Thursday 3 April 2014

Fat has the power to make you slim

Or rather, your adipose tissue does. No need for all that hogwash nonsense about BAT ( brown adipose tissue ) because it seems white adipose tissue is more than capable of  keeping you lean, provided it just gets the correct signal.

A less well known fact about leptin is that leptin receptors are present on the adipocytes themselves and leptin functions within paracrine loop ( link ). No need for leptin resistance in the brain, because leptin resistance at the level of the adipocyte is enough to cause metabolic derangement ( link )

You have to look at this study to really appreciate the power of leptin. Apparently, if you infect the liver with a virus that codes for the leptin gene such that the liver now secretes its own leptin, this leptin acts directly on adipocytes and causes them to completely oxidize all their contents within as little as 7 days.

The implication here is that there is no need to calorie restrict or exercise like a maniac to lose weight, you just need your leptin to be working (properly), and then the adipocyte itself is more than capable of regulating its own size. The novelty of this information is that the adipocytes themselves can massively increase their energy expenditure to keep you slim, the fats do not need to be released into circulation and used up by other tissues, which is what happens if you lower insulin.



Further, the hyperleptinemia induced by the liver-derived leptin did not increase hunger of the rats, even with a severe loss of bodyfat and massive energy expenditure increase, indicating once again that biology and body weight regulation is all about communication, not calories.

With this in mind aswell as what we know about leptin signalling in the brain it would be very easy to blame obesity on "leptin resistance" since clearly leptin is suppose to function within a negative feedback loop to keep bodyweight stable.








3 comments:

  1. fascinating stuff, Kindke! i would guess that Wooo's hypoleptinemia, then, is liver-based -- we know she has problems with gluconeogenesis at the liver, too....

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  2. I was thinking that, too. But was it genetic liver issues or did she damage her liver with the wonderful whole grain goodness of the SAD????

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  3. I bet some pharma companies are working on orally active, small molecule leptin receptor agonists.

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