Table 1.
Comparison of metabolic disturbances in chemical and genetic derived colitis rodent models.
| Model | Colitis Model | Evidence for m 0.75 Metabolic Defects | Trigger for Exaggerated Metabolic Defects |
|---|---|---|---|
| DSS | DSS exposure via drinking water; low doses (e.g., <3%) lead to mild symptoms and high doses (>3%) to acute disease. The ulceration is superficial, almost restricted to the colon [95]. | DSS per se does not cause liver damage [96] but alters the systemic metabolism. LDL-C, ketone bodies and tryptophan are elevated, while glucose and amino acids are reduced in DSS-induced colitis model [83,96,97,98]. |
HFD (60% cocoa butter or D12492 diet) [78,84], choline deficient diet [99] or ApoE−/− [85] model worsens pre-existing colitis scores, and further induced endotoxemia, glucose impairment, liver fibrosis and steatosis. |
| TNBS | TNBS causes transmural colitis, and it needs ethanol as vehicle for enema administrations, which also aid in disrupting intestinal barrier. | Cause liver damage [79,100,101], accompanied by intestinal inflammation and endotoxemia. | HFD (fat from lard) further worsens colitis scores [87,88], endotoxemia [86] and fat deposition in liver and colon [87]. |
| IL-10−/− | Spontaneous development of chronic inflammation due to exacerbated Th1 and Th17 response in the absence of the anti-inflammatory IL-10 cytokine [80]. | Decrease serum glucose [80] but increases in urine [102]. Increase serum VLDL [103]. | APN−/−, IL10−/− double knockout mice do not exaggerate the IL-10 deficiency induced colitis [80]. |
| Mdr1a−/− | Spontaneous development of bowel inflammation due to absence of P-glycoprotein, associated [104]. | Mdr1a−/− mice are similar to their congenic background strain FVB [104] which are resistant to diet induced obesity. | HFD (30.5% fat from lard) exposure only worsen IBD disease score, without affecting liver or glycemic response [81]. |
| Muc2−/− | Defective mucin secretion leads to spontaneous development of colitis [82]. | Muc2−/− mice show less body weight gain and impaired glucose homeostasis [82]. | HFD (59% fat, mostly from lard) does not worsen glucose intolerance but induces the fat deposition in the liver [82]. |
APN: adiponectin; DSS: dextran sulfate sodium; ApoE: apolipoprotein E; HFD: high-fat diet; LDL-C: low-density lipoprotein cholesterol; Mdr: multidrug resistance protein; Muc2: mucin2; TNBS: 2,4,6-trinitrobenzene sulfonic acid.