Skip to main content
. 2024 Feb 27;10(5):e26991. doi: 10.1016/j.heliyon.2024.e26991

Table 4.

Different applications of SCAFs as potential therapy for the treatment of NAFLD.

Categories Specific measures Results References
Individual application
  • ●Administration of sodium butyrate to male C57BL/6J mice at 4–5 weeks of age

  • ●Compared to the control group, TG, IL-6 and TNF-α levels were reduced in the dosing group, as were serum LPS concentrations

[86]
  • ●Administration of SCFAs to weaned pigs

  • ●LDL-c concentration were significantly reduced and GLP-1, PYY and leptin concentration were increased in dosing group

[87]
  • ●C57BL/6 mice were administered sodium acetate, sodium propionate or sodium butyrate during 6 weeks feeding period

  • ●The levels of TG, IL-6 and TNF-α decreased in the administered group compared to the control group, as did the serum concentration of LPS

[88]
  • ●Pigs were treated with 0.1% sodium acetate, 0.1% sodium propionate, 0.1% sodium butyrate, 0.1% mixed SCFAs, respectively

  • ●Compared to the control group, the concentration of TG, TC and LDL-c decreased significantly and the concentration of GLP-1, PYY and leptin increased significantly in the administration group

[89]
Prebiotics application
  • ●In a double-blind, randomized, placebo-controlled crossover design, 14 healthy, overweight obese men were given prebiotic inulin

  • ●Plasma glucose and insulin were lower after inulin ingestion and plasma free fatty acids were higher in the early post-inulin period and lower in the late postprandial period and SCFAs were increased in vivo

[90]
  • ●Male C57BL/6 mice given a high fat/high sugar diet supplemented with 10% FOS for 10 weeks

  • ●Significantly lower TC, TG and LDL levels and increased SCFAs in FOS-supplemented mice

[91]
  • ●12 weeks SP dietary supplementation for obese mice

  • ●In obese mice, body weight was reduced and serum lipid levels and liver triglyceride levels were also reduced, while SCFAs levels were increased

[92]
Clinical drugs application
  • ●Common carp were exposed to 0, 10, 100, and 250 μM OLA for 60 days

  • ●Decreased TC, LDL, TG, HDL, and increased abundance of SCFA-producing bacteria

[93]
  • ●Eight-week-old male C57BL/6J mice were randomly divided into five groups, the experimental group was established as a liver fibrosis model and given FTA

  • ●Compared to control group, there was no significant collagen deposition and the GM was altered, with significantly lower levels of LPS, MIP-1α and TNF-α, as well as increased levels of SCFAs in the administered mice

[94]
  • ●In the NAFLD model group, the Male 4-week-old C57BL/6J mice were divided into three subgroups: NAFLD MG (n = 8, fed by HFD), ECD group (EG, n = 8, fed by HFD and received ECD 5.7 g/kg/d) and SCFAs group

  • ●Both ECD and SCFAs reversed HFD-induced weight gain and serum ALT and AST, which inhibited liver TLR-4, TNF-α, IL-1β and NF-κB levels. ECD inhibited the decrease of IETJ protein induced by HFD and restored HFD-induced impaired SCFAs production

[95]
  • ●Male C57BL/6 mice were treated with SJP/saline for 6 weeks

  • After SJP treatment, TG, TC, ALT, and AST were significantly decreased and the level of PPARγ protein was steadily increased. In addition, SJP treatment regulated the relative abundance of SCFAs - producing bacteria

[96]

Abbreviations: SCFAs, short-chain fatty acid salts; FOS, Fructo-oligosaccharide; SP, seabuckthorn polysaccharide; OLA, Olanzapine; NAFLD, Nonalcoholic fatty liver disease; FTA, Forsythiaside A; ECD, Erchen decoction; SJP, Jiang Powder; TG, triglyceride; TC, total cholesterol; IL-6, interleukin-6; TNF-α, tumour necrosis factor-α; LPS, lipopolysaccharide; LDL-c, low-density lipoprotein cholesterol; GLP-1, glucagon-like peptide-1; PYY, Peptide YY; LDL, low-density lipoprotein; HDL, high-density lipoprotein; GM, gut microbiota; MIP-1α, macrophage inflammatory protein-1alpha; TLR-4, toll-like receptor 4; IL-1β, interleukin-1β; NF-κB, nuclear factor-kappaB; IETJ, intestinal epithelial tight junction; HFD, high fatty diet, ALT, alanine aminotransferase; AST, aspartate aminotransferase; PPARγ, peroxisome proliferator-activated receptor γ.