Dietary lectins are metabolic signals for the gut and modulate immune and hormone functions.
Although it is common knowledge that some dietary lectins can adversely affect the growth and health of young animals and that, therefore, lectins are implicated in nutritional disorders of the digestive system, it has not been rigorously established that findings with animals are also directly applicable to humans. However, because the glycosylation state of the human gut is basically similar to that of higher animals, it may be confidently predicted that the effects of dietary lectins will have similarities in both humans and animals. The more recent but not generally appreciated realization that lectins also have many beneficial effects on the gut and metabolism of animals makes the exploration of these for possible use in medical-clinical practice even more attractive. Most lectins in our diet are resistant to breakdown during gut passage and are bound and endocytosed by epithelial cells. These lectins are powerful exogenous growth factors for the small intestine, can induce dramatic shifts in its bacterial flora and interfere with its hormone secretion. In addition, lectins which are transported across the gut wall into the systemic circulation can modulate the body's hormone balance, metabolism and health. Although these physiological effects are mediated or reinforced by immune responses, they are primarily the result of the specific chemical reactivity of lectins with cell surface receptors of the gut. Clearly, as the interactions between lectins and the gut are predictable and may be manipulated to our advantage, the exciting scientific challenge is now to explore the possible transfer of the existing knowledge gained from animal experimentation to medical-clinical practice.
Pusztai
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Rowett Research Institute, Bucksburn, Aberdeen, UK.
D000818:Animals; D004032:Diet; D004064:Digestive System / Q000187:drug effects* / Q000378:metabolism / Q000382:microbiology; D004068:Digestive System Physiological Phenomena; D004702:Endocrine Glands / Q000187:drug effects*; D004705:Endocytosis; D006031:Glycosylation; D006801:Humans; D006969:Hypersensitivity, Immediate / Q000139:chemically induced* / Q000276:immunology; D037102:Lectins / Q000009:adverse effects / Q000502:physiology / Q000627:therapeutic use; D051381:Rats; D015398:Signal Transduction / Q000187:drug effects* / Q000502:physiology*
D037102:Lectins