Obese people are at an incredibly high risk of developing type 2 diabetes, high blood pressure, and heart disease, among other problems, which is why it is important to deal with this condition as soon as possible. The combination of health issues brought on by obesity – significantly higher than normal body fat percentage, blood sugar levels, blood pressure, and cholesterol – is collectively called “metabolic syndrome” and experts agree that the primary course of action center around dramatic changes in diet and exercise levels.
Of course, it can be difficult for an obese person to develop all the good habits needed for a big and fast lifestyle change all at once, so it is important to first focus on dietary changes that will help prevent the most dangerous issues, i.e. the development of diabetes.
Luckily, there is an early warning sign that shows if a person is likely to develop type 2 diabetes – a resistance to insulin i.e. lowered insulin sensitivity. The main culprit for this is a type of immune cell located in our fat tissue, and dietary fibers seem to be an effective way of battling metabolic syndrome, based on a number of studies.
Possible link between gut bacteria and prebiotic dietary fibers like Resistant Starch
In the past few years, we have seen some major breakthroughs in the gut microbiome, the name for the billions of bacteria living in our stomach, research. Scientists have shown that a well-balanced gut flora can help prevent a variety of diseases and that restoring balance to the gut flora using dietary supplements can help alleviate the symptoms of or even cure a number of health issues.
As some previous studies have shown certain benefits from short-chain fatty acids, which we get as a result of fibers like resistant starch being fermented by the bacteria in our gut, there was some speculation on just how important of a role our gut flora plays in the process. Can resistant starch help improve insulin sensitivity independently of gut microbiota, or do these helpful bacteria play a major role in this process?
Resistant Starch Study
In a recently published study, scientists at the University of Nebraska decided to take two types of mice – one which had a balanced gut flora, and one which had virtually no gut bacteria – and feed them a typical Western diet, high in sugar and fat, then add resistant starch to their diets and compare the results.
To conduct this study they had to have a control first. The type of mice typically used in obesity studies, B6 mice, are not affected by the Western diet when they are free of any gut bacteria, while the C3H mice are generally quite susceptible to the bad effects of the Western diet.
The researchers created four groups using of C3H and B6 mice that were conventionalized, i.e. they were given the bacteria and developed a balanced gut flora. These four types of mice – CH3 germ-free, CH3 with gut bacteria, B6 germ-free, and B6 with gut bacteria – were fed a Western diet for 8 weeks. The scientists measured how much weight each group mice had gained.
They then took CH3 and B6 mice and fed them with either the standard Western diet or a Western diet with 10% added resistant starch for another 8 weeks. The researchers then looked at their insulin resistance and other health markers and compared the results.
What did the study find and what are the implications?
After the first 8 weeks of the study the bacteria free B6 mice had gained a lot less weight than B6 mice that had gut bacteria, while both germ-free CH3 and CH3 mice with gut bacteria gained roughly the same amount of weight. The CH3 mice with gut bacteria did, however, gain more weight than B6 mice with gut bacteria, and they consumed more food. This meant that the germ-free CH3 rats were good test subjects for exploring the possible role the gut bacteria might play in helping fibers like resistant starch improve insulin sensitivity.
The two types of resistant starch used in the second 8 weeks of the experiment, RS2 and RS4, have proven positive effects on improving insulin sensitivity, but they also have a distinctive effect on the gut bacteria when consumed by humans. If anything was going to show that gut flora plays an important role here, it was this stuff.
CH3 mice that were fee RS4 had a noticeable improvement in insulin sensitivity, even though it did nothing to reduce their weight, body fat percentage or their appetite. The B6 mice fared almost the same.
In CH3 mice with gut bacteria, the addition of either RS2 or RS4 helped improve the diversity of the gut bacteria, which was previously reduced through eating a Western diet for 8 weeks. For the final test, determining whether resistant starch would improve insulin sensitivity in the absence of gut bacteria, germ-free CH3 and CH3 mice with gut bacteria were broken down into groups, some of which were fed the Western diet as a control, and others were fed a diet with 10% resistant starch.
Another form of control was also used, some mice were fed a low-fat diet to compare the weight gain with those who consumed a Western diet. Unsurprisingly, the Western diet increased body weight and fat percentage over those fed the low-fat diet, but resistant starch did little to improve any of this. Both germ-free CH3 and CH3 mice with gut bacteria feed a Western diet saw an increase in insulin and glucose levels over the low-fat diet group.
The addition of RS4 helped CH3 mice with gut bacteria reduce insulin levels, and it also caused some changes in their gut flora balance, which could possibly mean that the bacteria somehow contributed to these positive effects or was a necessary step in the process. However, when the germ-free CH3 mice were fed a diet that contained RS4 they experienced the same reduction in insulin levels, even though they had no gut bacteria to help them out.
The high blood sugar levels resulting from the Western diet were not directly affected by the addition of resistant starch, although both RS2 and RS4 dramatically improved insulin resistance and insulin secretion, regardless of whether the mice had gut bacteria or not.
There was another interesting find. Some previous studies have shown that a shift in bile acid pool composition can be a tell-tale sign of someone in a prediabetic state or of someone with type 2 diabetes. It was found that the a diet with resistant starch also affected the bile acid pool composition with or without gut bacteria.
The Conclusion
Although resistant starch has been shown to affect the composition of gut bacteria, the bacteria did not play a direct role in helping resistant starch “unleash” its health benefits. While diets with RS2 and RS4 had a fairly different effect on the gut flora, they produced quite similar results in terms of insulin sensitivity, the RS4 being slightly better at causing metabolic improvements.
An interesting thing that was shown in CH3 mice is that resistant starch improved insulin levels without affecting body weight or body composition, and similar results were previously observed in obese humans. The researchers also note that unlike in this study and some human clinical trials, a lot of studies with resistant starch fed to mice in the presence of a balanced gut flora show a reduction in body fat accompanies the improved insulin sensitivity.
They note that this is probably due to a larger amount of resistant starch used in such studies, around 30-50% of the diet, which is more readily fermented by bacteria in the stomach, which causes an increase in certain hormones that help with body weight reduction. However, this shouldn't get our hopes up, as such high doses fiber in a human diet are simply unrealistic, and would cause a different set of problems.
The main takeaway is that a diet with added resistant starch, around 10% of the overall daily diet, can improve insulin sensitivity, regardless of the state of gut bacteria in mice, but it probably also has some additional benefits to offer when processed by a well-balanced gut flora, as both RS2 and RS4 have been shown to affect its composition.
References
Bindels, Laure B., et al. "Resistant starch can improve insulin sensitivity independently of the gut microbiota." Microbiome 5.1 (2017): 12.