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Thursday, October 6, 2011

Fat Metabolism in Formerly Obese Women: Part III Energy Expended During Exercise

Continuing on from Part I and Part II:

Fat metabolism in formerly obese women
Ranneries,  AJP-Endo, 1998.

Overview:  An impaired fat oxidation has been implicated to play a role in the etiology of obesity, but it is unclear to what extent impaired fat mobilization from adipose tissue or oxidation of fat is responsible. The present study aimed to examine fat mobilization from adipose tissue and whole body fat oxidation stimulated by exercise in seven formerly obese women (FO) and eight matched controls (C).  They measured:
  • Lipolysis in the periumbilical subcutaneous adipose tissue 
  • Whole body energy expenditure (EE) 
  • Substrate oxidation rates (glucose, fatty acids) 
  • glycerol release (fat mobilization)
When obese, the FO subjects had body weights in excess of 120% normal weight.  They followed a conventional CRD to lose the weight and were weight stable for at least 2 months at 110% normal weight.  So weight losses were in excess of 10% bw and ranged from 15-20kg (33-44 lbs).    The FO & C groups were well matched as seen in Table 1.

So the subjects were fasted overnight, and had not engaged in strenuous activity for three days prior to the study.  They "sat quietly" for 15 minutes prior to the baseline measurement, and then exercised (cycle) at 50% VO2,max  for 60 minutes.  Measurements were taken every 15 minutes, with the last one at 75 minutes = 15 minutes after exercise stopped

The results are shown below: {click image to enlarge further, or click here to view table online}

In Part I it was noted that the resting REE was 23% less for the FO vs. C group and when I did the 24 calculation for basal metabolism this amounted to almost 400 calorie/day less!  In Part II the relative oxidations of carbs vs. fats were discussed, with the controls getting almost 80% from fatty acids and less than 10% from carb.  This was in stark contrast to the FO getting almost 50% from carb and under 35% from fat.  But moving to the exercise portion and we see two things:
  1. The slightly lower energy expenditure is on the order of the differences in REE's -- In other words the FO burn about the same amount less all day.
  2. The plot at right shows even more vividly how the "metabolism" during activity is indistinguishable between the groups.
Furthermore when they measured glycerol (a measure of fat released from stores), they saw no difference.  The authors conclude: 

... fat mobilization both at rest and during exercise is intact in FO, whereas fat oxidation is subnormal despite higher circulation NEFA levels. The lower resting EE and the failure to use fat as fuel contribute to a positive fat balance and weight gain in FO subjects.
I have a quibble with the last part of that statement, as the so-called "failure to use fat as fuel" disappeared with activity while the slight differential in energy expenditure persisted.  Furthermore, if the mitochondria were somehow dysfunctional, the dysfunction should have been more manifest during activity when the mitochondria are being called upon to perform even more lipid oxidation.

Therefore, I don't see this study demonstrating mitochondrial dysfunction, rather that the reduced state seems to alter substrate usage (at least temporarily as discussed in Part II) at rest.  That this was accompanied by substantially lower insulin levels vs. controls puzzles me.

I've come across a couple of other interesting things on metabolism in FO.  So I'll be adding at least one more part to this series when I get a chance.


Duffy Pratt said...

I have to wonder where this is going. The formerly obese burn more carbs than fat compared with those who were not formerly obese. What is the practical implication? If calorie in/calorie out remains true, what difference does this make? When overeating, the source of the fat that people store will vary somewhat. When undereating, there might be different mechanisms that should, I would think, lead to the same end result. I think I must be missing something about this.

Lucas Tafur said...

Hi Evelyn,

Maybe the problem is not with mitochondrial dysfunction, but with altered levels of proteins mediating the glucose-fatty acid cycle.

The key elements which come to my mind are AMPK and malonyl CoA, both which are affected by exercise. High malonyl CoA and ACC, and low MCD, plus a low basal level of AMPK would shift the balance towards glucose oxidation.

Exercise increases AMPK and MCD, which reduces ACC and malonyl CoA levels. This fits nicely with the observed patterns of oxidation in this study.

Sue said...

The study shows the importance of FO exercising during maintenance.

Evelyn aka CarbSane said...

Yep Sue! If there's any advantage to "fat burning" then it was shown here that when active, the FO were indistinguishable from the controls.

@Duffy, I wrote in Part I some of the impetus for this. I do not believe that the results of this study demonstrate either the hypothesis du jour (broken metabolism, dysfunctional mitochondria) nor does the differential substrate use at rest really concern me. It is interesting that they had such low insulin though (vs. controls) yet weren't even greater fat burners as a result. I think this is more indicative of long-term underfeeding from a surplus state.

Interesting Lucas. Malonyl CoA is implicated in IR but then this makes the lower insulin levels in FO (generally indicating better insulin sensitivity) even more befuddling.

Tsimblist said...

Maybe it is not the skeletal muscle that is skewing the resting numbers?

This article makes it sound like there are other significant components of resting metabolism:
The Myth about Muscle and Metabolism

Tsimblist said...

The following is from @bently (see

Sorry blogger doesn't like me the past few days and evaporates my posts but wanted to ask if this is possible ...

Hmmm, interesting. I wonder if this has anything to do with the twichoo or "X-factor" of low carb relief from elevated appetite.

Pure speculation of course but if the fat metabolism has some sort of impairment with the body strongly favoring glucose metabolism what happens when you run out of glucose but still have considerable body fat needed to be tapped for fuel?

Obviously the insulin hypothesis has been shot full of holes but it does seem that there is some credible evidence that endocrine derangement of SOME sort is involved. Am I misreading?

Tsimblist said...

Correction: The above post is from @bentley.

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