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.The researchershave suggested that properly timed bromocriptine dosing actually redirects theirmetabolism to one of lean animals (46).Now, if this doesn t sound like some of theinformation on leptin I ve presented, you really haven t been paying attention.Theultimate point is that, whatever mechanisms are involved, bromocriptine is working atthe brain to correct a lot of deficits elsewhere in the body, deficits similar to the ones seen with low leptin or leptin resistance.This includes not only metabolic defectsinvolved in metabolism and fat burning, but also those involved in the insulinresistance syndrome, diabetes, and calorie partitioning.While humans don t appear to be as sensitive to changing amounts of light,there is evidence that some of the same biological mechanisms are still operating(42,47).It may be that we lost those adaptations somewhere during our evolution orwe simply don t observe it to as great a degree in our modern environment.Undermost circumstances, humans don t go through the major parts of the annual light/darkcycles, because of our reliance on artificial lighting.I suspect that the same biology ispresent in humans, but we don t really see it because of the changes in ourenvironment.Now, so far I haven t really presented much to support the idea that what sgoing on in the Syrian hamster is operating in humans.It would make sense, mindyou, based on our evolutionary past, but the data just really isn t there, not in terms ofresearch on the brain.And while people typically get fatter in the winter, and leaner inthe summer, it s hard to distinguish changes in our physiology from changes in ourbehavior.During the winter, most people eat more and tend to be less active, whichwe would expect to cause fat gain; during the summer, we want to look better in abathing suit and get back in the gym and start eating more healthily.You can tconclude it s all from changes in physiology, because behavior patterns can be justas (or more) important.This is all sort of tangential to the point of this section anyhow.The point I reallywant to make here is that there are characteristic alterations in brain chemistry thatare involved in changes insulin sensitivity/resistance as well as the metabolicconsequences of those changes.The Syrian hamster goes through those changesseasonally, making it relatively easy to study.If you recall the data on both the OBand DB mice, these same changes in overall physiology also are associated withlow/no leptin levels (OB mouse), or leptin resistance (DB mouse).In all threemodels, correcting the neurobiological defects (in this case, with bromocriptine) fixesthe other problems as well.So, with that said, let s look at the rest of the metabolic effects of bromocriptine. Effects on animals: other metabolic effectsIn addition to its effects on bodyfat levels, researchers have examined othermetabolic effects of bromocriptine in animal models.I already mentioned one or twoof these effects above, mentioning bromocriptine lowers both total cholesterol andtriglyceride levels in most animal models (33).That observation alone, a change inboth cholesterol and triglyceride levels, suggests an overall change in the animal s fatmetabolism.Liver metabolism of cholesterol, as well as changes in liver productionof triglycerides (or the body s utilization or both) would both explain these results.These changes would also be consistent with improvements in insulin sensitivity forcomplex reasons that aren t that important for this booklet.However, the early research isn t quite as exciting as some of the more recentstuff.I already bored you to death with the different animal models of obesity and I mgoing to be referring back to one of them in this section: the OB mouse.To refreshyour memory, OB mice produce no leptin and their brains basically always think thatthey re starving to death.Because of this, the OB mouse show a significantlydecreased metabolic rate and fat burning, as well as severe hunger and increasedbodyfat deposition.Similar to the DB (diabetic) mice, the OB mice also have super high insulin,blood glucose, blood free fatty acid, blood cholesterol, and blood triglyceride levels.Like the DB mouse, they are insulin resistant.To reiterate, the OB mouse isn t really agood example of human obesity, since only one or two humans have been found wholack leptin completely.However, recall that the effects of no leptin are at least similarto what happens in the case of either low leptin (due to low bodyfat levels and dieting)or leptin resistance.In all cases, the brain receives a diminished leptin signal.Sostudies of the OB mouse can be informative [ Pobierz całość w formacie PDF ]
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.The researchershave suggested that properly timed bromocriptine dosing actually redirects theirmetabolism to one of lean animals (46).Now, if this doesn t sound like some of theinformation on leptin I ve presented, you really haven t been paying attention.Theultimate point is that, whatever mechanisms are involved, bromocriptine is working atthe brain to correct a lot of deficits elsewhere in the body, deficits similar to the ones seen with low leptin or leptin resistance.This includes not only metabolic defectsinvolved in metabolism and fat burning, but also those involved in the insulinresistance syndrome, diabetes, and calorie partitioning.While humans don t appear to be as sensitive to changing amounts of light,there is evidence that some of the same biological mechanisms are still operating(42,47).It may be that we lost those adaptations somewhere during our evolution orwe simply don t observe it to as great a degree in our modern environment.Undermost circumstances, humans don t go through the major parts of the annual light/darkcycles, because of our reliance on artificial lighting.I suspect that the same biology ispresent in humans, but we don t really see it because of the changes in ourenvironment.Now, so far I haven t really presented much to support the idea that what sgoing on in the Syrian hamster is operating in humans.It would make sense, mindyou, based on our evolutionary past, but the data just really isn t there, not in terms ofresearch on the brain.And while people typically get fatter in the winter, and leaner inthe summer, it s hard to distinguish changes in our physiology from changes in ourbehavior.During the winter, most people eat more and tend to be less active, whichwe would expect to cause fat gain; during the summer, we want to look better in abathing suit and get back in the gym and start eating more healthily.You can tconclude it s all from changes in physiology, because behavior patterns can be justas (or more) important.This is all sort of tangential to the point of this section anyhow.The point I reallywant to make here is that there are characteristic alterations in brain chemistry thatare involved in changes insulin sensitivity/resistance as well as the metabolicconsequences of those changes.The Syrian hamster goes through those changesseasonally, making it relatively easy to study.If you recall the data on both the OBand DB mice, these same changes in overall physiology also are associated withlow/no leptin levels (OB mouse), or leptin resistance (DB mouse).In all threemodels, correcting the neurobiological defects (in this case, with bromocriptine) fixesthe other problems as well.So, with that said, let s look at the rest of the metabolic effects of bromocriptine. Effects on animals: other metabolic effectsIn addition to its effects on bodyfat levels, researchers have examined othermetabolic effects of bromocriptine in animal models.I already mentioned one or twoof these effects above, mentioning bromocriptine lowers both total cholesterol andtriglyceride levels in most animal models (33).That observation alone, a change inboth cholesterol and triglyceride levels, suggests an overall change in the animal s fatmetabolism.Liver metabolism of cholesterol, as well as changes in liver productionof triglycerides (or the body s utilization or both) would both explain these results.These changes would also be consistent with improvements in insulin sensitivity forcomplex reasons that aren t that important for this booklet.However, the early research isn t quite as exciting as some of the more recentstuff.I already bored you to death with the different animal models of obesity and I mgoing to be referring back to one of them in this section: the OB mouse.To refreshyour memory, OB mice produce no leptin and their brains basically always think thatthey re starving to death.Because of this, the OB mouse show a significantlydecreased metabolic rate and fat burning, as well as severe hunger and increasedbodyfat deposition.Similar to the DB (diabetic) mice, the OB mice also have super high insulin,blood glucose, blood free fatty acid, blood cholesterol, and blood triglyceride levels.Like the DB mouse, they are insulin resistant.To reiterate, the OB mouse isn t really agood example of human obesity, since only one or two humans have been found wholack leptin completely.However, recall that the effects of no leptin are at least similarto what happens in the case of either low leptin (due to low bodyfat levels and dieting)or leptin resistance.In all cases, the brain receives a diminished leptin signal.Sostudies of the OB mouse can be informative [ Pobierz całość w formacie PDF ]