A Novel L-Arginine/L-Glutamine Coupling Hypothesis: Implications for Type 1 Diabetes

Bittencourt, P. de; Newsholme, Philip

doi:10.5772/20759

Cited by 3 publications

(3 citation statements)

References 218 publications

(209 reference statements)

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“…HSPs are categorized in families according to their molecular sizes and include HSP110, HSP100, HSP90, HSP70, HSP60, HSP30 and HSP10 subclasses [52]. Among these subclasses, the most studied in the context of muscle is the 70-kDa family (HSP70), which comprises several related proteins with molecular weights ranging from 66 to 78 kDa [53]. The specific roles and functions of each of these proteins are beyond the scope of this review and have been thoroughly discussed elsewhere [54].…”

Section: Heat Tolerance In Myofibersmentioning

confidence: 99%

The Role of Skeletal Muscles in Exertional Heat Stroke Pathophysiology

2021

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The active participation of skeletal muscles is a unique characteristic of exertional heat stroke. Nevertheless, the only well-documented link between skeletal muscle activities and exertional heat stroke pathophysiology is the extensive muscle damage (e. g., rhabdomyolysis) and subsequent leakage of intramuscular content into the circulation of exertional heat stroke victims. Here, we will present and discuss rarely explored roles of skeletal muscles in the context of exertional heat stroke pathophysiology and recovery. This includes an overview of heat production that contributes to severe hyperthermia and the synthesis and secretion of bioactive molecules, such as cytokines, chemokines and acute phase proteins. These molecules can alter the overall inflammatory status from pro- to anti-inflammatory, affecting other organ systems and influencing recovery. The activation of innate immunity can determine whether a victim is ready to return to physical activity or experiences a prolonged convalescence. We also provide a brief discussion on whether heat acclimation can shift skeletal muscle secretory phenotype to prevent or aid recovery from exertional heat stroke. We conclude that skeletal muscles should be considered as a key organ system in exertional heat stroke pathophysiology.

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Section: Heat Tolerance In Myofibersmentioning

confidence: 99%

The Role of Skeletal Muscles in Exertional Heat Stroke Pathophysiology

2021

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“…Indeed, O-GlcNAc signaling and its crosstalk with phosphorylation reactions affects the post-translational state of hundreds of proteins in response to nutrients and stress, and is also altered in several metabolic diseases and inflammatory processes [229]. For instance, glutamine stimulates the expression of the argininosuccinate synthetase (ASS) gene (involved in the regulation of NO production via NOS in many cells [230]) via O-GlcNAcylation of Sp1 [54,231], a key transcription factor required for full HS response [54,105,231]. Glutamine availability has also been identified as a limiting step for the activation of the mammalian target of rapamycin (mTOR) [232].…”

Section: Glutamine Metabolism and Its Importance For The Heat Shock Rmentioning

confidence: 99%

“…Nevertheless, TPN is very invasive and may expose the patient to increased risk of infections, so that, as far as possible, enteral alternatives should be chosen. Moreover, enteral routes are much more physiological and provide the physiological generation of other amino acid derivatives (e.g., citrulline and arginine), which can only be accounted for if glutamine is given enterally [64,230].…”

Section: Physical Exercise Glutamine and Hs Response In Agingmentioning

confidence: 99%

Physiological regulation of the heat shock response by glutamine: implications for chronic low-grade inflammatory diseases in age-related conditions

Leite

Cruzat

Krause

et al. 2016

Nutrire

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Aging is an intricate process modulated by different molecular and cellular events, such as genome instability, epigenetic and transcriptional changes, molecular damage, cell death and senescence, inflammation, and metabolic dysfunction. Particularly, protein quality control (chaperone systems) tends to be negatively affected by aging, thus leading to cellular senescence in metabolic tissues and, as a consequence, to the increasing dissemination of inflammation throughout the body. The heat shock (HS) response and its associated expression of the 70 kDa family of heat shock proteins (HSP70), which are anti-inflammatory molecular chaperones, are found to be markedly decreased during muscle inactivity and aging, while evidence supports the loss of HSP70 as a key mechanism which may drive muscle atrophy, contractile dysfunction, and reduced regenerative capacity. In addition, abnormal stress response is linked with higher incidence of neurodegenerative diseases as well as low-grade inflammatory diseases that are associated with physical inactivity and obesity. Therefore, strategies to increase or, at least, to maintain the levels of HSP70, and its accompanying HS response to stress, are key to reduce biological cell dysfunctions that occur in aging. In this sense, physical exercise is of note as it is the most powerful inducer of the HS response, comparable only to heat stress and fever-like conditions. On the other hand, the amino acid L-glutamine, whose production within the skeletal muscle and liberation into the blood stream is dependent on muscle activity, is a potentializer of HSP70 expression and HS response, particularly via its entering in hexosamine biosynthetic pathway (HBP). Herein, we discuss the collaborative role of glutamine (and its donors/precursors) and physical exercise (mostly responsible for glutamine release into the circulation) as potential tools to increase HSP70 expression and the HS response in the elderly.

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