High-
fructose diet induced changes in gut microbiota structure and function, which have been linked to inflammatory response. However, the effect of small or appropriate doses of
fructose on gut microbiota and inflammatory
cytokines is not fully understood. Hence, the abundance changes of gut microbiota in
fructose-treated Sprague-Dawley rats were analyzed by
16S rRNA sequencing. The effects of
fructose diet on metabolic disorders were evaluated by blood biochemical parameter test, histological analysis,
short-chain fatty acid (SCFA) analysis, ELISA analysis, and Western blot. Rats were intragastrically administered with pure
fructose at the dose of 0 (Con), 2.6 (Fru-L), 5.3 (Fru-M), and 10.5 g/kg/day (Fru-H) for 20 weeks. The results showed that there were 36.5% increase of
uric acid level in the Fru-H group when compared with the Con group. The serum proinflammatory
cytokines (IL-6, TNF-α, and MIP-2) were significantly increased (P < 0.05), and the anti-inflammatory
cytokine IL-10 was significantly decreased (P < 0.05) with
fructose treatment. A higher
fructose intake induced
lipid accumulation in the liver and inflammatory cell infiltration in the pancreas and colon and increased the abundances of Lachnospira, Parasutterella, Marvinbryantia, and Blantia in colonic contents.
Fructose intake increased the expressions of
lipid accumulation
proteins including
perilipin-1, ADRP, and Tip-47 in the colon. Moreover, the higher level intake of
fructose impaired intestinal barrier function due to the decrease of the expression of
tight junction proteins (ZO-1 and
occludin). In summary, there were no negative effects on
body weight, fasting
blood glucose, gut microbiota, and SCFAs in colonic contents of rats when
fructose intake is in small or appropriate doses. High intake of
fructose can increase
uric acid, proinflammatory
cytokines, intestinal permeability, and
lipid accumulation in the liver and induce inflammatory response in the pancreas and colon.