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This new study looked at something new, although I'm surprised it's not something that's been studied extensively in the past. In this study, the researchers sought to determine if exposure to cold can influence the "browning" of WAT. Previous studies have shown that activity of brown fat is increased by a cold environment (activity of brown fat follows a cyclical pattern, reaching a high in winter when exposed to cold temperatures), while little is known of the response of WAT to the cold.
To study this, the researchers examined both abdominal and thigh subcutaneous WAT from 71 subjects who were biopsied in the summer or winter, and adipose expression was assessed after an acute cold stimulus applied to the thigh of physically active young subjects.
Results showed that in winter, UCP1 and PGC1α mRNA were increased 4 to 10-fold, and 1.5 to 2-fold, respectively; along with beige adipose markers, and UCP1 protein was 3-fold higher in the winter.
If you're not a subscriber or haven't read my book, and you're hearing UCP1 for the first time, let me explain. UCP1 stands for uncoupling protein type 1, and it's highly expressed in brown fat. What this protein does, is that it takes the stored potential energy in the mitochondria, and instead of converting it to chemical energy (as ATP, which is in the case of most other tissues), UCP1 takes that stored potential energy and converts it to heat. Those who've read my book may remember this is the basis behind the evolution of warm-bloodedness.
The benefit of this to obesity and weight loss is that now we can use up that stored energy and burn it off as heat. Similarly, too much stored energy when demand is low (as in a sedentary person), can cause weight gain, but also the production of toxic free-radicals in the mitochondria, which doesn't usually end well for us. Having sufficient amounts of brown fat is said to be protective of obesity and a host of other degenerative health conditions (like diabetes).
Now back to this study's results... what was interesting here was that the seasonal increase in abdominal WAT UCP1 mRNA was considerably diminished in overweight subjects (BMI > 30), suggesting that dysfunctional WAT in obesity inhibits adipose thermogenesis.
After applying an acute cold stimulus to the thigh of subjects for 30 min, PGC1α and UCP1 mRNA was stimulated 2.7-fold (p < 0.05) and 1.9-fold, respectively. Presence of an inflammatory compound, however, was shown to inhibit this response (meaning chronic inflammation blunts the positive changes seen in WAT and BAT upon cold exposure).
So this study has confirmed what I would have guessed was already known--that WAT increases thermogenic genes both seasonally and acutely in response to a cold stimulus. A couple interesting points, however, are that this browning of WAT is inhibited by obesity and inflammation.
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Source: The effects of temperature and seasons on subcutaneous white adipose tissue inhumans: evidence for thermogenic gene induction.
Other related posts on brown fat: