Phospholipids:
Amphipathic molecules with hydrophilic (polar) heads and hydrophobic (non-polar) tails.
Essential in cell membrane structure and function, including signaling and as lung surfactant.
Ketone Bodies:
Water-soluble compounds (acetone, acetoacetate, and β-hydroxybutyrate) produced in the liver during fatty acid oxidation.
Serve as alternative energy sources during fasting or glucose deprivation.
Structure:
Two main types:
Glycerophospholipids: Contain glycerol as the backbone.
Sphingophospholipids: Contain sphingosine, predominant in nerve tissue (e.g., sphingomyelin).
Functions:
Structural components of cell membranes.
Reservoirs for intracellular messengers.
Essential in bile and lung surfactant production.
Degradation:
Phospholipases hydrolyze phosphodiester bonds, releasing molecules like arachidonic acid.
Remodeling of membrane-bound phospholipids involves replacing fatty acids.
Clinical Relevance:
Niemann-Pick Disease:
Caused by defective sphingomyelin degradation due to sphingomyelinase deficiency.
Type A: Rapid neurodegeneration.
Type B: Affects visceral organs, leading to chronic disease.
Glycolipids:
Found in all membranes but most abundant in nerve tissue.
Involved in cellular interactions, growth, and development.
Prostaglandins:
Potent, hormone-like compounds produced in small amounts in nearly all tissues.
Act locally with a short half-life, regulating inflammation and other processes.
Production:
Synthesized in the liver during fasting or carbohydrate restriction from fatty acid oxidation.
Steps include conversion of acetyl-CoA to acetoacetate, β-hydroxybutyrate, and acetone.
Usage:
Transported in the blood to peripheral tissues (muscles, brain), where they are reconverted to acetyl-CoA for energy production via the TCA cycle.
Excessive Production:
Leads to ketonemia and ketonuria in conditions like uncontrolled diabetes and prolonged fasting.
Diabetic ketoacidosis (DKA): Results in acidemia due to the loss of protons from circulating ketones, causing severe dehydration and acidosis.