Fat Metabolism in Formerly Obese Women: Part II Resting Substrate Usage

Continuing the discussion from Part I

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

In this part I wish to address the respiratory quotient, RQ.  The RQ is a measure of the relative amounts of energy derived from glucose oxidation vs. fatty acid oxidation.  

To recap the subjects of this study, when obese, the FO (formerly obese) 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 which is all I'm going to discuss here.  The results "cropped" for just the resting substrate use are shown in the table at right {as always, click to enlarge}.  Now this is quite dramatic!  As a percentage, controls utilized less than 10% carbs and almost 80% from fat, while the formerly obese utilized almost 50% from carbs and only about 35% from fat.  This is a rather startling difference.  

The resting RQ was significantly higher in FO (0.849 ± 0.07) vs. the controls (0.742 ± 0.015).   The authors point out that the elevated NEFA (988 vs. 704 μM) and lower insulin levels (34.4 vs. 69.0 pM) in the FO might indicate a persisting negative energy balance, but note that underfeeding generally reduces RQ which was the opposite of what was observed.  

Thus the authors conclude:

Despite higher circulating levels of NEFA, the FO had lower fat oxidation during rest ... and the difference in fat oxidation was more pronounced when we adjusted for differences in plasma NEFA concentrations. Therefore, the study suggests that the major cause of the lower fat oxidation in FO may be an impaired skeletal muscle uptake and/or oxidation of fatty acids.

I'm going to discuss the exercise portion of this separately in Part III, but it bears pointing out that there were no differences in substrate usage during exercise.  However, these subjects apparently had no impaired fatty acid uptake or oxidation in the exercised state -- when required rates to sustain activity were much higher.  So  why would the impairment manifest itself only at rest?  Still, if there's something to the FO burning more carbs at rest, and they appear to be more insulin sensitive (as demonstrated by reduced insulin levels), I don't get the logic of eating a VLC/HF diet as some means to "repair" things.  Fire up the engines and the substrate utilization differences disappeared.

I found another paper looking at the formerly obese.  This time from the National Weight Control Registry.  Here, the 40 FO's (including 7 men) had maintained at least the minimum weight loss to qualify (30 lbs) for one year, and the average maintenance was almost 10 years.  What they found is shown in the table at right.  No significant differences!

Whatever effect Ranneries et.al. saw after 2 months seems to have almost entirely disappeared by 1 year and beyond.   So ... do the obese have broken metabolisms that are retained even with weight loss??

There's one other thing that bothers me about this whole notion of mitochondrial function.  The only difference between energy derived from glucose and fatty acids as far as the mitochondria are concerned is that most of glycolysis occurs outside the mitochondria.  Pyruvate dehydrogenase is associated with the mitochondria and converts the pyruvate into acetyl CoA.  The very same acetyl CoA that is produced by the oxidation of fatty acids within the mitochondria.  Your mitochondria don't really function any differently from this point on -- acetyl CoA feeds into the Krebs cycle and the reducing equivalents feed into the very same electron transport chain (ETC).  Many of the mitochondrial dysfunction studies I've seen deal with the ETC so something just doesn't quite sit right when I see these associated with lipid oxidation alone.  Just thinking out loud ...

In Part III I'll address the exercise portion of the Ranneries study.