Tuesday, 13 August 2013

New model for carbohydrate sensitive obesity

The carbohydrate sensitive rat as a model of obesity.    ( link here aswell )

To sum up, these guys have been working on a new model of obesity that can be induced by high-carbohyrate diets, as opposed to be bog standard high-fat diets researchers use to induce obesity in rodents. The important point here is its a model. This is EXACTLY what science is. Scientists create models in an attempt to imitate and predict the real world.

The study is already short and direct to the point so its not worth me paraphrasing it ( its free full text at moment so read it you lazy bums! ) however still I want to highlight a few key points.

The first point is that, not all rats exhibit the same propensity to develop obesity on either the high-fat or the high-carb diet. I.E. some rats just DONT get fat. This is good news for the model because this is what we have observed in humans. Some humans are clearly obesity resistant. While others are quite clearly highly prone to obesity.

BMR and TEF values did not correlate to adiposity gain during either HCD or HFD. Otherwise stated, rats with a low BMR and/or a low TEF did not exhibit any greater propensity to become obese than rats with a high BMR or TEF.

Having a higher energy expenditure does not mean you are less likely to become obese. sucks for CICO. Everytime you here someone say "he/she doesnt gain weight because they have a high metabolism", just think to yourself, thats rubbish!
Considering RQ, no relationship was observed between adiposity gain and Activity-RQ, indicating no link between substrate utilization by muscles and propensity to adiposity.

SO in this model, the fuel you burn during exercise doesnt seem to predict your obesity prone-ness

Now heres the punchline, the strongest predictor of being sensitive to carbohydrate induced obesity the researchers found was your respiratory quotient in the postprandial state.

 In general, the Rest-RQ response increased above High-Carb-Diet food quotient (FQ; 0.955) only in Carb-sensitive rats (Figure S5) which means that during this period, the proportion of fat used to fuel energy metabolism was less than the proportion of fat in the meal and was significantly higher than in CR rats between 120 and 180 minutes after ingestion of the meal.
Calculation of resting glucose and lipid oxidation (Rest-Gox and Rest-Lox) from Rest-RQ and REE showed that ingestion of the HC test-meal increased Rest-Gox and decreased Rest-Lox significantly more in CS rats

So, in this model of obesity, ( which may or may not accurately reflect human obesity ), it is the postprandial handling of the nutrients that determines if you become fat or not. ( on high-carb diet only ) If you are carbohydrate-obesity-sensitive, then what happens is when you eat carbohydrate, fat oxidation is overly suppressed. Wonder why that is? Insulin hyper-secretion?

 in Carb-Sensitive rats, already under High-Carb diet since weaning (though chow rather than the high quality synthetic HCD used during this experiment), a defective post-prandial substrate partitioning characterized by a larger post-meal increase in Rest-Glucose-oxidation and a larger post-meal inhibition of Rest-Lipid-oxidation can be considered as potentially responsible for the larger adiposity gain.
Since this observation was made early in the life of the rats, this metabolic difference can be considered as a cause rather than a consequence of sensitivity to adiposity gain under HCD 

Whoa, it almost looks like the researchers are saying that ( in this model ), your propensity to become obese on a high-carb diet is determined from birth, possibly through genetic/epigenetic factors I might guess?

This rings so painfully true for me because I was fat right from a very young age and I was raised on a high-carbohydrate diet. Lowcarb will unfortunately probably have to be a lifelong thing for me if I want to keep my weight down.


  1. If " the postprandial handling of the nutrients that determines if you become fat or not" then eating fewer meals a day could also make a difference .

    1. I dont think it would make any difference

    2. I guess the postprandial response doesn't last longer than 4 hours, so if somebody eats like Kitovans once a day, while being carb-sensitive, it would be less fattening than snacking through the day.

  2. what a great find, Kindke -- fascinating possibilities open up!

  3. Kindke this was fabulous.

    Depressed lipid oxidation in the near postprandial phase is exactly the same defect found in obesity sensitive humans, and this explains the near universal palliative effect of a low carb diet.

    Metabolic rate has zero relationship to proneness to body fat anabolism. It is entirely possible to have a very high metabolic rate and build body fat , or to have a very low metabolic rate and also preferentially build body fat. THe metabolic rate is independent of body fat proneness other than to say a low metabolic rate may be a sign of neuroendocrine or mitochondrial disorder that heralds body fat gain as a symptom... for example myopathy or thyroidal illness or severe IR, will usually have low metabolic rate due to metabolic disorder but also body fat gain in lieu of other tissues.

    My favorite example is pregnant female; her metabolic rate is much higher than baseline because of progesterone as well as growing fetus, but her body is driven to very specifically grow/store body fat. It is the normal effects of pregnancy.

    In practice, what "CICO" people are advising is "starve yourself until you become so energy deficient even the most body fat anabolic metabolism is forced to catabolize fat tissue". This is precisely what CICO advocates encourage with stuff like "reduce calories by x amount until you drop weight; if you aren't losing weight its because you arent in a caloric deficit; we all have different metabolisms so just cut back from your baseline until you see progress".

    1. Yes, pregnant and breastfeeding females are the perfect examples of hormone importance for one's weight.

  4. Great post, Kindke.
    Chris Gardner's work in humans is tangentially similar to this - he showed, among other things, how insulin resistance and insulin secretion interact with various diet-induced weight loss interventions (not exactly groundbreaking, but he spells it out very clearly). I tried to summarize a lot of the stuff he discussed in a blog post (http://caloriesproper.com/?p=2172), but here is a review he wrote in case you're interested: http://www.nature.com/ijosup/journal/v2/n1s/abs/ijosup20124a.html.

  5. I always love your posts Kindke :)