Gut dysbiosis and systemic inflammation promote cardiomyocyte abnormalities in an experimental model of steatohepatitis

Table 1 Atherogenic ratios, inflammation and endothelial dysfunction markers in a nutritional model of steatohepatitis

Variable	Control (n = 10)	Intervention (n = 10)	P value
AC	0.6 (0.2–0.9)	2.5 (1.5–3.4)	< 0.001a
CRI-I	1.6 (± 0.4)	3.5 (± 1.1)	< 0.001a
CRI-II	0.3 (± 0.1)	0.8 (± 0.2)	< 0.001a
IL-1β (pg/mL)	367.7 (± 31.2)	465.9 (± 52.7)	0.001a
MCP-1 (ng/mL)	2.7 (± 0.6)	3.8 (± 0.9)	0.005a
TIMP-1 (ng/mL)	7.1 (± 1.4)	12.4 (± 2.3)	< 0.001a
PAI-1 (ng/mL)	0.11 (± 0.05)	0.17 (± 0.06)	0.037a

Data are means ± standard deviation or medians (25^th-75^th percentiles).

^aP ≤ 0.05 was considered statistically significant.

AC: Atherogenic coefficient; CRI: Castelli’s risk index; IL: Interleukin; MCP: Monocyte chemoattractant protein; PAI: Plasminogen activator inhibitor; TIMP: Tissue inhibitor of metalloproteinase.