CLA Producing Bacteria, an Effective Alternative to Regular Supplements for Lean Individuals on Low(ish) Fat Bulks?

This is not a CLA supplementation study, but a study probing the effects of CLA-producing bacteria supplementation may explain the ambiguous results of previous CLA studies.

From previous SuppVersity articles on CLA you will remember that the real world benefits of CLA are by far not as earth-shatteringly impressive as the body-fat destructive effects that were reported in previous rodent studies would suggest.

Now, one reason that "your" CLA supplement did not work as promised is the isoform mix of commonly available supplements, where the cis-9, trans-11-conjugated linoleic acid content may actually hamper the fat burning effects of trans-10, cis-12-conjugated linoleic acid. This alone does yet probably not explain the very mixed results from previous CLA for fatloss studies. So, if it's not the "mix" that explains the ambiguity (learn more), what else could it be?

You can learn more about CLA at the SuppVersity

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Cis-9,11 o trans-10,12 Which to Take?

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If we put any faith into the results of a recent study from the College of Biological Sciences at the China Agricultural University in Beijing offers another explanation for the difference between mind-boggling weight loss and total failure that has been observed in human (and rodent studies).

To find out whether the degree of obesity and macronutrient composition of the diet would affect the efficacy of CLA the scientists did something very interesting: Instead of feeding the rodents CLA directly, they supplemented their diets with bacteria that would produce CLA in the tummy of the animals. More specifically, they used t10c12-producing recombinant food-grade Lactococcus lactis transformed with the pai isomerase gene. The protocol was inspired by previous studies by Lee et al. (2006 & 2007), in which the researchers observed a significant loss of body weight loss in C57BL/6J male mice that received native t10c12- and c9t11-CLA co-producing L. rhamnosus PL60 (Lee. 2006) or L. plantarum PL62 (Lee. 2007) during the period of diet-induced obesity (DIO).

What's the difference to regular CLA studies? Well, first of all, this is the first study to investigate the interactions between CLA, diet and body weight. More importantly, though, this study uses CLA producing bacteria, instead of regular CLA. The latter will transform dietary fatty acids to CLA and, more specifically, to the more powerful t10c12 isomer of CLA, which is only one of the two forms you will find in commercially available supplements, i.e. the form of CLA of which previous studies have shown that it is responsible for the fat-burning, but also the pro-diabetic and pro-fatty-liver effects CLA is hailed and dreaded for.

Since Rosberg-Cody et al. (2011) were unable to replicate the results in Balb/c male mice that received recombinant L. paracasei t10c12-producing NFBC338 during a maintenance period with normal-fat diets, the Li et al (2015) speculated that "the host dietary fat intake or obesity might influence the activity of t10c12-CLA in animals" (Li. 2015).

Figure 1: The scientists administered six different diets to their lab animals. Of these, only the PAI-75 diets contained CLA producing bacteria delivering 3mg of t10c-12 CLA per 3.9g and 26.3g of fat - not exactly much.

All in all, the study did have 6 different diets with two different baseline (normal and high fat) diets with and without CLA producing and placebo bacteria. These diets were then fed to three groups of animals:

"The mice were divided into three groups at random. (1) Lean mice were fed with a 4% normal-fat diet supplemented with PAI-75 (n = 28) or PAI-79 (n = 28) for 60 days; (2) obesity-induced mice were fed with a 26% high-fat diet containing PAI-75 (n = 16) or PAI-79 (n = 16) for 60 days to induce obesity; and (3) obese mice initially induced by a high-fat diet without bacterial supplementation were fed with a high-fat diet containing PAI-75 (n = 16) or PAI-79 (n = 16) for 50 days" (Li. 2015).

Considering the low amount of CLA in the diets, the effects the scientists observed in the lean mix were quite impressive. With only 0.1% of the total fat from CLA, the lean rodents showed a significantly reduced weight gain.

Figure 2: Weight development in lean mice on regular (low fat) chow, lean mice on HFD chow and obese mice with and without CLA producing bacteria in the chow (Li. 2015).

In conjunction with significantly reduced ratios of total cholesterol/HDL, and LDL/HDL (p < 0.05), the results in the lean mice confirm almost everything the claims you will find on most of the conventional CLA supplements at GNC & co. What is not mentioned on the labels in the increase in liver fat that did not reach significance, though (probably due to the low dose of CLA) in the study at hand (see Figure 3, top - red bars).

The clogged up livers of the lean mice are yet not the only negative result Lee et al. observed. In the obesity-induced mice (the ones on the high fat diet), the body weight and abdominal adipose tissue were unexpectedly increased (p < 0.05) (!) and the TG/HDL ratio (p < 0.05) rose.

Figure 3: Changes in liver, abdominal fat and brown fat, as well as carcass (fat free) mass in response to 60 days on diets containing CLA producing (PAI-75) and "placebo" bacteria (PAI-79 | Li. 2015).

Bottom line: In view of the negative effects in the rodents on the obesogenic diets and the non-existing weight loss effects and only modest improvements in cholesterol in the obese rodents on the normal diets, the scientists hypothesis that diet and baseline-adiposity modulate the effects of CLA-producing bacteria appears to be confirmed. The increase in liver fat in the lean mice is disconcerting, but (probably due to the low dose of CLA) probably not a problem. All this would make CLA-producing bacteria a viable fat loss or rather fat gain prevention tool for lean individuals.

There's  however one thing we must not forget: "[T]he possibility of generalizing from the results of studies on mice to humans is limited" (Li. 2015). Accordingly, we do now have "deeper insights that the health effect of t10c12-CLA [producing bacteria] is also influenced by the dietary fat content or host obesity degree" (Li. 2015), but we do still need human clinical trials that would allow us to find out if similar interactions would occur in lean vs. obese human beings on diff. diets | Comment on Facebook!

References:

• Lee, Hui-Young, et al. "Human originated bacteria, Lactobacillus rhamnosus PL60, produce conjugated linoleic acid and show anti-obesity effects in diet-induced obese mice." Biochimica et Biophysica Acta (BBA)-Molecular and Cell Biology of Lipids 1761.7 (2006): 736-744.
• Lee, K., et al. "Antiobesity effect of trans‐10, cis‐12‐conjugated linoleic acid‐producing Lactobacillus plantarum PL62 on diet‐induced obese mice." Journal of applied microbiology 103.4 (2007): 1140-1146.
• Li et al. "Effects of trans-10, cis-12-conjugated linoleic acid on mice are influenced by the dietary fat content and the degree of murine obesity." European Journal of Lipid Science and Technology (2015): Early view article.
• Rosberg-Cody, Eva, et al. "Recombinant lactobacilli expressing linoleic acid isomerase can modulate the fatty acid composition of host adipose tissue in mice." Microbiology 157.2 (2011): 609-615.