal muscle mass impairs glucose homeostasis, but it may also be caused by glucose dysregulation. Gut microbiota modulates lipopolysaccharide (LPS) production, short-chain fatty acids (SCFA), and various metabolites that affect the host metabolism, including skeletal muscle tissues, and may have a role in the sarcopenia etiology. Here, we aimed to review the relationship between skeletal muscle mass, glucose homeostasis, and gut microbiota, and the effect of consuming probiotics and prebiotics on the development and pathological consequences of sarcopenia in the aging human population. This review includes discussions about the effects of glucose metabolism and gut microbiota on skeletal muscle mass and sarcopenia and the interaction of dietary intake, physical activity, and gut microbiome to influence sarcopenia through modulating the gut–muscle axis. Emerging evidence suggests that the microbiome can regulate both skeletal muscle mass and function, in part through modulating the metabolisms of short-chain fatty acids and branch-chain amino acids that might act directly on muscle in humans or indirectly through the brain and liver. Dietary factors such as fats, proteins, and indigestible carbohydrates and lifestyle interventions such as exercise, smoking, and alcohol intake can both help and hinder the putative gut–muscle axis. The evidence presented in this review suggests that loss of muscle mass and function are not an inevitable consequence of the aging process, and that dietary and lifestyle interventions may prevent or delay sarcopenia.
16
Magaña, Juan Carlos, Cláudia M. Deus, Maria Giné-Garriga, Joel Montané, and Susana P. Pereira. "Exercise-Boosted Mitochondrial Remodeling in Parkinson’s Disease." Biomedicines 10, no. 12 (December 12, 2022): 3228. http://dx.doi.org/10.3390/biomedicines10123228.
Повний текст джерелаАнотація:
Parkinson’s disease (PD) is a movement disorder characterized by the progressive degeneration of dopaminergic neurons resulting in dopamine deficiency in the striatum. Given the estimated escalation in the number of people with PD in the coming decades, interventions aimed at minimizing morbidity and improving quality of life are crucial. Mitochondrial dysfunction and oxidative stress are intrinsic factors related to PD pathogenesis. Accumulating evidence suggests that patients with PD might benefit from various forms of exercise in diverse ways, from general health improvements to disease-specific effects and, potentially, disease-modifying effects. However, the signaling and mechanism connecting skeletal muscle-increased activity and brain remodeling are poorly elucidated. In this review, we describe skeletal muscle–brain crosstalk in PD, with a special focus on mitochondrial effects, proposing mitochondrial dysfunction as a linker in the muscle–brain axis in this neurodegenerative disease and as a promising therapeutic target. Moreover, we outline how exercise secretome can improve mitochondrial health and impact the nervous system to slow down PD progression. Understanding the regulation of the mitochondrial function by exercise in PD may be beneficial in defining interventions to delay the onset of this neurodegenerative disease.
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Sallum, Beatriz Gamel, Fernanda Veeck Sosa, Izadora de Godoy de Orleães, Sarah Brandão, Julia Vitória Bonelli Loureiro, Thaís Maciel Kimo de Almeida Pena, Isabelle Bicalho Negri, et al. "SARCOPENIA AND COGNITIVE DECLINE IN THE ELDERLY: A LITERATURE REVIEW TAILORING THE MUSCLE-BRAIN AXIS." International Journal of Health Science 4, no. 11 (January 24, 2024): 2–6. http://dx.doi.org/10.22533/at.ed.1594112423018.
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Cammisuli, Davide Maria, Jonathan Fusi, Giorgia Scarfò, Simona Daniele, Gianluca Castelnuovo, and Ferdinando Franzoni. "A Minireview Exploring the Interplay of the Muscle-Gut-Brain (MGB) Axis to Improve Knowledge on Mental Disorders: Implications for Clinical Neuroscience Research and Therapeutics." Oxidative Medicine and Cellular Longevity 2022 (September 15, 2022): 1–8. http://dx.doi.org/10.1155/2022/8806009.
Повний текст джерелаАнотація:
What benefit might emerge from connecting clinical neuroscience with microbiology and exercise science? What about the influence of the muscle-gut-brain (MGB) axis on mental health? The gut microbiota colonizes the intestinal tract and plays a pivotal role in digestion, production of vitamins and immune system development, but it is also able to exert a particular effect on psychological well-being and appears to play a critical role in regulating several muscle metabolic pathways. Endogenous and exogenous factors may cause dysbiosis, with relevant consequences on the composition and function of the gut microbiota that may also modulate muscle responses to exercise. The capacity of specific psychobiotics in ameliorating mental health as complementary strategies has been recently suggested as a novel treatment for some neuropsychiatric diseases. Moreover, physical exercise can modify qualitative and quantitative composition of the gut microbiota and alleviate certain psychopathological symptoms. In this minireview, we documented evidence about the impact of the MGB axis on mental health, which currently appears to be a possible target in the context of a multidimensional intervention mainly including pharmacological and psychotherapeutic treatments, especially for depressive mood.
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Burtscher, Johannes, Barbara Strasser, Giuseppe Pepe, Martin Burtscher, Martin Kopp, Alba Di Pardo, Vittorio Maglione, and Andy V. Khamoui. "Brain–Periphery Interactions in Huntington’s Disease: Mediators and Lifestyle Interventions." International Journal of Molecular Sciences 25, no. 9 (April 25, 2024): 4696. http://dx.doi.org/10.3390/ijms25094696.
Повний текст джерелаАнотація:
Prominent pathological features of Huntington’s disease (HD) are aggregations of mutated Huntingtin protein (mHtt) in the brain and neurodegeneration, which causes characteristic motor (such as chorea and dystonia) and non-motor symptoms. However, the numerous systemic and peripheral deficits in HD have gained increasing attention recently, since those factors likely modulate disease progression, including brain pathology. While whole-body metabolic abnormalities and organ-specific pathologies in HD have been relatively well described, the potential mediators of compromised inter-organ communication in HD have been insufficiently characterized. Therefore, we applied an exploratory literature search to identify such mediators. Unsurprisingly, dysregulation of inflammatory factors, circulating mHtt, and many other messenger molecules (hormones, lipids, RNAs) were found that suggest impaired inter-organ communication, including of the gut–brain and muscle–brain axis. Based on these findings, we aimed to assess the risks and potentials of lifestyle interventions that are thought to improve communication across these axes: dietary strategies and exercise. We conclude that appropriate lifestyle interventions have great potential to reduce symptoms and potentially modify disease progression (possibly via improving inter-organ signaling) in HD. However, impaired systemic metabolism and peripheral symptoms warrant particular care in the design of dietary and exercise programs for people with HD.
20
Song, Wen-Shin, Tai-Ho Hung, Shing-Hwa Liu, Yin-Ting Zheng, Hsin-Mei Lin, and Feng-Yi Yang. "Neuroprotection by Abdominal Ultrasound in Lipopolysaccharide-Induced Systemic Inflammation." International Journal of Molecular Sciences 24, no. 11 (May 26, 2023): 9329. http://dx.doi.org/10.3390/ijms24119329.
Повний текст джерелаАнотація:
Systemic inflammation is associated with intestinal inflammation and neuroinflammation by imbalancing the gut–brain axis. Low-intensity pulsed ultrasound (LIPUS) has neuroprotective and anti-inflammatory effects. This study explored LIPUS’s neuroprotective effects against lipopolysaccharide (LPS)-induced neuroinflammation through transabdominal stimulation. Male C57BL/6J mice were intraperitoneally injected with LPS (0.75 mg/kg) daily for seven days, and abdominal LIPUS was applied to the abdominal area for 15 min/day during the last six days. One day after the last LIPUS treatment, biological samples were collected for microscopic and immunohistochemical analysis. Histological examination showed that LPS administration leads to tissue damage in the colon and brain. Transabdominal LIPUS stimulation attenuated colonic damage, reducing histological score, colonic muscle thickness, and villi shortening. Furthermore, abdominal LIPUS reduced hippocampal microglial activation (labeled by ionized calcium-binding adaptor molecule-1 [Iba-1]) and neuronal cell loss (labeled by microtubule-associated protein 2 [MAP2]). Moreover, abdominal LIPUS attenuated the number of apoptotic cells in the hippocampus and cortex. Altogether, our results indicate that abdominal LIPUS stimulation attenuates LPS-induced colonic inflammation and neuroinflammation. These findings provide new insights into the treatment strategy for neuroinflammation-related brain disorders and may facilitate method development through the gut–brain axis pathway.
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Schlegel, Petr, Michal Novotny, Blanka Klimova, and Martin Valis. "“Muscle-Gut-Brain Axis”: Can Physical Activity Help Patients with Alzheimer’s Disease Due to Microbiome Modulation?" Journal of Alzheimer's Disease 71, no. 3 (October 1, 2019): 861–78. http://dx.doi.org/10.3233/jad-190460.
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Ibrahim, Iddrisu, Soumyakrishnan Syamala, Joseph Atia Ayariga, Junhuan Xu, Boakai K. Robertson, Sreepriya Meenakshisundaram, and Olufemi S. Ajayi. "Modulatory Effect of Gut Microbiota on the Gut-Brain, Gut-Bone Axes, and the Impact of Cannabinoids." Metabolites 12, no. 12 (December 10, 2022): 1247. http://dx.doi.org/10.3390/metabo12121247.
Повний текст джерелаАнотація:
The gut microbiome is a collection of microorganisms and parasites in the gastrointestinal tract. Many factors can affect this community’s composition, such as age, sex, diet, medications, and environmental triggers. The relationship between the human host and the gut microbiota is crucial for the organism’s survival and development, whereas the disruption of this relationship can lead to various inflammatory diseases. Cannabidiol (CBD) and tetrahydrocannabinol (THC) are used to treat muscle spasticity associated with multiple sclerosis. It is now clear that these compounds also benefit patients with neuroinflammation. CBD and THC are used in the treatment of inflammation. The gut is a significant source of nutrients, including vitamins B and K, which are gut microbiota products. While these vitamins play a crucial role in brain and bone development and function, the influence of gut microbiota on the gut-brain and gut-bone axes extends further and continues to receive increasing scientific scrutiny. The gut microbiota has been demonstrated to be vital for optimal brain functions and stress suppression. Additionally, several studies have revealed the role of gut microbiota in developing and maintaining skeletal integrity and bone mineral density. It can also influence the development and maintenance of bone matrix. The presence of the gut microbiota can influence the actions of specific T regulatory cells, which can lead to the development of bone formation and proliferation. In addition, its metabolites can prevent bone loss. The gut microbiota can help maintain the bone’s equilibrium and prevent the development of metabolic diseases, such as osteoporosis. In this review, the dual functions gut microbiota plays in regulating the gut-bone axis and gut-brain axis and the impact of CBD on these roles are discussed.
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Olsen, C. L., and W. R. Jeffery. "A forkhead gene related to HNF-3beta is required for gastrulation and axis formation in the ascidian embryo." Development 124, no. 18 (September 15, 1997): 3609–19. http://dx.doi.org/10.1242/dev.124.18.3609.
Повний текст джерелаАнотація:
We have isolated a member of the HNF-3/forkhead gene family in ascidians as a means to determine the role of winged-helix genes in chordate development. The MocuFH1 gene, isolated from a Molgula oculata cDNA library, exhibits a forkhead DNA-binding domain most similar to zebrafish axial and rodent HNF-3beta. MocuFH1 is a single copy gene but there is at least one other related forkhead gene in the M. oculata genome. The MocuFH1 gene is expressed in the presumptive endoderm, mesenchyme and notochord cells beginning during the late cleavage stages. During gastrulation, MocuFH1 expression occurs in the prospective endoderm cells, which invaginate at the vegetal pole, and in the presumptive notochord and mesenchyme cells, which involute over the anterior and lateral lips of the blastopore, respectively. However, this gene is not expressed in the presumptive muscle cells, which involute over the posterior lip of the blastopore. MocuFH1 expression continues in the same cell lineages during neurulation and axis formation, however, during the tailbud stage, MocuFH1 is also expressed in ventral cells of the brain and spinal cord. The functional role of the MocuFH1 gene was studied using antisense oligodeoxynucleotides (ODNs), which transiently reduce MocuFH1 transcript levels during gastrulation. Embryos treated with antisense ODNs cleave normally and initiate gastrulation. However, gastrulation is incomplete, some of the endoderm and notochord cells do not enter the embryo and undergo subsequent movements, and axis formation is abnormal. In contrast, the prospective muscle cells, which do not express MocuFH1, undergo involution and later express muscle actin and acetylcholinesterase, markers of muscle cell differentiation. The results suggest that MocuFH1 is required for morphogenetic movements of the endoderm and notochord precursor cells during gastrulation and axis formation. The effects of inhibiting MocuFH1 expression on embryonic axis formation in ascidians are similar to those reported for knockout mutations of HNF-3beta in the mouse, suggesting that HNF-3/forkhead genes have an ancient and fundamental role in organizing the body plan in chordates.
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Li, Zefang, Xueqiang Wu, Zhaojun Yan, Yiping Cui, Yueling Liu, Song Cui, Yining Wang, and Tianyu Liu. "Unveiling the muscle-brain axis: A bidirectional mendelian randomization study investigating the causal relationship between sarcopenia-related traits and brain aging." Archives of Gerontology and Geriatrics 123 (August 2024): 105412. http://dx.doi.org/10.1016/j.archger.2024.105412.
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Paoletti, Ilaria, and Roberto Coccurello. "Irisin: A Multifaceted Hormone Bridging Exercise and Disease Pathophysiology." International Journal of Molecular Sciences 25, no. 24 (December 16, 2024): 13480. https://doi.org/10.3390/ijms252413480.
Повний текст джерелаАнотація:
The fibronectin domain-containing protein 5 (FNDC5), or irisin, is an adipo-myokine hormone produced during exercise, which shows therapeutic potential for conditions like metabolic disorders, osteoporosis, sarcopenia, obesity, type 2 diabetes, and neurodegenerative diseases, including Alzheimer’s disease (AD). This review explores its potential across various pathophysiological processes that are often considered independent. Elevated in healthy states but reduced in diseases, irisin improves muscle–adipose communication, insulin sensitivity, and metabolic balance by enhancing mitochondrial function and reducing oxidative stress. It promotes osteogenesis and mitigates bone loss in osteoporosis and sarcopenia. Irisin exhibits anti-inflammatory effects by inhibiting NF-κB signaling and countering insulin resistance. In the brain, it reduces amyloid-β toxicity, inflammation, and oxidative stress, enhancing brain-derived neurotrophic factor (BDNF) signaling, which improves cognition and synaptic health in AD models. It also regulates dopamine pathways, potentially alleviating neuropsychiatric symptoms like depression and apathy. By linking physical activity to systemic health, irisin emphasizes its role in the muscle–bone–brain axis. Its multifaceted benefits highlight its potential as a therapeutic target for AD and related disorders, with applications in prevention, in treatment, and as a complement to exercise strategies.
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D’Amico, Federica, Cecilia Lugarà, Giovanni Luppino, Carlo Giuffrida, Ylenia Giorgianni, Eleonora Maria Patanè, Sara Manti, Antonella Gambadauro, Mariarosaria La Rocca, and Tiziana Abbate. "The Influence of Neurotrophins on the Brain–Lung Axis: Conception, Pregnancy, and Neonatal Period." Current Issues in Molecular Biology 46, no. 3 (March 15, 2024): 2528–43. http://dx.doi.org/10.3390/cimb46030160.
Повний текст джерелаАнотація:
Neurotrophins (NTs) are four small proteins produced by both neuronal and non-neuronal cells; they include nerve growth factor (NGF), brain-derived neurotrophic factor (BDNF), neurotrophin-3 (NT-3), and neurotrophin-4 (NT-4). NTs can exert their action through both genomic and non-genomic mechanisms by interacting with specific receptors. Initial studies on NTs have identified them only as functional molecules of the nervous system. However, recent research have shown that some tissues and organs (such as the lungs, skin, and skeletal and smooth muscle) as well as some structural cells can secrete and respond to NTs. In addition, NTs perform several roles in normal and pathological conditions at different anatomical sites, in both fetal and postnatal life. During pregnancy, NTs are produced by the mother, placenta, and fetus. They play a pivotal role in the pre-implantation process and in placental and embryonic development; they are also involved in the development of the brain and respiratory system. In the postnatal period, it appears that NTs are associated with some diseases, such as sudden infant death syndrome (SIDS), asthma, congenital central hypoventilation syndrome (CCHS), and bronchopulmonary dysplasia (BPD).
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Sun, Yi, Youfeng Yang, Anisha Banerjee, Amrisha Verma, Qiuhong Li, Christy Carter, and Thomas Buford. "Effects of Angiotensin (1-7) Expressing Lactobacillus and Exercise on Gut-Brain Axis in Aged Rats." Innovation in Aging 4, Supplement_1 (December 1, 2020): 887–88. http://dx.doi.org/10.1093/geroni/igaa057.3275.
Повний текст джерелаАнотація:
Abstract Aging is associated with gut dysbiosis – a condition linked with altered central nervous system function (“gut-brain axis”). Age-related health benefits have been ascribed to the renin-angiotensin system, mediated partially via the angiotensin(1-7) axis. Research has shown exercise altering gut microbiota composition and function. This study explored the effects of a genetically modified probiotic expressing angiotensin (1-7) and exercise on the gut-brain axis. Sixty-two male F344/BN rats were randomized at 24-months-old to receive oral gavage of angiotensin (1-7) Lactobacillus paracasei (LP) or LP-A, wide-type LP, or control 3-times/week for 12 weeks; with or without exercise. Rats in exercise groups were walking on a treadmill 10-minutes/day for 5-days/week. Microbiome taxonomic analysis of fecal samples post intervention was performed via 16S-based PCR. A battery of behavior tests were performed before and after the intervention. PCoA revealed that groups differed in the overall fecal microbiota community structure by weighted UniFrac (p=0.034). Indices of alpha-diversity, including Shannon (p=0.02) and Simpson (p=0.019) indexes, displayed LP-A groups with more diverse microbiome than controls. Grip strength (p=0.042) and exercise tolerance (p<0.001) tests showed exercise groups had more muscle strength and aerobic capacity than the sedentary groups. Exercise groups had more lean mass (p=0.019); both LP-A and LP groups had lower fat mass compared to the controls in body composition measurement. LP-A travelled longer distance in the central area than the control in the open field test showing reduced anxiety (p=0.029). Therefore, we conclude LP-A and exercise have distinct and possibly overlapping beneficial effects on the gut-brain axis.
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Suryawanshi, Aditya Rajendra, Santosh Bhimray Kallur, Sujata Maruti Shendage, Shruti Rajendra Dhamale, Mamata Gurunath Vishe, and Yash Rajendra Dhamale. "To study impact of drug abuse in adolescence." Indian Journal of Forensic and Community Medicine 11, no. 3 (October 15, 2024): 96–104. http://dx.doi.org/10.18231/j.ijfcm.2024.023.
Повний текст джерелаАнотація:
Adolescent drug usage can lead to a variety of outcomes that are different from those associated with adult drug use. Alcohol is a common illicit substance in youth, and the molecular mechanisms behind alcohol-induced neuro inflammation, brain injury, and behavioural dysfunction caused by ethanol are not fully understood. In the adult brain, alcoholism is associated with a higher chance of neuropsychiatric diseases. Adolescent alcohol use can cause long-lasting modifications to the control of cytokines and the sensitivity of the hypothalamic-pituitary-adrenal (HPA) axis, which can impact neuropathology and behaviour long into adulthood... Synthetic androgens used for muscle and strength gain, especially in adolescence, are called alcoholic androgenic steroids (AAS). Adult neuropathology and alcoholism can be prevented and treated using AAS, an anabolic steroid.
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Feng, Meina, Qin Zhou, Wenxian Tu, Yunfeng Wang, Yuanmin Du, and Kang Xu. "ATF4 promotes brain vascular smooth muscle cells proliferation, invasion and migration by targeting miR-552-SKI axis." PLOS ONE 17, no. 7 (July 20, 2022): e0270880. http://dx.doi.org/10.1371/journal.pone.0270880.
Повний текст джерелаАнотація:
Background Studies have indicated vascular smooth muscle cells (VSMCs) played a crucial role in atherosclerosis and microRNAs (miRNAs) played key roles in biological functions of VSMCs. Whereas, the potential function and mechanism of miR-552 in VSMCs remains unclear. Our aim was to explore the role of miR-552 on VSMCs and underlying mechanism. Material/Methods MTT assay and transwell assay were used to measure the proliferation, invasion, and migration of human brain VSMCs (HBVSMCs) and mice VSMCs (mVSMCs), respectively. Bioinformatics tools and luciferase assay were adopted to verify the association between miR-552 and SKI. Rescue experiments were employed to assess the interaction of miR-552 and SKI in modulating biological functions in HBVSMCs and mVSMCs. The expression level of transcription factors (TFs)was measured via qRT-PCR assay. The effect of ATF4 on miR-552 and SKI expression was tested by qRT-PCR or western blot assay. Finally, chromatin immunoprecipitation (ChIP) assay and JASPAR databases were used to analyze the regulatory linkage between ATF4 and miR-552. Results We found that miR-552 was upregulated in HBVSMCs treated with PDGF-bb and miR-552 overexpression could promote proliferation, invasion, and migration of HBVSMCs and mVSMCs, whereas, miR-552 knockdown had the opposite impact. In addition, we also found that SKI was a direct target of miR-552, which reversed miR-552-mediated proliferation, invasion, and migration in HBVSMCs and mVSMCs. Furthermore, we also discovered that miR-552 overexpression promoted the effects of ATF4 elevation on proliferation, migration and invasion of HBVSMCs and mVSMCs, but, miR-552 decline had the opposite impact. Conclusions ATF4-miR-552-SKI axis played critical roles in the proliferation and migration of HBVSMCs and mVSMCs, which were closely involved in atherosclerosis (AS). Therefore, our findings might offer a novel therapeutic target for AS.
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Parolaro, S., F. Mottarlini, L. Da Dalt, B. Rizzi, S. Taddini, F. Bonacina, F. Vairano, et al. "Activity-based anorexia dysregulates the Irisin-BDNF neurometabolic axis in female rats: a muscle-to brain crosstalk." Neuroscience Applied 3 (2024): 104896. https://doi.org/10.1016/j.nsa.2024.104896.
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Wada, Taira, Yuya Ichihashi, Emi Suzuki, Yasuhiro Kosuge, Kumiko Ishige, Taketo Uchiyama, Makoto Makishima, Reiko Nakao, Katsutaka Oishi, and Shigeki Shimba. "Deletion of Bmal1 Prevents Diet-Induced Ectopic Fat Accumulation by Controlling Oxidative Capacity in the Skeletal Muscle." International Journal of Molecular Sciences 19, no. 9 (September 18, 2018): 2813. http://dx.doi.org/10.3390/ijms19092813.
Повний текст джерелаАнотація:
Brain and muscle arnt-like protein 1 (BMAL1), is a transcription factor known to regulate circadian rhythm. BMAL1 was originally characterized by its high expression in the skeletal muscle. Since the skeletal muscle is the dominant organ system in energy metabolism, the possible functions of BMAL1 in the skeletal muscle include the control of metabolism. Here, we established that its involvement in the regulation of oxidative capacity in the skeletal muscle. Muscle-specific Bmal1 KO mice (MKO mice) displayed several physiological hallmarks for the increase of oxidative capacity. This included increased energy expenditure and oxygen consumption, high running endurance and resistance to obesity with improved metabolic profiles. Also, the phosphorylation status of AMP-activated protein kinase and its downstream signaling substrate acetyl-CoA carboxylase in the MKO mice were substantially higher than those in the Bmal1flox/flox mice. In addition, biochemical and histological studies confirmed the substantial activation of oxidative fibers in the skeletal muscle of the MKO mice. The mechanism includes the regulation of Cacna1s expression, followed by the activation of calcium—nuclear factor of activated T cells (NFAT) axis. We thus conclude that BMAL1 is a critical regulator of the muscular fatty acid level under nutrition overloading and that the mechanism involves the control of oxidative capacity.
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Knauf, Claude, Anne Abot, Eve Wemelle, and Patrice D. Cani. "Targeting the Enteric Nervous System to Treat Metabolic Disorders? “Enterosynes” as Therapeutic Gut Factors." Neuroendocrinology 110, no. 1-2 (July 2, 2019): 139–46. http://dx.doi.org/10.1159/000500602.
Повний текст джерелаАнотація:
The gut-brain axis is of crucial importance for controlling glucose homeostasis. Alteration of this axis promotes the type 2 diabetes (T2D) phenotype (hyperglycaemia, insulin resistance). Recently, a new concept has emerged to demonstrate the crucial role of the enteric nervous system in the control of glycaemia via the hypothalamus. In diabetic patients and mice, modification of enteric neurons activity in the proximal part of the intestine generates a duodenal hyper-contractility that generates an aberrant message from the gut to the brain. In turn, the hypothalamus sends an aberrant efferent message that provokes a state of insulin resistance, which is characteristic of a T2D state. Targeting the enteric nervous system of the duodenum is now recognized as an innovative strategy for treatment of diabetes. By acting in the intestine, bioactive gut molecules that we called “enterosynes” can modulate the function of a specific type of neurons of the enteric nervous system to decrease the contraction of intestinal smooth muscle cells. Here, we focus on the origins of enterosynes (hormones, neurotransmitters, nutrients, microbiota, and immune factors), which could be considered therapeutic factors, and we describe their modes of action on enteric neurons. This unsuspected action of enterosynes is proposed for the treatment of T2D, but it could be applied for other therapeutic solutions that implicate communication between the gut and brain.
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Collins, Stephen M., Harvey P. Weingarten, and Kevin McHugh. "The Gut-Brain Axis in IBD: An Investigator’s Perspective." Canadian Journal of Gastroenterology 9, no. 5 (1995): 257–60. http://dx.doi.org/10.1155/1995/729863.
Повний текст джерелаАнотація:
Three clinical observations in inflammatory bowel disease (IBD) prompt an examination of the role of gut-brain interactions in the pathophysiology of IBD. The first is the recognition that anorexia is among several factors that lead to malnutrition in IBD patients. The second is the suspicion that stressful life events may precipitate exacerbations of IBD. The third is that IBD and irritable bowel syndrome (IBS) seem to be related. Recent work in animal models has provided insights into these clinical observations. Animal models of colitis exhibit a marked reduction in feeding during the acute phase of inflammation. Interestingly, thirst mechanisms are preserved and meal pattern analysis reveals that meal frequency is unchanged while meal size is reduced. These observations suggest that the anorexia does not reflect a general debility or malaise phenomenon. The anorexia is mediated in part by prostaglandins and interleukin-10. In another set of experiments, the authors evaluated the effect of stress on colitis induced by trinitrobenzene (TNB) in rats. Mild restraint stress had no effect on the histology or activity of myeloperoxidase in rats that had not previously had colitis. In contrast, stress caused an acute exacerbation of colitis, reflected histologically and by myeloperoxidase activity, in rats with TNB colitis six weeks previously. These results provide new evidence in support of a causal relationship between stress and reactivation of intestinal inflammation. The apparent relationship between IBD and IBS has prompted speculation of a causal relationship between inflammation and gut ‘irritability’. Studies in animal models of colitis and jejunitis have shown that mucosal injury and inflammation are associated with neuromuscular dysfunction and abnormal motility. Neuromuscular dysfunction often persists after the mucosa has healed. More recent studies indicate that cells in the muscularis externa, which includes smooth muscle, are capable of cytokine and other inflammatory mediator production. Thus, one may speculate that the local production of mediators outlasts the mucosal injury and maintains a state of persistent dysfunction in the tissue. This may contribute to postinflammatory irritability in the gut. In summary, recent studies provide a tangible basis for further investigation of the inter-relationships between behaviour and inflammation in the clinical expression of IBD.
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Zhang, Ting, Yu Yue, Chen Li, Xuangao Wu, and Sunmin Park. "Vagus Nerve Suppression in Ischemic Stroke by Carotid Artery Occlusion: Implications for Metabolic Regulation, Cognitive Function, and Gut Microbiome in a Gerbil Model." International Journal of Molecular Sciences 25, no. 14 (July 17, 2024): 7831. http://dx.doi.org/10.3390/ijms25147831.
Повний текст джерелаАнотація:
The vagus nerve regulates metabolic homeostasis and mediates gut–brain communication. We hypothesized that vagus nerve dysfunction, induced by truncated vagotomy (VGX) or carotid artery occlusion (AO), would disrupt gut–brain communication and exacerbate metabolic dysregulation, neuroinflammation, and cognitive impairment. This study aimed to test the hypothesis in gerbils fed a high-fat diet. The gerbils were divided into four groups: AO with VGX (AO_VGX), AO without VGX (AO_NVGX), no AO with VGX (NAO_VGX), and no AO without VGX (NAO_NVGX). After 5 weeks on a high-fat diet, the neuronal cell death, neurological severity, hippocampal lipids and inflammation, energy/glucose metabolism, intestinal morphology, and fecal microbiome composition were assessed. AO and VGX increased the neuronal cell death and neurological severity scores associated with increased hippocampal lipid profiles and lipid peroxidation, as well as changes in the inflammatory cytokine expression and brain-derived neurotrophic factor (BDNF) levels. AO and VGX also increased the body weight, visceral fat mass, and insulin resistance and decreased the skeletal muscle mass. The intestinal morphology and microbiome composition were altered, with an increase in the abundance of Bifidobacterium and a decrease in Akkermansia and Ruminococcus. Microbial metagenome functions were also impacted, including glutamatergic synaptic activity, glycogen synthesis, and amino acid biosynthesis. Interestingly, the effects of VGX were not significantly additive with AO, suggesting that AO inhibited the vagus nerve activity, partly offsetting the effects of VGX. In conclusion, AO and VGX exacerbated the dysregulation of energy, glucose, and lipid metabolism, neuroinflammation, and memory deficits, potentially through the modulation of the gut–brain axis. Targeting the gut–brain axis by inhibiting vagus nerve suppression represents a potential therapeutic strategy for ischemic stroke.
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Gil-Lozano, Manuel, Diego Pérez-Tilve, Mayte Alvarez-Crespo, Aurelio Martís, Ana M. Fernandez, Pablo A. F. Catalina, Lucas C. Gonzalez-Matias, and Federico Mallo. "GLP-1(7-36)-amide and Exendin-4 Stimulate the HPA Axis in Rodents and Humans." Endocrinology 151, no. 6 (April 2, 2010): 2629–40. http://dx.doi.org/10.1210/en.2009-0915.
Повний текст джерелаАнотація:
Glucagon-like peptide-1 (GLP-1) is a potent insulinotropic peptide expressed in the gut and brain, which is secreted in response to food intake. The levels of GLP-1 within the brain have been related to the activity of the hypothalamic-pituitary-adrenal (HPA) axis, and hence, this peptide might mediate some responses to stress. Nevertheless, there is little information regarding the effects of circulating GLP-1 on the neuroendocrine control of HPA activity. Here, we have studied the response of corticoadrenal steroids to the peripheral administration of GLP-1 (7-36)-amide and related peptides [exendin (Ex)-3, Ex-4, and Ex-4(3-39)] in rats, mice, and humans. GLP-1 increases circulating corticosterone levels in a time-dependent manner, both in conscious and anaesthetized rats, and it has also increased aldosterone levels. Moreover, GLP-1 augmented cortisol levels in healthy subjects and diabetes mellitus (DM)-1 patients. The effects of GLP-1/Ex-4 on the HPA axis are very consistent after distinct means of administration (intracerebroventricular, iv, and ip), irrespective of the metabolic state of the animals (fasting or fed ad libitum), and they were reproduced by different peptides in this family, independent of glycaemic changes and their insulinotropic properties. Indeed, these effects were also observed in diabetic subjects (DM-1 patients) and in the DM-1 streptozotocin-rat or DM-2 muscle IGF-I receptor-lysine-arginine transgenic mouse animal models. The mechanisms whereby circulating GLP-1 activates the HPA axis remain to be elucidated, although an increase in ACTH after Ex-4 and GLP-1 administration implicates the central nervous system or a direct effect on the pituitary. Together, these findings suggest that GLP-1 may play an important role in regulating the HPA axis.
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Chowdhury, Sabarna, Subhendu K. Chatterjee, Samir Bhattacharya, Sudipta Maitra та Surjya K. Saikia. "Acidic ambiance induced post-oxidative stress affects AMPK- PGC1α-SIRT1 axis in the skeletal muscles of zebrafish Danio rerio Hamilton, 1822". Acta Biologica Szegediensis 64, № 2 (10 квітня 2021): 191–98. http://dx.doi.org/10.14232/abs.2020.2.191-198.
Повний текст джерелаАнотація:
The present study was aimed to understand whether acidic pH induces oxidative stress in zebrafish affecting metabolic sensor protein and thereby, the mitochondrial functions in the skeletal muscle of zebrafish. The experiments performed in aquaria involved the study of the changes of HIF1α, AMPK, PGC1α and SIRT1 levels together with the levels of mitochondrial Tfam and Nrf1. The results obtained from investigation of superoxide dismutase (SOD), catalase and glutathione revealed that the fish undergoes oxidative stress within a short duration of exposure to acidic ambiance. Further analysis with MDA and HIF1α helped to understand the effects of post oxidative stress on skeletal muscle of the fish at pH 5.0 (± 0.5). Of the three tissues studied (gill, brain and skeletal muscle) the effect was maximum in skeletal muscle as depicted by MDA level at 2 hours beyond which it declines augmenting death or mortality (15%) to the fish. Consequently, HIF1α was increased as an adaptive strategy against metabolic disruption during the first 2 hours period. However, on exposure to pH 5.0 (± 0.5) for 2 hours, there were decrease of the metabolic sensors viz. AMPK and SIRT1 followed by mitochondrial gene transcriptional co-activator PGC1α. The expression of mitochon-drial transcription factors Tfam and Nrf1 were also reduced confirming perturbation in mitochondrial function affecting low ATP production compared to control. This was also supported by the decrease of COXII as well as mitochondrial complex I activity. All these results confirm that the metabolic machinery of zebrafish is affected when pH was lowered to 5.0 (± 0.5).
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Sonkodi, Balázs. "Delayed-Onset Muscle Soreness Begins with a Transient Neural Switch." International Journal of Molecular Sciences 26, no. 5 (March 5, 2025): 2319. https://doi.org/10.3390/ijms26052319.
Повний текст джерелаАнотація:
Unaccustomed and/or strenuous eccentric contractions are known to cause delayed-onset muscle soreness. In spite of this fact, their exact cause and mechanism have been unknown for more than 120 years. The exploration of the diverse functionality of the Piezo2 ion channel, as the principal proprioceptive component, and its autonomously acquired channelopathy may bring light to this apparently simple but mysterious pain condition. Correspondingly, the neurocentric non-contact acute compression axonopathy theory of delayed-onset muscle soreness suggests two damage phases affecting two muscle compartments, including the intrafusal (within the muscle spindle) and the extrafusal (outside the muscle spindle) ones. The secondary damage phase in the extrafusal muscle space is relatively well explored. However, the suggested primary damage phase within the muscle spindle is far from being entirely known. The current manuscript describes how the proposed autonomously acquired Piezo2 channelopathy-induced primary damage could be the initiating transient neural switch in the unfolding of delayed-onset muscle soreness. This primary damage results in a transient proprioceptive neural switch and in a switch from quantum mechanical free energy-stimulated ultrafast proton-coupled signaling to rapid glutamate-based signaling along the muscle–brain axis. In addition, it induces a transient metabolic switch or, even more importantly, an energy generation switch in Type Ia proprioceptive terminals that eventually leads to a transient glutaminolysis deficit and mitochondrial deficiency, not to mention a force generation switch. In summary, the primary damage or switch is likely an inward unidirectional proton pathway reversal between Piezo2 and its auxiliary ligands, leading to acquired Piezo2 channelopathy.
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Arslanova, Alisa, Aksiniya Tarasova, Anastasia Alexandrova, Vera Novoselova, Ilnar Shaidullov, Dilyara Khusnutdinova, Tatiana Grigoryeva, Dina Yarullina, Olga Yakovleva, and Guzel Sitdikova. "Protective Effects of Probiotics on Cognitive and Motor Functions, Anxiety Level, Visceral Sensitivity, Oxidative Stress and Microbiota in Mice with Antibiotic-Induced Dysbiosis." Life 11, no. 8 (July 29, 2021): 764. http://dx.doi.org/10.3390/life11080764.
Повний текст джерелаАнотація:
Accumulating clinical and preclinical data indicate a prominent role of gut microbiota in regulation of physiological functions. The gut-brain axis imbalance due to gut dysbiosis is associated with a range of neurodegenerative diseases. Probiotics were suggested not only to restore intestinal dysbiosis but also modulate stress response and improve mood and anxiety symptoms. In this study, we assessed the effects of probiotic lactobacilli on behavioral reactions, the level of oxidative stress and microbiota content in mice administered to broad-spectrum antibiotics. Our study demonstrates that antibiotic treatment of adolescent mice for two weeks resulted in higher mortality and lower weight gain and induced significant changes in behavior including lower locomotor and exploratory activity, reduced muscle strength, visceral hypersensitivity, higher level of anxiety and impaired cognitive functions compared to the control group. These changes were accompanied by decreased diversity and total amount of bacteria, abundance of Proteobacteria and Verrucomicrobia phyla, and reduced Firmicutes/Bacteroides ratio in the gut microbiota. Moreover, a higher level of oxidative stress was found in brain and skeletal muscle tissues of mice treated with antibiotics. Oral administration of two Lactobacillus strains prevented the observed changes and improved not only microbiota content but also the behavioral alterations, suggesting a neuroprotective and antioxidant role of probiotics.
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Urits, Ivan, Purna Mukherjee, Joshua Meidenbauer, and Thomas N. Seyfried. "Dietary Restriction Promotes Vessel Maturation in a Mouse Astrocytoma." Journal of Oncology 2012 (2012): 1–10. http://dx.doi.org/10.1155/2012/264039.
Повний текст джерелаАнотація:
Mature vasculature contains an endothelial cell lining with a surrounding sheath of pericytes/vascular smooth muscle cells (VSMCs). Tumor vessels are immature and lack a pericyte sheath. Colocalization of vascular endothelial growth factor receptor 2 (VEGFR-2) and platelet-derived growth factor receptor beta (PDGF-Rβ) reduces pericyte ensheathment of tumor vessels. We found that a 30% dietary restriction (DR) enhanced vessel maturation in the mouse CT-2A astrocytoma. DR reduced microvessel density and VEGF expression in the astrocytoma, while increasing recruitment of pericytes, positive for alpha-smooth muscle actin (α-SMA). Moreover, DR reduced colocalization of VEGF-R2 and PDGF-Rβ, but did not reduce total PDGF-Rβexpression. These findings suggest that DR promoted vessel normalization by preventing VEGF-induced inhibition of the PDGF signaling axis in pericytes. DR appears to shift the tumor vasculature from a leaky immature state to a more mature state. We suggest that vessel normalization could improve delivery of therapeutic drugs to brain tumors.
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Xiong, Lin, Xixi Yao, Jie Pei, Xingdong Wang, Shaoke Guo, Mengli Cao, Pengjia Bao, Hui Wang, Ping Yan, and Xian Guo. "Do microbial-gut-muscle mediated by SCFAs, microbial-gut-brain axis mediated by insulin simultaneously regulate yak IMF deposition?" International Journal of Biological Macromolecules 257 (February 2024): 128632. http://dx.doi.org/10.1016/j.ijbiomac.2023.128632.
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Ivanova, Elena P., Andrey A. Lobanov, Sergey V. Andronov, Anatoliy D. Fesyun, Andrey P. Rachin, Gleb N. Barashkov, Elena N. Bogdanova, et al. "Fresh Water Aquatic Training in Patients with Upright Posture Maintaining Disorders." Bulletin of Rehabilitation Medicine 20, no. 6 (December 21, 2021): 58–66. http://dx.doi.org/10.38025/2078-1962-2021-20-6-58-66.
Повний текст джерелаАнотація:
The use of the fresh water aquatic training course, as a more gentle training method, may allow patients to ensure effective restoration of muscle functions responsible for maintaining an upright body position. A more accurate control of the course results can be performed using a virtual analysis carried out using the «Habilect» system that allows to determine the body parts attitude. Aim. To study the effect of training in fresh water using the Habilect system based on the Microsoft Kinect infrared sensor (video stabilometry) on motor functions that contribute to maintaining an upright body posture in patients with mild gait disturbances. Material and methods. An open descriptive study was conducted including 12 patients (7 men, 5 women), aged 40 to 62 years, with upright posture maintaining disorders, which correspond to the functional diagnosis encoded by the ICF «Gait Stereotype Functions» B770.1 – mild violations (5–24%). A group of subjects (n = 12), in addition to basic therapy and training with an exercise therapy instructor, underwent aquatic training in fresh water for two weeks (30 minutes, 6 days a week). Assessment methods: the research was carried out using the Habilect gait video analysis system before and after the rehabilitation course. The χ2 test was used to assess the significance of differences between groups of qualitative variables. When analyzing quantitative variables, the Shapiro-Wilk’s (W) test was performed. For abnormal distribution, the data is in Me format [Q25-Q75]. The Wilcoxon T-test was used to assess the significance of differences in quantitative variables of the two studied groups. The processing of the obtained research results was carried out using the Statistica for Windows, v. 8.0 (StatSoft Inc., USA) and Microsoft Excel (Microsoft, USA). The significance of the differences was considered established at p <0.05. Result and discussion. When examining the amplitude of body deflection along the X-axis before training, they were 3.25 cm [-98 cm; 93.9 cm], after – -9.96 cm [-100.92 cm; -81.96 cm], on the Y-axis before training – -29.01 cm [-29.01 cm; 13.76 cm], after –-30.59 cm [-30.59 cm; 31.09 cm], on the Z-axis before training – 388.1 cm [369.22 cm; 393.39 cm], after training – 380.96 cm [377.98cm, 400.05 cm], deviation of the body movement vector before training 16.45 cm [7.46 cm; 338.67 cm], after training – 324.7 cm [324.7 cm; 342.56 cm]. When examining the amplitude of head deflection along the X-axis before training, they were -0.92 cm [-1.24 cm; -0.92 cm], after – 1.5 cm [-10.19 cm; 2.38 cm], Y-axis before training – 125.33 cm [61.13 cm; 128.94 cm], after – 107.42 cm [52.49 cm; 107.42 cm], along the Z-axis before training – -8.59 cm [-8.97 cm; -5.33 cm], after training – -14.89 cm [-14.89 cm, -3.45cm]. When calculating the increase in deviation (deviations of the main body axes from the initial value) using the Wilcoxon T-test revealed statistically significant deviations in the X-axis (an increase of 306.5%, p = 0.0504), the Z-axis (an increase of 112.68%, p =0.0225) and the Body Angle parameter (an increase of 1973.86% p = 0.0323). When calculating the increase in the deviation of the head axes from the initial value using the Wilcoxon T-test, statistically significant deviations were revealed along the X axis (increase of 163.04%, p = 0.0280), the Y axis (increase of 85.71%, p = 0.0199) and the parameter Z (an increase of 173.34% p = 0.0292). The study revealed a decrease in the body axes deviations amplitude in all 3 planes, which indicates an improvement in the work of all brain parts that are responsible for the coordination of motor functions and their vegetative support, an improvement in functional interaction within individual muscle chains. The reduction in the head and neck muscles in compensatory balancing participation during walking and maintaining a vertical body posture mainly due to the muscles of the lower extremities and pelvis contributes to the prevention of arterial and venous circulation disorders in the head and neck and makes training not only more effective, but also safer. Conclusion. Due to the decrease in the amplitude of deviations along all three axes (Z, Y, X), the course of aquatic training contributes to the correction of upright posture maintaining disorders, a statistically significant decrease in the amplitude of head and neck movements.
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Brunette-Clement, Tristan, Evan Kalin-Hajdu, and Pascal Lavergne. "Endoscopic transorbital approach for left anterior clinoidectomy, optic canal decompression and spheno-orbital meningioma resection." Neurosurgical Focus: Video 12, no. 2 (April 2025): V6. https://doi.org/10.3171/2025.1.focvid24199.
Повний текст джерелаАнотація:
Endoscopic transorbital approaches have been increasingly used to treat lesions of the middle fossa, such as sphenoid wing meningiomas or cavernous sinus disease, eschewing the cosmetic and functional consequences of a frontotemporal craniotomy, as well as technical shortcomings of endoscopic endonasal approaches. In this video, the authors present a case of a spheno-orbital meningioma for which an endoscopic transorbital approach was used for tumor resection, optic canal decompression, and anterior clinoidectomy. The advantages of this approach are demonstrated, particularly the direct, shorter distance to target along the axis of the middle fossa, which avoids neurovascular structures, brain retraction, and temporal muscle manipulation. The video can be found here: https://stream.cadmore.media/r10.3171/2025.1.FOCVID24199
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Staresinic, Mario, Mladen Japjec, Hrvoje Vranes, Andreja Prtoric, Helena Zizek, Ivan Krezic, Slaven Gojkovic, et al. "Stable Gastric Pentadecapeptide BPC 157 and Striated, Smooth, and Heart Muscle." Biomedicines 10, no. 12 (December 12, 2022): 3221. http://dx.doi.org/10.3390/biomedicines10123221.
Повний текст джерелаАнотація:
First, we review the definitively severed myotendinous junction and recovery by the cytoprotective stable gastric pentadecapeptide BPC 157 therapy, its healing that might combine both transected and detached tendon and transected muscle, ligament and bone injuries, applied alone, as native peptide therapy, effective in rat injury, given intraperitoneally or in drinking water or topically, at the site of injury. As a follow up, we reviewed that with the BPC 157 therapy, its cytoprotective ability to organize simultaneous healing of different tissues of and full recovery of the myotendinous junction might represent the particular muscle therapy against distinctive etiopathology muscle disabilities and weakness. In this, BPC 157 therapy might recover many of muscle disabilities (i.e., succinylcholine, vascular occlusion, spinal cord compression, stroke, traumatic brain injury, severe electrolyte disturbances, neurotoxins, neuroleptics, alcohol, serotonin syndrome and NO-system blockade and tumor-cachexia). These might provide practical realization of the multimodal muscle-axis impact able to react depending on the condition and the given agent(s) and the symptoms distinctively related to the prime injurious cause symptoms in the wide healing concept, the concept of cytoprotection, in particular. Further, the BPC 157 therapy might be the recovery for the disabled heart functioning, and disabled smooth muscle functioning (various sphincters function recovery). Finally, BPC 157, native and stable in human gastric juice, might be a prototype of anti-ulcer cytoprotective peptide for the muscle therapy with high curing potential (very safe profile (lethal dose not achieved), with suited wide effective range (µg-ng regimens) and ways of application).
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Garofalo, Cinzia, Costanza Maria Cristiani, Sara Ilari, Lucia Carmela Passacatini, Valentina Malafoglia, Giuseppe Viglietto, Jessica Maiuolo, et al. "Fibromyalgia and Irritable Bowel Syndrome Interaction: A Possible Role for Gut Microbiota and Gut-Brain Axis." Biomedicines 11, no. 6 (June 13, 2023): 1701. http://dx.doi.org/10.3390/biomedicines11061701.
Повний текст джерелаАнотація:
Fibromyalgia (FM) is a serious chronic pain syndrome, characterised by muscle and joint stiffness, insomnia, fatigue, mood disorders, cognitive dysfunction, anxiety, depression and intestinal irritability. Irritable Bowel Syndrome (IBS) shares many of these symptoms, and FM and IBS frequently co-exist, which suggests a common aetiology for the two diseases. The exact physiopathological mechanisms underlying both FM and IBS onset are unknown. Researchers have investigated many possible causes, including alterations in gut microbiota, which contain billions of microorganisms in the human digestive tract. The gut-brain axis has been proven to be the link between the gut microbiota and the central nervous system, which can then control the gut microbiota composition. In this review, we will discuss the similarities between FM and IBS. Particularly, we will focus our attention on symptomatology overlap between FM and IBS as well as the similarities in microbiota composition between FM and IBS patients. We will also briefly discuss the potential therapeutic approaches based on microbiota manipulations that are successfully used in IBS and could be employed also in FM patients to relieve pain, ameliorate the rehabilitation outcome, psychological distress and intestinal symptoms.
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Dong, Kang, Zhishuai Hou, Zhao Li, Yuling Xu, and Qinfeng Gao. "Extended Photoperiod Facilitated the Restoration of the Expression of GH-IGF Axis Genes in Submerged Rainbow Trout (Oncorhynchus mykiss)." International Journal of Molecular Sciences 25, no. 24 (December 19, 2024): 13583. https://doi.org/10.3390/ijms252413583.
Повний текст джерелаАнотація:
Salmonids, classified as physostomous fish, maintain buoyancy by ingesting air to inflate their swim bladders. Long-term submergence has been shown to cause body imbalance and reduced growth performance in these fish. Previous studies have demonstrated that extended photoperiod can promote growth in salmonids. This study aimed to investigate the regulatory effects of prolonged lighting on the growth of submerged rainbow trout (Oncorhynchus mykiss) by examining the transcriptional expression of genes in the growth hormone (GH)-insulin-like growth factor (IGF) axis. Rainbow trout were individually reared in one of the six environments, defined by the combination of three photoperiods (0L:24D, 12L:12D, and 24L:0D) and two spatial rearing modes (routine and submerged), for 16 weeks. We compared the growth performance of rainbow trout in different environments and further analyzed the transcription profiles and correlations of GH-IGF axis genes in the brain, liver, and muscle. The findings of this study were as follows: growth performance of rainbow trout gradually increased with photoperiod duration. Specifically, final body weight (FBW) and specific growth rate (SGR) increased, while feed conversion ratio (FCR) decreased. Extended photoperiod partially mitigated the adverse effects of long-term submergence on rainbow trout growth. Under 24L:0D photoperiod conditions, growth performance (FBW, SGR, and FCR) in submerged and routine rainbow trout was more closely aligned compared to 0L:24D and 12L:12D photoperiod conditions. In response to variations in the photoperiod, GH-IGF axis genes of rainbow trout exhibited significant transcriptional differences, particularly between treatments with 0L:24D and 24L:0D light exposure. An extended photoperiod facilitated the restoration of the expression of GH-IGF axis genes in submerged rainbow trout towards routine levels, including the up-regulation of sst and sstr2 genes in the brain. Correlation analysis implied differentiation of physiological functions of ghr and igfbp paralogs. This study provided insights into the feasibility of enhancing the growth performance of submerged salmonids through photoperiod manipulation.
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Thomas, Gregory, Kaysie L. Banton, Raymond Garrett, Carlos H. Palacio, David Acuna, Robert Madayag, and David Bar-Or. "Hypoxia Dysregulates the Transcription of Myoendothelial Junction Proteins Involved with Nitric Oxide Production in Brain Endothelial Cells." Biomedicines 12, no. 1 (December 28, 2023): 75. http://dx.doi.org/10.3390/biomedicines12010075.
Повний текст джерелаАнотація:
Myoendothelial junctions (MEJs) are structures that allow chemical signals to be transmitted between endothelial cells (ECs) and vascular smooth muscle cells, which control vascular tone. MEJs contain hemoglobin alpha (Hbα) and endothelial nitric oxide synthase (eNOS) complexes that appear to control the production and scavenging of nitric oxide (NO) along with the activity of cytochrome b5 reductase 3 (CYB5R3). The aim of this study was to examine how hypoxia affected the regulation of proteins involved in the production of NO in brain ECs. In brief, human brain microvascular endothelial cells (HBMEC) were exposed to cobalt chloride (CoCl2), a hypoxia mimetic, and a transcriptional analysis was performed using primers for eNOS, CYB5R3, and Hbα2 with ΔΔCt relative gene expression normalized to GAPDH. NO production was also measured after treatment using 4,5-diaminofluorescein diacetate (DAF-DA), a fluorescent NO indicator. When HBMEC were exposed to CoCl2 for 48 h, eNOS and CYB5R3 messenger RNA significantly decreased (up to −17.8 ± 4.30-fold and −10.4 ± 2.8, respectively) while Hbα2 increased to detectable levels. Furthermore, CoCl2 treatment caused a redistribution of peripheral membrane-generated NO production to a perinuclear region. To the best of our knowledge, this is the first time this axis has been studied in brain ECs and these findings imply that hypoxia may cause dysregulation of proteins that regulate NO production in brain MEJs.
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Gahr, Scott A., Roger L. Vallejo, Gregory M. Weber, Brian S. Shepherd, Jeffrey T. Silverstein, and Caird E. Rexroad. "Effects of short-term growth hormone treatment on liver and muscle transcriptomes in rainbow trout (Oncorhynchus mykiss)." Physiological Genomics 32, no. 3 (February 2008): 380–92. http://dx.doi.org/10.1152/physiolgenomics.00142.2007.
Повний текст джерелаАнотація:
Although studies have established that exogenous growth hormone (GH) treatment stimulates growth in fish, its effects on target tissue gene expression are not well characterized. We assessed the effects of Posilac (Monsanto, St. Louis, MO), a recombinant bovine GH, on tissue transcript levels in rainbow trout selected from two high-growth rate and two low-growth rate families. Transcript abundance was measured in liver and muscle with the Genome Research in Atlantic Salmon Project (GRASP) 16K cDNA microarray. A selection of the genes identified as altered by the microarray and transcripts for insulin-like growth factors, growth hormone receptors (GHRs), and myostatins were measured by real-time PCR in the liver, muscle, brain, kidney, intestine, stomach, gill, and heart. In general, transcripts identified as differentially regulated in the muscle on the microarray showed similar directional changes of expression in the other nonhepatic tissues. A total of 114 and 66 transcripts were identified by microarray as differentially expressed with GH treatment across growth rate for muscle and liver, respectively. The largest proportion of these transcripts represented novel transcripts, followed by immune and metabolism-related genes. We have identified a number of genes related to lipid metabolism, supporting a modulation in lipid metabolism following GH treatment. Most notable among the growth-axis genes measured by real-time PCR were increases in GHR1 and -2 transcripts in liver and muscle. Our results indicate that short-term GH treatment activates the immune system, shifts the metabolic sectors, and modulates growth-regulating genes.
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Czerwiec, Frank S., Jeffrey Drajesk, Sarah Hooper, Kimberly Hunsicker, Robert Jacks, Jamie MacPherson, Tonya Marmon, and David A. Katz. "PMON72 The "RESCUE" Trial: 11beta-Hydroxysteroid Dehydrogenase Type 1 (HSD-1) Inhibition for ACTH-Dependent Cushing's Syndrome." Journal of the Endocrine Society 6, Supplement_1 (November 1, 2022): A87. http://dx.doi.org/10.1210/jendso/bvac150.179.
Повний текст джерелаАнотація:
Abstract Background HSD-1, an intracellular enzyme, converts cortisone to cortisol in tissues where cortisol excess is associated with morbidity including liver, adipose, bone, brain, muscle, skin, and eye. SPI-62 is a potent and specific HSD-1 inhibitor in development for treatment of Cushing's syndrome and autonomous cortisol secretion, and as adjunctive therapy to prednisolone in polymyalgia rheumatica. In Phase 1 clinical trials SPI-62 was generally well tolerated and associated with maximal liver and brain HSD-1 inhibition. SPI-62 decreased urinary cortisol metabolites indicating a similar decrease of hepatocellular cortisol in this important target tissue. After a corresponding transient decrease, circulating cortisol homeostasis was restored by ACTH increase which also resulted in a moderate adrenal androgen increase. SPI-62's effects on androgens did not result in adverse effects. Urinary free cortisol was unaffected. The RESCUE trial will assess SPI-62 safety and efficacy in patients with a dysregulated HPA axis, ie., ACTH-dependent Cushing's syndrome. Methods In this randomized, placebo-controlled, crossover, multinational, Phase 2 clinical trial, adult patients (N=26) with ACTH-dependent Cushing's syndrome with active and consistently elevated urinary free cortisol (UFC) will be randomized to receive SPI-62 and placebo for 12 weeks each. A diagnosis of an inadequately treated pituitary adenoma (Cushing's disease) or ectopic ACTH or CRH producing tumor based on established criteria is required. Evidence of Cushing's associated morbidities including at least 2 of A) insulin-resistance/type-2 diabetes mellitus, B) dyslipidemia, C) hypertension, or D) osteopenia is required. Subjects must not have had recent Cushing's surgical, radiation other approved or experimental medical therapies for cortisol excess. Medical conditions or treatments likely to interfere with study assessments or subject safety are also excluded. The primary outcome is pharmacological suppression of the urinary ratio of hepatic 5- and 3-steroid reductase metabolites of cortisol and cortisone (tetrahydrocortisol+allotetrahydrocortisol)/tetrahydrocortisone). Safety is assessed by adverse events, vital signs, ECG, and clinical laboratory analyses including effects on HPA/HPG axis biomarkers. Efficacy is assessed by reduction of Cushing's features and morbidities of hyperglycemia, dyslipidemia, adiposity, hepatic steatosis, hypertension, glaucoma, osteopenia, muscle strength, cognition, sleep, and mood. Assessments include tumor-imaging by MRI, ocular tonometry, timed up-and-go and hand-grip strength tests, dual-energy x-ray absorptiometry, oral glucose tolerance, continuous glucose monitoring, and ambulatory blood pressure monitoring. Results This trial is ongoing; results are pending. Discussion This Phase 2 explores SPI-62 safety, HSD-1 inhibition, effects on HPA/HPG axes, and clinical effects in patients with ACTH-dependent Cushing's syndrome. Presentation: Monday, June 13, 2022 12:30 p.m. - 2:30 p.m.
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Deus, Lysleine Alves, Hugo de Luca Corrêa, Rodrigo Vanerson Passos Neves, Andrea Lucena Reis, Fernando Sousa Honorato, Victor Lopes Silva, Michel Kendy Souza, et al. "Are Resistance Training-Induced BDNF in Hemodialysis Patients Associated with Depressive Symptoms, Quality of Life, Antioxidant Capacity, and Muscle Strength? An Insight for the Muscle–Brain–Renal Axis." International Journal of Environmental Research and Public Health 18, no. 21 (October 27, 2021): 11299. http://dx.doi.org/10.3390/ijerph182111299.
Повний текст джерелаАнотація:
Background: Hemodialysis patients are suffering from depressive symptoms. Brain-derived neurotrophic factor (BDNF) levels are negatively associated with depressive symptoms and decrease during a single hemodialysis session. Resistance training (RT) might be an additional non-pharmacological tool to increase BDNF and promote mental health. Methods: Two randomized groups of hemodialysis patients: control (CTL, n = 76/F36; 66.33 ± 3.88 years) and RT (n = 81/F35; 67.27 ± 3.24 years). RT completed six months of training thrice a week under the supervision of strength and conditioning professional immediately before the dialysis session. Training loads were adjusted using the OMNI rating of perceived exertion. The total antioxidant capacity (TROLOX), glutathione (GSH), thiobarbituric acid reactive substance (TBARS), and BDNF levels were analyzed in serum samples. Quality of life (assessed through Medical Outcomes—SF36), and Beck Depression Inventory was applied. Results: RT improved handgrip strength (21.17 ± 4.38 vs. 27.17 ± 4.34; p = 0.001) but not for CTL (20.09 ± 5.19 vs. 19.75 ± 5.54; p = 0.001). Post-training, RT group had higher values as compared to CTL related to TROLOX (RT,680.8 ± 225.2 vs. CTL,589.5 ± 195.9; p = 0.001) and GSH (RT, 9.33 ± 2.09 vs. CTL,5.00 ± 2.96; p = 0.001). RT group had lower values of TBARS as compared to CTL at post-training (RT, 11.06 ± 2.95 vs. CTL, 13.66 ± 2.62; p = 0.001). BDNF increased for RT (11.66 ± 5.20 vs. 19.60 ± 7.23; p = 0.001), but decreased for CTL (14.40 ± 4.99 vs. 10.84 ± 5.94; p = 0.001). Quality of life and mental health increased (p = 0.001) for RT, but did not change for CTL (p = 0.001). BDNF levels were associated with emotional dimensions of SF36, depressive symptoms, and handgrip (p = 0.001). Conclusions: RT was effective as a non-pharmacological tool to increased BDNF levels, quality of life, temper the redox balance and decrease depressive symptoms intensity in hemodialysis patients.
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Sonkodi, Balázs. "Proton-Mediated PIEZO2 Channelopathy: Linking Oxaliplatin Treatment to Impaired Proprioception and Cognitive Deficits." Cancers 16, no. 23 (November 21, 2024): 3898. http://dx.doi.org/10.3390/cancers16233898.
Повний текст джерелаАнотація:
Oxaliplatin induces acute neuropathy within a few hours post-treatment, with symptoms persisting for several days. Delayed onset muscle soreness also causes the delayed onset of mechanical pain sensation starting at about 6–8 h and lasting up to a week after exercise. Both conditions come with impaired proprioception and could be chronic if these bouts are repeated frequently. The involvement of PIEZO2 ion channels, as the principal mechanosensory channels responsible for proprioception, is theorized in both conditions as well. The current opinion manuscript is meant to explain how the minor stretch-related microdamage of PIEZO2 on Type Ia proprioceptive terminals could explain the aforementioned symptoms of impaired proprioception. This includes a platinum-induced proton affinity ‘switch’ on these proprioceptive endings with PIEZO2 content, resulting in this being the likely initiating cause. Furthermore, it postulates how the proton-based ultrafast long-range oscillatory synchronization to the hippocampus could be impaired due to this microdamage on Type Ia proprioceptive terminals. Finally, the manuscript provides insight into how the impairment of the PIEZO2-initiated ultrafast muscle–brain axis may contribute to chemobrain and its associated cognitive and memory deficits.