Talk:Lipid metabolism

Mistake with Acyl CoA Dehydrogenase

The image shown, titled 'Beta oxidation of palmitic acid' is mostly correct, but incorrectly shows that FAD is converted to FADH. The reaction is instead FAD --> FADH_2. This may be confirmed to be a mistake by referencing other diagrams on the matter, as well as Wikipedia's own image here: File:LCHAD deficiency.svg, and the net reaction in this article '7 FAD + 7 NAD⁺ + 7 CoASH + 7 H₂O + H(CH₂CH₂)₇CH₂CO-SCoA → 8 CH₃CO-SCoA + 7 FADH₂ + 7 NADH + 7 H⁺' (I have emboldened the FADH2).

I have corrected the image on my own but am unsure how to. Showder98 (talk) 03:52, 30 April 2023 (UTC)

explain biosynthesis and catabolism of purine nucleotide with purine metabolism disorder?

Biosynthesis and catabolism of purine nucleotides are fundamental processes in purine metabolism, which involves the synthesis and breakdown of purine nucleotides, such as adenosine and guanosine, essential for DNA, RNA, and energy metabolism.

Biosynthesis of purine nucleotides: Purine nucleotides are synthesized de novo from simpler molecules like amino acids and bicarbonate. The pathway starts with the formation of inosine monophosphate (IMP) from phosphoribosyl pyrophosphate (PRPP) and amino acids like glycine and glutamine. IMP is further converted into adenosine monophosphate (AMP) and guanosine monophosphate (GMP) through separate pathways. These nucleotides can be phosphorylated to form their respective diphosphate (ADP, GDP) and triphosphate (ATP, GTP) forms, which are crucial for cellular energy metabolism. Catabolism of purine nucleotides: Purine nucleotides can be broken down into simpler compounds through two major pathways: the salvage pathway and the deamination pathway. In the salvage pathway, purine bases released from nucleotide degradation are recycled to form nucleotides again using PRPP. In the deamination pathway, purine nucleotides are deaminated by enzymes like adenosine deaminase (ADA) and guanosine deaminase, producing hypoxanthine and xanthine, respectively. Xanthine is further converted into uric acid, which is excreted in urine. Disorders in purine metabolism can lead to various diseases, such as gout and Lesch-Nyhan syndrome:

Gout results from the accumulation of uric acid crystals in joints due to overproduction or underexcretion of uric acid. Lesch-Nyhan syndrome is a genetic disorder caused by a deficiency in the enzyme hypoxanthine-guanine phosphoribosyltransferase (HGPRT), leading to excessive uric acid production, neurological abnormalities, and self-injurious behavior.

 Not done - propose a specific change to the article and provide a WP:BMI source to support the change. Zefr (talk) 16:24, 7 May 2024 (UTC)