It looks like you're using an Ad Blocker.
Please white-list or disable AboveTopSecret.com in your ad-blocking tool.
Thank you.
Some features of ATS will be disabled while you continue to use an ad-blocker.
•Smoking burns up to 200 calories a day in a heavy smoker
•Because smoking burns calories, metabolism is boosted (increased) slightly
•Nicotine is an appetite suppressant
These studies examined the cellular mechanisms for lower adiposity seen with nicotine ingestion. Rats were infused with nicotine or saline for 1 wk and adipocytes isolated from epididymal fat pads. Nicotine-infused rats gained 37% less weight and had 21% smaller fat pads. Basal lipolysis was 78% higher, whereas the maximal lipolytic response to isoproterenol was blunted in adipocytes from nicotine-infused rats. The antilipolytic actions of adenosine and the levels of serum catecholamines were unaffected by nicotine. The nicotine-induced alteration in lipolysis was not associated with any changes in hormone-sensitive lipase. Nicotine caused a 30% decrease in lipoprotein lipase (LPL) activity, without any changes in LPL mass or mRNA levels, in epididymal fat in the fed state. In contrast, LPL activity, mass, and mRNA levels in heart were increased by nicotine whether animals were fed or fasted.
These studies provide evidence for multiple mechanistic events underlying nicotine-induced alterations in weight and suggest that nicotine diverts fat storage away from adipose tissue and toward utilization by muscle.
Nicotine was injected intraperitoneally to rats and 2 h later lipoprotein lipase was determined in isolated perfused hearts. There was a significant increase in heparin releasable lipoprotein lipase activity which represents the functional pool without increase in total enzyme activity. When 1 microliter/h of a solution of nicotine (120 mg/ml) was delivered for 3 days from subcutaneously implanted miniosmotic pumps, total lipoprotein lipase activity in the heart increased 1.5-3.0 fold. Endogenous lipoprotein lipase activity in plasma doubled and there was a significant fall in plasma triglyceride levels. The effect of nicotine on heart lipoprotein lipase activity was evident also after 6 days of continuous delivery and was accompanied by a fall in adipose tissue lipoprotein lipase activity. No effect was seen when the dose of nicotine was halved. A positive correlation was seen between plasma nicotine levels and heart lipoprotein lipase activity, while adipose tissue lipoprotein lipase correlated negatively with plasma nicotine levels. Chronic administration of nicotine was accompanied by either weight loss or diminished weight gain. It is concluded that in the rat the acute effect of nicotine on the shift of lipoprotein lipase to the functional pool could be related to enhanced beta-adrenergic stimulation. The chronic effect of nicotine could have been mediated by the loss in body weight, due to reduced caloric intake.
Adipose tissue lipoprotein lipase was studied in smokers (n= 17) aged 18–47 years and compared with enzyme activity in non-smokers of comparable age (n= 8) and a second time in some of the subjects 5–9 weeks after cessation of smoking (n= 7). Serum cotinine levels served to validate the smoking status of the subjects. Fasting enzyme activity was similar in smokers and non-smokers, when expressed per 106 cells, but was significantly increased when normalized for cell size. When lipoprotein lipase was determined in the same individual 4 h after an oral glucose load, a significant decrease (P< 0.002) occurred in the smokers, while enzyme activity rose in the non-smokers (P
Originally posted by Wyn Hawks
...really interesting stuff you posted though... give up carbs, huh?... does that include beer?... if it does, its an evil conspiracy...
...maybe nervousness causes folks to eat more when they stop smoking... they dont know what to do with their hands and, then, theres that oral need... sucking on a drinking straw helps if you can convince yourself that it does...