Chitosan is a natural polysaccharide that consists of glucosamine and N-acetylglucosamine copolymers ⁽¹⁴⁾. It has been described as biodegradable, nontoxic, non-immunogenic, and biocompatible ⁽²⁵⁾, with properties similar to cellulose ⁽²⁾.

In an in vitro study, chitosan demonstrated antioxidant effects by reducing albumin carobonyls and hydroperoxides in a time-dependent manner ⁽⁹⁾.

In animal models, antiobesity effects may occur through serum leptin and C-reactive protein modulation ⁽¹⁴⁾ or AMPK activation and lipogenesis-associated gene inhibition ⁽¹⁵⁾. In porcine models, chitosan altered genes influencing appetite and feeding behavior in the small intestine (NPY), adipose tissue (Leptin), and the brain (HCRT, INSR, NMB, GHR, PPARG, NPY5R) ⁽¹⁷⁾. It also downregulated FABP2 gene expression, increased serum leptin, and significantly altered gut microbial populations ⁽¹⁶⁾. In high-fat diet-induced obese rodents, chitosan oligosaccharides improved dyslipidemia and prevented body weight gain by inhibiting adipocyte differentiation ⁽¹⁹⁾. As an insoluble fiber, low molecular weight chitosan polyglucosamines can bind to fat in the intestinal lumen, forming a complex that is partially utilized by colon bacteria and partially eliminated ^{(22) (26) (27)}, but appropriate concentrations are needed. In one of these animal studies, it was suggested that the more likely mechanisms for weight loss could include bacterial energy wasting, as increased acetate and glucose excretion were also present, suggesting that larger amounts of lipids and glucose were available as fuel for bacteria in the colon ⁽²⁶⁾.

Hypocholesterolemic effects from chitosan in murine models were not due to reduced cholesterol absorption efficiency or increases in fecal sterol output, so that a major bile acid-binding capacity was ruled out ⁽²⁸⁾. The more likely scenario is that the fiber’s influence on satiation and satiety reduces food intake suppression and therefore cholesterol ⁽²⁹⁾.

Human studies suggest that it is unlikely that chitosan binds fat in intestines, and could therefore not support this purported mechanism of action ^(21) (30).

Topical application enhances wound healing by stimulation of granulation tissue. Possible mechanisms include formation of a gel-like fibronectin matrix that facilitates inward epithelial cell migration and the formation of heparin-chitosan complexes that activate growth factors that bind to stabilized heparin ⁽¹²⁾.