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      Procyanidins and sensory nutrition; do procyanidins modulate homeostasis via astringent taste receptors?

      , , ,
      Bioscience, Biotechnology, and Biochemistry
      Oxford University Press (OUP)

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          ABSTRACT

          Long-term intake of procyanidins has been suggested to reduce the risk of cardiovascular disease, dementia, and sensory function decline associated with aging. However, most of the ingested procyanidins are not absorbed and are excreted in the feces, so the mechanism of their beneficial impact is unknown. Procyanidins are the components of astringency in plant foods and their stimulation appears to be directly transmitted to the central nervous system via sensory nerves. Recent attention has been focused on the taste receptors expressed in the extra-oral gastrointestinal tract may regulate homeostasis via the neuroendocrine system. In this paper, we have reviewed recent findings on the relationship between the astringency of procyanidins and their bioregulatory effects.

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          Most cited references43

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          TRP channels as cellular sensors.

          TRP channels are the vanguard of our sensory systems, responding to temperature, touch, pain, osmolarity, pheromones, taste and other stimuli. But their role is much broader than classical sensory transduction. They are an ancient sensory apparatus for the cell, not just the multicellular organism, and they have been adapted to respond to all manner of stimuli, from both within and outside the cell.
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            Neural regulation of endocrine and autonomic stress responses.

            The survival and well-being of all species requires appropriate physiological responses to environmental and homeostatic challenges. The re- establishment and maintenance of homeostasis entails the coordinated activation and control of neuroendocrine and autonomic stress systems. These collective stress responses are mediated by largely overlapping circuits in the limbic forebrain, the hypothalamus and the brainstem, so that the respective contributions of the neuroendocrine and autonomic systems are tuned in accordance with stressor modality and intensity. Limbic regions that are responsible for regulating stress responses intersect with circuits that are responsible for memory and reward, providing a means to tailor the stress response with respect to prior experience and anticipated outcomes.
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              A mechanosensory complex that mediates the endothelial cell response to fluid shear stress.

              Shear stress is a fundamental determinant of vascular homeostasis, regulating vascular remodelling, cardiac development and atherogenesis, but the mechanisms of transduction are poorly understood. Previous work showed that the conversion of integrins to a high-affinity state mediates a subset of shear responses, including cell alignment and gene expression. Here we investigate the pathway upstream of integrin activation. PECAM-1 (which directly transmits mechanical force), vascular endothelial cell cadherin (which functions as an adaptor) and VEGFR2 (which activates phosphatidylinositol-3-OH kinase) comprise a mechanosensory complex. Together, these receptors are sufficient to confer responsiveness to flow in heterologous cells. In support of the relevance of this pathway in vivo, PECAM-1-knockout mice do not activate NF-kappaB and downstream inflammatory genes in regions of disturbed flow. Therefore, this mechanosensing pathway is required for the earliest-known events in atherogenesis.
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                Author and article information

                Contributors
                (View ORCID Profile)
                Journal
                Bioscience, Biotechnology, and Biochemistry
                Oxford University Press (OUP)
                1347-6947
                November 01 2023
                November 01 2023
                Article
                10.1093/bbb/zbad154
                37930827
                b6b41363-193c-412e-9cb6-f571b2d8196d
                © 2023

                https://academic.oup.com/journals/pages/open_access/funder_policies/chorus/standard_publication_model

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