Nicotine and leptin levels

[JJFigure]

I've come across a few references to nicotine's ability to raise leptin levels, and the guys over at Avant Labs have played with this theory as well, with anectdotal success.

I know MS has a theory that Nolvadex will boost leptin levels in a very lean woman; has anyone looked at using a short cycle of nicotine to boost leptin levels? By nicotine, I'm talking gum, patches, or lozenges, not the tar based type.

 

[MS]

Nicotine may assist when getting down to or maintaining low bodyfat levels, similar to WellButrin or bromocriptine. It is still debateable whether or not this is leptin mediated (the research is conflicting), or related to changes in uncoupling protein expression, or changes in other appetite related gene systems (or all of the above).

Of course you wouldn't want to get your nicotine by smoking it! And remember that nicotine is addictive....

 

[JJFigure]

I was hoping you'd jump on this, MS. Do you know of anyone who's tried it?

Could this be one of the reasons people who quit smoking put on weight relatively quickly? Ignoring the fact they may be substituting food for cigs.

 

[JJFigure]

I want to expand on my second question - I have a friend who quit smoking for Lent and hasn't started up again (due to my nagging - he says he got rid of the God pressure but now he's got me pressuring him). Anyway, he's putting on weight hand over fist; mainly because his appetite is out of control. Is it the impact of nicotine on leptin causing his appetite to increase (leptin levels are raising without nicotine), or just lack of nicotine?

 

[MS]

I don't know anyone who's tried it for BB dieting purposes. As I alluded, there is sketchy and conflicting evidence that nicotine actually increases leptin levels in humans. However it may be that nicotine somehow increases the sensitivity of leptin receptors, or assists with uptake of leptin into the brain, or maybe even increases recycling of leptin. This is all speculation on my part. However it does not appear to directly increase circulating leptin levels, but it does increase mRNA transcripts for a mitochondrial uncoupling protein called UCP1.

 

[slinky]

I remember a report that stated that smoking cigarettes does not necessarily keep the weight off. They observed several test subjects that had quit smoking and noticed, on average, 5lb gain. I've got to find that. It's been awhile, but was very interesting.

JJ, what is the behaviour pattern of this friend? Is he rather obsessive compulsive? I just believe that you're right in that most people who smoke are "substituting food for cigs."

However that, a good friend of mine has written a article on leptin/diet. I'll see if he'll let me post it here, if anyones interested. It's been published in a issue of MM, btw.

 

[JJFigure]

He is rather obsessive compulsive. And naturally, he just went cold turkey when he quit smoking. I thought, if this were a leptin issue, he could cycle in a little Nicorette to help get his appetite under control, and then wean off the Nicorette. Of course, that may just be fighting fire with fire. It would probably be better just to have him try some EC to try and control his appetite.

I'd be interested to see your friend's article.

 

[valerie]

Hey JJ I had been reading on this too. Thanks for bringing it up-valerie

 

[JJFigure]

According to this study, adding nicotine wouldn't help increase my friend's leptin levels to normal levels, since with the added bodyfat, they're probably already increasing on their own (duh, didn't think of that):

Leptin levels in smokers and long-term users of nicotine gum.

Eliasson B, Smith U.

Lundberg Laboratory for Diabetes Research, Sahlgrenska University Hospital, Goteborg, Sweden. [email protected]

BACKGROUND: The aim of this study was to examine the effects of cigarette smoking and other forms of long-term nicotine consumption on circulating leptin levels as well as the relationship between leptin levels and insulin sensitivity, measured with the euglycaemic hyperinsulinaemic clamp, in healthy middle-aged men. STUDY DESIGN: Samples from 73 subjects were analysed: 23 non-smokers, 31 smokers and 19 long-term nicotine gum chewers (NGCs) with similar ranges of age, body mass index (BMI) and per cent body fat. RESULTS: Leptin levels were higher in NGCs and smokers than in the non-smoking matched control subjects. Smoking cessation for 8 weeks further increased the leptin levels, probably due to the concomitant increase in body fat (mean +/- SD, 2.2 +/- 1.8 kg). Acute administration of one dose of nicotine nasal spray or smoking one cigarette did not significantly change the circulating leptin levels during the following 60 min. Plasma leptin concentrations were positively correlated with the proportion of body fat and negatively correlated with the degree of insulin sensitivity in each of the three subject groups. In a stepwise multiple linear regression analysis, plasma leptin concentrations were significantly correlated with the proportion of body fat, degree of insulin sensitivity and smoking status. CONCLUSION: These data show that long-term use of nicotine is associated with elevated circulating leptin levels. The increased leptin levels may be an important reason for the lower body weight in smokers. The results of this study also support the view that leptin is directly or indirectly related to insulin sensitivity in men.

 

[JJFigure]

But here's another interesting study on how nicotine may stimulate lipolysis:

Systemic nicotine stimulates human adipose tissue lipolysis through local cholinergic and catecholaminergic receptors

K Andersson and P Arner

Departments of Medicine and Research Center, Huddinge Hospital, Karolinska Institute, Huddinge, Sweden


Correspondence to: P Arner, Center for Metabolism and Endocrinology, M63, Huddinge University Hospital, S-141 86 Stockholm, Sweden. E-mail: [email protected]


Abstract

OBJECTIVE: To evaluate whether the lipolytic effects of systemic nicotine are not only attributed to indirect adrenergic mechanisms, but also to a direct action of nicotine on fat cells.

DESIGN: The effect of a systemic nicotine infusion (0.5 µg/kg/min for 30 min) on lipolysis in subcutaneous adipose tissue was investigated in situ in 11 non-obese, non-smoking, healthy male subjects under placebo-controlled conditions.

MEASUREMENTS: By using microdialysis probes the glycerol levels (lipolysis index) and blood flow were monitored locally in subcutaneous adipose tissue.

RESULTS: Plasma nicotine levels peaked (7.2 ng/ml) at the end of the infusion. Nicotine induced a mean (±s.e.) percentage peak increase in adrenaline and noradrenaline plasma levels of 213±30% (P<0.01) and 118±5% (P<0.05), respectively. Nicotine increased venous plasma glycerol levels by 144±9% (P<0.001), arterialized plasma glycerol levels by 148±12% (P<0.001) and adipose glycerol levels by 148±16% (P<0.001), but did not alter blood flow. By inducing a local cholinoceptor blockade with mecamylamine (10-5 M) via the microdialysis system, the increase in adipose glycerol levels was inhibited by ~45% (P=0.02). A corresponding local beta-adrenoceptor blockade with propranolol (10-4 M), inhibited the increase in adipose glycerol levels by ~60% (P=0.02). Infusion of saline (ie placebo) had no effect on the parameters mentioned above.

CONCLUSION: Systemically administered nicotine induces lipolysis, in part by activating the classical adrenergic mechanism (mediated by a nicotine-induced release of catecholamines stimulating beta-adrenoceptors), and in part by directly activating a nicotinic cholinergic lipolytic receptor located in adipose tissue.

International Journal of Obesity (2001) 25, 1225-1232

Here's the website, if you want to read the whole thing:

http://www.nature.com/cgi-taf/DynaPage.taf?file=/ijo/journal/v25/n8/full/0801654a.html