Effect of 1-Kestose on Lipid Metabolism in a High-Fat-Diet Rat Model

Abstract

Objectives: Hyperlipidemia is a risk factor for various diseases. Identifying food components that can help reduce the levels of blood lipids, such as cholesterol and triglycerides, is a global research priority. It has been reported that 1-Kestose, a fructooligosaccharide, can reduce blood cholesterol and triglyceride levels in rats; however, the underlying mechanisms remain unclear. Therefore, we aimed to elucidate the effects of 1-kestose supplementation on lipid metabolism and the gut environment in rats. Methods: Twenty male Sprague-Dawley rats (age 8 weeks) were provided 1-kestose-containing water and were maintained for two weeks. After dissection, the blood components, hepatic gene expression, gut microbiota, and bile acid composition in the cecal contents of the rats were analyzed. Results: The 1-Kestose intake reduced plasma cholesterol and triglyceride levels. Additionally, an increase in cytochrome P450 family 7 subfamily A member 1 mRNA expression, a key gene for bile acid synthesis in the liver, and a decrease in lipid synthesis-related mRNA expression were observed. In the cecum, the levels of deconjugated bile acids, which are involved in the regulation of lipid synthesis, were increased. Furthermore, the 1-kestose intake altered the gut microbiota in the cecum, leading to an increase in the abundance of specific bacteria, such as Bifidobacterium, which are involved in the deconjugation of conjugated bile acids. Conclusions: The intake of 1-kestose alters the gut microbiota and bile acid metabolism in the cecum, potentially influencing lipid metabolism in the host.

Keywords: 1-kestose; bile acids; cholesterol; gut microbiota; lipid metabolism.

Figure 1

(A) Body weight gain after 2 weeks of feeding, (B) food intake, and (C) water intake along with (D) liver weight. Data are presented as means ± standard errors (n = 10 animals per group). * p < 0.05, ** p < 0.01. +KES, 4% (w/v) 1-kestose treatment; −KES, control.

Figure 2

Concentrations of (A) glucose, (B) insulin, (C) free fatty acids, (D) cholesterol, and (E) triglycerides in plasma. Data are presented as means ± standard deviations (n = 10 animals per group). ** p < 0.01. +KES, 4% (w/v) 1-kestose treatment; −KES, control.

Figure 3

(A) The relative abundance of cholesterol metabolism-related genes, including Abcg5, Abcg8, Srebp2, Cyp7a1 and Baat, in liver tissues of rats. (B) The relative abundance of triglyceride metabolism-related genes, including Gpam, Fasn and Srebp1, in liver tissues of rats. Data are presented as mean ± standard deviation (n = 10 animals per group). * p < 0.05, ** p < 0.01, *** p < 0.001. Abcg5, ATP-binding cassette sub-family G member 5; Abcg8, ATP-binding cassette sub-family G member 8; Srebp2, sterol regulatory element-binding protein 2; Cyp7a1, cytochrome P450 family 7 subfamily A member 1; Baat, bile acid-CoA: amino acid N-acyltransferase; Gpam, glycerol-3-phosphate acyltransferase mitochondrial; Fasn, fatty acid synthase; Srebp1, sterol regulatory element-binding protein 1; +KES, 4% (w/v) 1-kestose treatment; −KES, control.

Figure 4

Cecal content (A), weight, and (B) pH. (C) Concentrations of T-CA, CA, CDCA, DCA, and LCA in cecal contents. (D) Correlation analysis between bile acids and mRNA expression levels was performed using Spearman’s correlation. Data are presented as the mean ± standard deviation (n = 10 animals per group). * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001 +KES, 4% (w/v) 1-kestose treatment; −KES, control; T-CA, taurocholic acid; CA, cholic acid; CDCA, chenodeoxycholic acid; DCA, deoxycholic acid; LCA, lithocholic acid.

Figure 5

Alpha diversity indices: (A) Chao1, (B) Shannon, and (C) principal component analysis score plot; relative abundances of gut microbiota at the (D) phylum and (E) genus levels; abundances of (F) Bifidobacterium and (G) Anaerostipes; and (H) predicted BSH gene abundance in the cecal contents of rats. (I) Correlation analysis between gut microbiota and bile acids was performed using Spearman’s correlation. Data are presented as the mean ± standard deviation (n = 10 animals per group). * p < 0.05, ** p < 0.01, **** p < 0.0001. +KES, 4% (w/v) 1-kestose treatment; −KES, control; BSH, bile salt hydrolase.