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Mechanisms of Disease: the pathological basis of gastroparesis—a review of experimental and clinical studies

Nature Clinical Practice Gastroenterology & Hepatology volume 4, pages 336–346 (2007)Cite this article

Abstract

The pathogenesis of gastroparesis is complicated and poorly understood. This lack of understanding remains a major impediment to the development of effective therapies for this condition. Most of the scientific information available on the pathogenesis of gastroparesis has been derived from experimental studies of diabetes in animals. These studies suggest that the disease process can affect nerves (particularly those producing nitric oxide, but also the vagus nerve), interstitial cells of Cajal and smooth muscle. By contrast, human data are sparse, outdated and generally inadequate for the validation of data obtained from experimental models. The available data do, however, suggest that multiple cellular targets are involved. In practice, though, symptoms seldom correlate with objective measures of gastric function and there is still a lot to learn about the pathophysiology of gastroparesis. Future studies should focus on understanding the molecular pathways that lead to gastric dysfunction, in animal models and in humans, and pave the way for the development of rational therapies.

Key Points

  • The pathogenesis of gastroparesis is complex; disruption of gastric function occurs at multiple cellular levels

  • Evidence suggests that the pathogenesis of gastroparesis might involve nerves (particularly those producing nitric oxide, but also the vagus nerve), interstitial cells of Cajal and smooth muscle

  • Most research into the pathogenesis of gastroparesis has been performed in animals; human studies are limited

  • Further studies in animal models and humans are needed to increase our understanding of the molecular pathways that lead to gastric dysfunction so that viable treatment options can be developed

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Figure 1: The importance of inhibitory nitrergic mechanisms in gastric emptying
Figure 2: The main cellular elements involved in gastric motility and sensation
Figure 3: Effects of diabetes on gastric nNOS
Figure 4: Effects on gastric smooth muscle in a patient with type 1 diabetes
Figure 5: Interstitial cells of Cajal and gastroparesis
Figure 6: Enteric neurons and gastroparesis

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Acknowledgements

This work was supported, in part, by grants NIDDK U01 DK073983-01 (PJ Pasricha) and DK DK68055 (G Farrugia). Figure 1 was kindly supplied by H Mashimo, and Figures 5 and 6 were kindly supplied by N Zarate.

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Authors and Affiliations

  1. H Vittal is an Advanced Endoscopy Fellow at the Maine Medical Center, G Gomez is Professor of Surgery, and PJ Pasricha is Bassel and Frances Blanton Distinguished Professor of Internal Medicine and Professor of Neuroscience and Cell Biology, at the University of Texas Medical Branch, Galveston, TX.,

    Harsha Vittal, Guillermo Gomez & Pankaj J Pasricha

  2. G Farrugia is Professor of Medicine at the Mayo Clinic College of Medicine, Rochester, MN, USA.,

    Gianrico Farrugia

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Correspondence to Pankaj J Pasricha.

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Vittal, H., Farrugia, G., Gomez, G. et al. Mechanisms of Disease: the pathological basis of gastroparesis—a review of experimental and clinical studies. Nat Rev Gastroenterol Hepatol 4, 336–346 (2007). https://doi.org/10.1038/ncpgasthep0838

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