How are fatty acid metabolized?
फैटी एसिड कैसे चयापचय होते हैं?
What is fatty acid metabolism called?
What are steps of fatty metabolism?
Where is fatty acid metabolism?
What are the types of fat metabolism?
What are two types of metabolism?
What are the 3 main types of fat?
What are 2 types of metabolism?
What are the products of fat metabolism?
What is the formula for triglycerides?
What are the three parts of metabolism?
What are the 3 stages of metabolism?
What are fatty acid types?
फैटी एसिड के टूटने की तीन भागों की प्रक्रिया क्या है?
Beta oxidation of fatty acids.
Beta oxidation of unsaturated fatty acids.
What is important for fatty acid metabolism.
#mbbs #medicalcollege #fattyliver #fate #metabolism #oxidation #fattyacids #biological
Fatty Acid metabolism||Beta oxidation||Omega oxidation||Ketogenesis||Adipose tissue metabolism|| Alpha oxidation.
Fatty acid metabolism can contribute to important needs of cancer cells: energy, growth, and membrane synthesis. Furthermore, fatty acids are catabolized by fatty acid oxidation, which is an important source of nicotinamide adenine dinucleotide phosphate (NADPH). Cancer cells require NADPH, which is used during fatty acid synthesis and oxidative stress inhibition. Fatty acid synthase is variably expressed among NB cell lines . Curiously, stem cell-like NB cells showed remarkably high expression of enzymes involved in cholesterol biosynthesis as a result of elevated expression of sterol regulatory element binding factors (SREBFs).
MYCN plays an important role in fatty acid metabolism in MYCN-amplified NB. The inhibition of MYCN signaling results in the downregulation of glycolysis and β-oxidation, mitochondrial dysfunction, and consequently, lipid accumulation in NB cells . The major cause of lipid accumulation by MYC inhibition in NB seems to be related to reduced oxidation rather than de novo fatty acid synthesis . In line, knockdown of the carnitine palmitoyltransferase (CPT1), which is highly expressed in NB, also leads to lipid accumulation in NB.
Fatty acid metabolism has been shown to fuel the production of mitochondrial ROS in zebrafish macrophages following infection of embryos with S. enterica Typhimurium (Hall et al., 2013). Immunoresponsive gene 1 (irg1), an infection-inducible and macrophage-specific gene encoding a homolog of bacterial 2-methylcitrate dehydratase, was found to be required for the utilization of fatty acids during this response, and knockdown of this gene increased the susceptibility to infection (Hall et al., 2013). This study showed that also murine macrophages require fatty acid β-oxidation for infection-induced mitochondrial ROS production and bactericidal activity. ROS production is also dependent on glucose metabolism and overproduction of ROS, which can have tissue-damaging effects, has been associated with diabetes (Coughlan & Sharma, 2016). Studies in a zebrafish model for hyperinsulinemia suggest that the metabolic switch between insulin-sensitive and insulin-resistant states is mediated by protein tyrosine phosphatase nonreceptor type 6 (Ptpn6), which is well known as a negative regulator of the innate immune response (Kanwal et al., 2013; Marin-Juez et al., 2014). The dual role of this phosphatase in the regulation of glucose metabolism and immunity is particularly interesting in the light of the emerging coepidemic of TB and diabetes (Pizzol et al., 2016). There are many ongoing efforts to develop zebrafish models for metabolic diseases, including diabetic complications, providing new opportunities to study the relation with infectious diseases.
https://youtube.com/watch?v=xRn-hjGit58&feature=shares—–Human body diseases
https://youtube.com/watch?v=jGyn8bpX4h0&feature=shares—- Respiratory system and its disease
https://youtube.com/watch?v=Ua-xZzOl4xw&feature=shares—— Nervous system and its diseases
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https://youtube.com/watch?v=8iJAbGlMd64&feature=shares—-Digestive system and its diseases
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