synaptic cleft? nuerotransmitters and being hungry?

Question

im doing research on xenical and meridia( weight loss pills) how does the 3 work?

Answer 1

Xenical (orlistat) doesn't really effect neurotransmitter. It works by inhibiting the absorption of fats. It does this by inhibiting an enzyme called pancreatic lipase; this enzyme normally breaks fats down into fatty acids, which can be absorbed by the intestines. No lipase, fat absorption (that's why people on xenical can't eat lots of fat, if they do, they have fatty liquid faeces).

Meridia (Sibutramine) is a different matter. It does work on the brain, actually reducing hunger. It works by blocking the reuptake of the neurotransmitters serotonin and noradrenaline (AKA norephinephrine). These neurotransmitters are released by neurons that project from the brainstem into the rest of the brain. Once the neurotransmitters are released (not into a true synaptic cleft, but more into the interstial/extracellular fluid), they are removed by uptake by molecular transporters.

By inhibiting these transporters, meridia increases the levels of noradrenaline and serotonin in the brain. How these neurotransmitters then effect the neurons that produce the sensation of hunger is not really understood, but importantly, somehow noradrenaline and serotonin reduce hunger.

It is believed that an area of the brain called the hypothalamus is very important in controlled both energy intake and energy expenditure in the body. There are a huge number of neurotransmitters that somehow modify this pathway, but the exact roles they all play is elusive. Important neurotransmitters in this pathway are ghrelin (a protein released by the stomach that increases hunger), Obestatin (which works as the inhibitor of ghrelin), leptin (produced by fat cells, inhibits hunger, animals with no leptin become massively obsese). Actually the list goes on and on; neuropeptide Y, agouti related peptide, melanocyte stimulating hormone, histamine orexin.......

It's very complicated.