High-fat diet reduces the formation of butyrate, but increases succinate, inflammation, liver fat and cholesterol in rats, while dietary fibre counteracts these effects.
BACKGROUND
Obesity is linked to type 2 diabetes and risk factors associated to the metabolic syndrome. Consumption of dietary fibres has been shown to have positive metabolic health effects, such as by increasing satiety, lowering blood glucose and cholesterol levels. These effects may be associated with short-chain fatty acids (SCFAs), particularly propionic and butyric acids, formed by microbial degradation of dietary fibres in colon, and by their capacity to reduce low-grade inflammation.


OBJECTIVE
To investigate whether dietary fibres, giving rise to different SCFAs, would affect metabolic risk markers in low-fat and high-fat diets using a model with conventional rats for 2, 4 and 6 weeks.


METHODS
Conventional rats were administered low-fat or high-fat diets, for 2, 4 or 6 weeks, supplemented with fermentable dietary fibres, giving rise to different SCFA patterns (pectin - acetic acid; guar gum - propionic acid; or a mixture - butyric acid). At the end of each experimental period, liver fat, cholesterol and triglycerides, serum and caecal SCFAs, plasma cholesterol, and inflammatory cytokines were analysed. The caecal microbiota was analysed after 6 weeks.


CONCLUSIONS
Fermentable dietary fibre decreased weight gain, liver fat, cholesterol and triglyceride content, and changed the formation of SCFAs. The high-fat diet primarily reduced formation of SCFAs but, after a longer experimental period, the formation of propionic and acetic acids recovered. The concentration of succinic acid in the rats increased in high-fat diets with time, indicating harmful effect of high-fat consumption. The dietary fibre partly counteracted these harmful effects and reduced inflammation. Furthermore, the number of Bacteroides was higher with guar gum, while noticeably that of Akkermansia was highest with the fibre-free diet.
Department of Applied Nutrition and Food Chemistry, Lund University, Lund, Sweden.
Greta
G
Jakobsdottir
Jie
J
Xu
Göran
G
Molin
Siv
S
Ahrné
Margareta
M
Nyman
D000818:Animals; D001835:Body Weight; D002087:Butyrates / Q000097:blood / Q000378:metabolism*; D018932:Chemokine CCL2 / Q000097:blood; D002784:Cholesterol / Q000097:blood / Q000378:metabolism*; D003106:Colon / Q000378:metabolism / Q000382:microbiology; D004032:Diet; D059305:Diet, High-Fat / Q000009:adverse effects*; D004043:Dietary Fiber / Q000378:metabolism*; D005232:Fatty Acids, Volatile / Q000097:blood / Q000378:metabolism; D007249:Inflammation / Q000378:metabolism*; D008099:Liver / Q000378:metabolism* / Q000473:pathology*; D008297:Male; D064307:Microbiota; D009929:Organ Size; D010368:Pectins / Q000378:metabolism; D051381:Rats; D019802:Succinic Acid / Q000097:blood / Q000378:metabolism*; D013997:Time Factors
D002087:Butyrates; D018932:Chemokine CCL2; D004043:Dietary Fiber; D005232:Fatty Acids, Volatile; D010368:Pectins; D002784:Cholesterol; D019802:Succinic Acid