Obese prone CD rats robustly ferment resistant starch (RS) with no increased weight and fat accretion
Authors: Obanda Diana , Page Ryan , Guice Justin , Kyereh Emmanuel , Raggio Anne , Tuuri Georgianna , Husseneder Claudia , Martin Roy , Marx Brian , Coulon Diana , Stout Rhett , Keenan Michael 
Published: November 2023

We compared the efficacy of switching to a low fat diet or a low fat diet supplemented with resistant starch (RS) in attenuating diet induced obesity in CD rats. This rat species exhibits two phenotypes with regard to obesity. The obese prone (OP) rats develop obesity on a high calorie diet while the obese resistant (OR) remain lean. The obesity trait in OP rats is linked to a polygenic pattern of inheritance similar to the human obese phenotype. Using isocaloric diets, intake of RS that escapes digestion in the small intestine and is available to colonic microbiota reduces abdominal fat in various models of obesity by increasing energy expenditure and fat oxidation. Fermentation of RS by gut bacteria has been shown to be the mechanism involved. Using OR and OP rats we evaluated changes in the gut microbiota in relation to development of obesity and its associated comorbidities. We focused on the species Methanobrevibacter smithii the predominant archaeon in the human gut that increases fermentation and methanogenesis. Based on previous studies, we hypothesized that OR rats would remain lean on a high fat diet, ferment RS better than OP rats and have higher amounts of total bacteria and M. smithii when the diet includes RS.

Five week old rats (OP; n=32; OR; n=32) were each stratified based on weight and insulin sensitivity into two groups. Ten rats were fed a LF diet while 22 were fed high fat (HF) diet for 4 weeks. Then four rats were euthanized from each diet group to determine body fat accumulation. The remaining 6 rats in the LF group continued on the same diet. The 18 remaining rats from the HF group were divided into three groups of 6 each. Group 1 continued on the HF diet, group 2 was switched to a LF diet, and group 3 was switched to the low fat diet containing RS (20% wt of diet) for 4 weeks. Food and water were provided ad libitum. At the end of the study, fermentation variables were determined. Gene copies of total bacteria and M. smithii were determined by qPCR. Results described are significant at p< 0.05 divided by number of pairwise comparisons.

As expected OP rats fed a HF diet significantly accumulated fat and gained weight compared to OR rats. Switching to a LF diet or a LF diet containing RS both significantly reduced emboweled body weight (no gut contents) and fat pad accumulation. Surprisingly, OP rats fermented RS more robustly than OR rats as evidenced by increased weight of the empty and full cecum, short chain fatty acids, and a drop in pH of cecal contents. RS increased gene copies of total bacteria and M. smithii in the cecum only in OP rats. M. smithii gene copy numbers were not significantly different in diets without RS in both OP and OR rats. The robust fermentation in OP rats resulted in significantly higher GLP‐1 levels. Body fat accumulation and insulin sensitivity were not different in OP and OR rats switched to a LF diet or LF with RS. Rats fed the HF diet throughout the study gained most weight and had the worst insulin sensitivity. We concluded that the increased fermentation observed did not contribute to greater weight gain as is commonly believed to be one of the causes of obesity.

Support or Funding Information

Funding: LSU AgCenter and Ingredion Incorporated.