TLDR: Forced lipolysis gives weight reduction and elevates FFAs that cause insulin resistance. Forced adipocyte distension causes obesity with secondary FFA release leading to worse insulin resistance even. Well, I got a full-text copy (thanks again to Mike Eades) of the acipimox in mice under intermittent hypoxia study. It’s an extremely strange paper. But some aspects are acquired by it that I find interesting. They took groups of mice and kept them in a chamber for 14 days which either exposed these to severe intermittent hypoxia or no intermittent hypoxia.
With or without acipimox. Intermittent hypoxia induces weight reduction mediated via the sympathoadrenal system. The mice began at 24.8g and finished up two weeks at 22 later.6g. The increased lipolysis elevated free fatty acids and impaired blood sugar tolerance. This is simple and is exactly what you might expect pretty. These mice (still black circles) lived in the same apparatus, were exposed to IH but do drink acipimox for two weeks never.
3. That is very glucose intolerant. I have no idea what happened to their weight because the paper doesn’t say. But you are not getting the weights. I am suspicious that the weight gains were such that stating them would have demanded a debate of exactly why they happened. So a combination to be in the equipment and taking in acipimox made the mice fats enough to mangle their glucose tolerance.
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The group also treated a set of mice with acipimox without placing them in the apparatus. Just remaining them in routine cages with or without acipimox. No problems with putting on weight or glucose tolerance. BTW Simply for fun here is the effect of injecting exogenous insulin into those fat mice after fourteen days on acipimox under control chamber conditions. Insulin does nothing. I believe very insulin resistant is an acceptable description. Just what exactly is it possible to take from the paper away? They have a quirky finding. A “That’s unusual” moment. A bit like Sauer discovering that placing a rat directly into starvation allows its xenografted cancer to develop like wildfire.
But, unlike Sauer, they’ve just stepped round it and pretended it was unimportant. Their core finding, that inappropriately elevated free fatty acids (especially after acipimox) result in blood sugar intolerance and insulin level of resistance, hits me as very important. Lowering FFA with acipimox acutely (1-2 days) goes quite a distance to ameliorating metabolic symptoms (acutely), a lot of studies on this. There is a significant role for FFAs in metabolic syndrome, related to adipocyte distention/dysfunction generally.
It’s not all of metabolic syndrome, but a big chunk. So from here I wandered around other causes for raised FFAs. Late additional thought: IH mice are thin and have elevated FFAs credited to sympathetic nervous system activation. Their adipocytes are half clear, like an individual on amphetamines or crystal meth.