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. 2020 Apr 14;26(14):1564–1579. doi: 10.3748/wjg.v26.i14.1564

Table 2.

Summary of current human and experimental data on molecular, morphological and functional changes in intestinal epithelial barrier and neuromuscular compartment in metabolic disorders

Metabolic disorder Morphofunctional changes in intestinal epithelial barrier Morphofunctional changes in enteric neuromuscular compartment Ref.
Human investigations
Obesity ↑ Circulating LPS NA [6]
↓ Occludin and tri-cellulin immunopositivity
↑ ZO-1
Diabetes ↑ Intestinal permeability (urinary excretion of lactulose) NA [6]
Experimental models
HFD-induced obese mice ↓ ZO-1, occludin and claudins ↓ Nitrergic and VIPergic neurons Altered smooth muscle cell excitability [89-91,93,94,96,97]
↑ Circulating LPS ↓ Enteric inhibitory neurotransmission
↑ Enteric excitatory tachykininergic neurotransmission
↑ SP immunopositivity
↑ A2B adenosine receptor expression
Lep ob/ob mice ↑ Intestinal permeability NA [92]
Alterations of villi/crypt length
↓ TJs and mucus-related genes
Ob/ob mice ↑ Paracellular permeability ↓ Intestinal motor activity [95]
Altered TJs ↓ ACh receptors
Delayed intestinal transit rate

↑: Increase; ↓: Decrease; A2B: Adenosine 2B receptor; Ach: Acetylcholine; HFD: High-fat diet; Lep: Leptin; LPS: Lipopolysaccharide; NA: Not available; Ob/ob: Obese mice; SP: Substance P; TJ: Tight junction; ZO-1: Zonulin-1.