Table 3 Comparison of biological and structural parameters between D-Gal-induced model and naturally aged animals.

Total feed

No increase in the first week; began to rise and stabilize in the second week. Decreased intake associated with reduced body weight

Not directly discussed

Decreased food intake due to loss of olfactory receptors; decreased leptin sensitivity

^{1,2,7,8,12,14,15,16,17,18,19}

Distal colon transit time

Shorter than control; possibly due to early inflammation or disruption of the enteric nervous system

In diabetic model: faster transit time due to inflammatory cytokines (TNF-α, IL-6)

Transit time generally slower, but not always clinically significant

^{3,6,7,14,15,20,29,30,31,32,33,34}

Fecal pellet output

Significantly lower than control; tendency toward diarrhea, although stool water content not significantly different

In diabetic model: increased fecal weight due to propulsive contractions

Pellet number and water content decrease with age

^14,15,32

Histological structure

Mild epithelial and smooth muscle damage; high lymphocyte infiltration; longer colon length

Thickening of mucosal and muscular layers (in diabetic model)

Decreased smooth muscle contractility; disrupted neurotransmission mechanisms

^{1,8,14,20,21,22}

Immunohistochemistry (p16Ink4a)

Higher expression than control; indicates accumulation of senescent cells

Not directly discussed

Expression increases with advancing age

^10,23,24

Immunohistochemistry (Lamin B1)

Higher expression; associated with telomere instability and DNA damage

Not directly discussed

Changes in expression (increase/decrease) affect cell proliferation

^9,25,26,27