Mobilisation of adipose triacylglycerol in fasting
In fasting, adipose tissue (fat tissue) releases its stored triacylglycerol (three fatty acids on a glycerol backbone) as fatty acids and glycerol, which enter the blood as fuel.
Remember
Low blood glucose lowers insulin and raises glucagon, so fat cells switch from storing fat to releasing fatty acids and glycerol. Without enough glycerol-3-phosphate (the activated glycerol backbone that fatty acids attach to), which fat cells make mainly from glucose, fatty acids cannot be rebuilt into triglycerides and so leave the cell.
Memory aid
insulin stores, glucagon releases
A short pairing of the two hormones: insulin is the storage signal and glucagon is the release signal.
Mobilisation means getting stored fuel out of its store and into the blood. In adipose tissue, the fuel is stored as triacylglycerol in adipocytes (fat cells). With a constant supply of glucose, the fatty acids in the store are not static, because they are constantly released from triacylglycerol and attached to glycerol again, in a continual cycle.
When blood glucose falls, insulin levels fall and the pancreas releases glucagon. Insulin is the storage signal and glucagon is the release signal. Glucagon activates hormone-sensitive lipase, the enzyme that breaks stored fat down into fatty acids and glycerol. This breakdown of triacylglycerol is called lipolysis.
Low glucose also removes the brake on release. To rebuild triacylglycerol, adipocytes need glycerol-3-phosphate, which they make mainly from glucose through glycolysis (the breakdown of glucose). When glucose is scarce there is too little glycerol-3-phosphate to put fatty acids back into triacylglycerol. That step is called re-esterification, and when it fails the fatty acids and glycerol leave the cycle.
The fatty acids and glycerol then enter the blood as an alternative fuel for other tissues. Lipoprotein lipase, the enzyme on adipose capillaries that takes fatty acids out of passing lipoproteins so that fat can be stored, is suppressed in adipose tissue during fasting, so fat is no longer being laid down. Adrenaline also helps to mobilise fat, but glucagon is the hormone tied to low glucose.
Key facts
- Trigger
- Blood glucose falls, so insulin falls and glucagon rises.
- Enzyme
- Glucagon activates hormone-sensitive lipase in adipocytes.
- Products
- Stored triacylglycerol is split into fatty acids and glycerol, which enter the blood as fuel.
- Rebuilding fat
- Adipocytes need glycerol-3-phosphate, made mainly from glucose, to rebuild triacylglycerol, so low glucose leaves too little glycerol-3-phosphate for fatty acids to be re-attached.
- Lipoprotein lipase
- It is suppressed in adipose tissue in fasting, so fat is no longer being laid down.
- Insulin
- It promotes the storage of fat and inhibits hormone-sensitive lipase.
Exam traps
- Insulin does not release fat from adipose tissue, because insulin is the hormone of the fed state (after a meal) and promotes glucose uptake and the storage of fat. In fasting it falls.
- Lipoprotein lipase does not release stored fat. It takes fatty acids out of passing lipoproteins so that fat can be stored, and in fasting its activity in adipose tissue is suppressed.
- Adrenaline does help to mobilise fat, but a change that raises glycerol-3-phosphate in adipocytes still favours storage, because adipocytes need it to rebuild triacylglycerol.
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