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| Methionine (MET) restriction (MR) has been shown to arrest cancer growth and sensitizes tumors to chemotherapy. -Many cancer cells rely heavily on exogenous methionine to sustain rapid growth and proliferation because they often have impaired methionine salvage pathways. -Methionine contributes to the synthesis of glutathione, a key antioxidant. (Methionine is a precursor of glutathione, a tripeptide that reduces reactive oxygen species.) -MR diets might influence the redox state of cancer cells, increasing oxidative stress and thereby leading to cell death in metabolically compromised tumor cells. -Proliferation and growth of several types of cancer cells are inhibited by MR, while normal cells are unaffected by limiting methionine as long as homocysteine is present. -Methionine restriction is effective when the non-essential amino acid, cysteine, is absent from the diet or media. methionine is the precursor for cysteine which is essential for the formation of GSH. -Malignant cells lack the enzyme required to recycle homocysteine therefore giving methionine restriction the capacity to alter cancer cells while maintaining normal, healthy cells. While vegan diets are typically low in methionine, some nuts and legumes (such as Brazil nuts and kidney beans) are rich in methionine. Foods to avoid for MR diet: Animal Proteins: -Red Meat (Beef, Pork, Lamb): -Poultry (Chicken, Turkey): -Fish and Seafood: -Eggs: Both the egg whites and yolks are protein rich. -Dairy Products: Milk, cheese, and yogurt Certain Plant Proteins: -Soy Products: -Legumes: Protein Supplements: Foods Lower in Methionine (Often Favorable on an MR Diet) Fruits & Vegetables: leafy greens, berries, apples, and citrus fruits. Grains & Cereals: rice, oats, and barley Nuts and Seeds: can vary in methionine content. Alternative Protein Sources: emphasize protein sources with a lower methionine-to-cysteine ratio.
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| • PPARα – Regulates fatty acid oxidation, lipid metabolism, and energy homeostasis. – Expressed primarily in liver, heart, kidney, and muscle, PPARα activation induces genes involved in β-oxidation and lipid transport. – It is also involved in modulating inflammatory responses, which may indirectly affect cellular proliferation and survival. – Expression and activation in cancers can vary: – In some liver cancers, PPARα expression or activity may be altered, reflecting its central role in hepatic metabolism. – Overactivation has been associated with liver proliferation in rodent models; however, species differences exist regarding the carcinogenic potential of PPARα agonists. – Outside the liver, PPARα’s role is less defined, but its regulation of inflammation and lipid metabolism may influence tumor metabolism and microenvironment. |
| 2272- | dietMet, | Methionine restriction - Association with redox homeostasis and implications on aging and diseases |
| - | Review, | Nor, | NA |
Query results interpretion may depend on "conditions" listed in the research papers. Such Conditions may include : -low or high Dose -format for product, such as nano of lipid formations -different cell line effects -synergies with other products -if effect was for normal or cancerous cells
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