Research of great importance for health. Chronic stress could induce adrenaline to activate lactate dehydrogenase A (LDHA) to produce lactic acid. Systemic lactic acidosis is associated with a negative survival prognosis in cancer. Most fruits and vegetables are basicity-producing foods since the metabolized products are precursors of organic anions such as citrate, succinate and conjugate bases of carboxylic acids. The acid-base balance in the body includes the adrenal production of cortisol. When bicarbonate levels are low, the kidneys increase glutaminase activity and trigger cortisol production. Studies in animals and humans have reported that systemic cortisol levels are increased by acid-base alteration through induced metabolic acidosis. Acidosis appears to mediate cortisol activity through the pituitary-adrenal cortex-renal glutaminase axis. The final metabolite of these precursors is the bicarbonate anion.
Chronic stress and stress hormones can upregulate the expression of stress-related proinflammatory genes in circulating white blood cells, which increases the release of proinflammatory cells and the production of proinflammatory cytokines, and may activate aging. inflammatory response without the trigger of exogenous inflammation, leading to the promotion of tumorigenesis and metastasis. Stress hormones promote the onset and development of cancers through several mechanisms, such as inducing DNA damage, increasing p53 degradation, and regulating the tumor microenvironment. Chronic stress can also activate the inflammatory response and the interaction between inflammatory cells and cancer cells to form the tumor microenvironment, thereby promoting all stages of tumorigenesis.
Studies have reported that systemic cortisol levels are increased by acid-base disruption through transiently induced metabolic acidosis. Acidosis mediates cortisol activity through the pituitary-adrenal cortex-renal glutaminase axis. Western diet-induced acidosis may play a role in modulating systemic cortisol levels. Excessive or chronic cortisol production acquired from a “Western” dietary lifestyle could play a role in upregulating the tryptophan metabolism pathway and driving downstream molecular events that promote carcinogenesis. Upregulated cortisol bioactivity driven by diet-induced acidosis may be a factor in metabolic syndrome by promoting insulin resistance.
Chronic hyperglucocorticoidism increases visceral obesity while reducing insulin sensitivity primarily in visceral adipocytes which appear to be more responsive to cortisol than subcutaneous adipocytes due to higher levels of glucocorticoid receptor expression. Visceral adipocytes also show increased activity that converts cortisone to bioactive cortisol.
Research of great importance for health. Chronic stress could induce adrenaline to activate lactate dehydrogenase A (LDHA) to produce lactic acid. Systemic lactic acidosis is associated with a negative survival prognosis in cancer. Most fruits and vegetables are basicity-producing foods since the metabolized products are precursors of organic anions such as citrate, succinate and conjugate bases of carboxylic acids. The acid-base balance in the body includes the adrenal production of cortisol. When bicarbonate levels are low, the kidneys increase glutaminase activity and trigger cortisol production. Studies in animals and humans have reported that systemic cortisol levels are increased by acid-base alteration through induced metabolic acidosis. Acidosis appears to mediate cortisol activity through the pituitary-adrenal cortex-renal glutaminase axis. The final metabolite of these precursors is the bicarbonate anion.
Chronic stress and stress hormones can upregulate the expression of stress-related proinflammatory genes in circulating white blood cells, which increases the release of proinflammatory cells and the production of proinflammatory cytokines, and may activate aging. inflammatory response without the trigger of exogenous inflammation, leading to the promotion of tumorigenesis and metastasis. Stress hormones promote the onset and development of cancers through several mechanisms, such as inducing DNA damage, increasing p53 degradation, and regulating the tumor microenvironment. Chronic stress can also activate the inflammatory response and the interaction between inflammatory cells and cancer cells to form the tumor microenvironment, thereby promoting all stages of tumorigenesis.
Studies have reported that systemic cortisol levels are increased by acid-base disruption through transiently induced metabolic acidosis. Acidosis mediates cortisol activity through the pituitary-adrenal cortex-renal glutaminase axis. Western diet-induced acidosis may play a role in modulating systemic cortisol levels. Excessive or chronic cortisol production acquired from a “Western” dietary lifestyle could play a role in upregulating the tryptophan metabolism pathway and driving downstream molecular events that promote carcinogenesis. Upregulated cortisol bioactivity driven by diet-induced acidosis may be a factor in metabolic syndrome by promoting insulin resistance.
Chronic hyperglucocorticoidism increases visceral obesity while reducing insulin sensitivity primarily in visceral adipocytes which appear to be more responsive to cortisol than subcutaneous adipocytes due to higher levels of glucocorticoid receptor expression. Visceral adipocytes also show increased activity that converts cortisone to bioactive cortisol.
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