Impaired pancreatic secretion in severely malnourished patients is a consequence of primary pancreatic dysfunction

Winter, Trevor A.; Marks, Tessa; Callanan, Marie; O’Keefe, Stephen J.; Bridger, Sharon

doi:10.1016/s0899-9007(00)00575-x

Cited by 13 publications

(15 citation statements)

References 29 publications

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“…Severely undernourished patients had lower pentagastrin-stimulated gastric acid output, and secretion of CCK-stimulated trypsin and other non-protease pancreatic enzymes compared with controls (Winter et al, 2000). Severely undernourished patients also secreted significantly less gastric acid and trypsin in response to both CCK and enteral feeding stimulation (Winter et al, 2001). After 2 weeks to 3 months of nutritional support, non-protease pancreatic enzyme concentrations returned to normal, whereas trypsin and gastric acid concentrations remained low (Winter et al, 2000; Winter et al, 2001).…”

Section: Consumers Differ In Digestive Capacitymentioning

confidence: 99%

“…Severely undernourished patients also secreted significantly less gastric acid and trypsin in response to both CCK and enteral feeding stimulation (Winter et al, 2001). After 2 weeks to 3 months of nutritional support, non-protease pancreatic enzyme concentrations returned to normal, whereas trypsin and gastric acid concentrations remained low (Winter et al, 2000; Winter et al, 2001). This lack of recovery likely corresponds to longer term gastric parietal and pancreatic acinar cell dysfunction (Winter et al, 2001).…”

Section: Consumers Differ In Digestive Capacitymentioning

confidence: 99%

“…After 2 weeks to 3 months of nutritional support, non-protease pancreatic enzyme concentrations returned to normal, whereas trypsin and gastric acid concentrations remained low (Winter et al, 2000; Winter et al, 2001). This lack of recovery likely corresponds to longer term gastric parietal and pancreatic acinar cell dysfunction (Winter et al, 2001). However, because many of the undernourished patients in these test groups had coincident gastrointestinal disease, including Crohn’s disease, small bowel disease and short bowel, more research is needed to determine whether undernourishment, in the absence of gastrointestinal disease, causes lower gastric acid and trypsin production.…”

Section: Consumers Differ In Digestive Capacitymentioning

confidence: 99%

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Personalizing protein nourishment

Dallas

Sanctuary

et al. 2017

Critical Reviews in Food Science and Nutrition

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Proteins are not equally digestible—their proteolytic susceptibility varies by their source and processing method. Incomplete digestion increases colonic microbial protein fermentation (putrefaction), which produces toxic metabolites that can induce inflammation in vitro and have been associated with inflammation in vivo. Individual humans differ in protein digestive capacity based on phenotypes, particularly disease states. To avoid putrefaction-induced intestinal inflammation, protein sources and processing methods must be tailored to the consumer’s digestive capacity. This review explores how food processing techniques alter protein digestibility and examines how physiological conditions alter digestive capacity. Possible solutions to improving digestive function or matching low digestive capacity with more digestible protein sources are explored. Beyond the ileal digestibility measurements of protein digestibility, less invasive, quicker and cheaper techniques for monitoring the extent of protein digestion and fermentation are needed to personalize protein nourishment. Biomarkers of protein digestive capacity and efficiency can be identified with the toolsets of peptidomics, metabolomics, microbial sequencing and multiplexed protein analysis of fecal and urine samples. By monitoring individual protein digestive function, the protein component of diets can be tailored via protein source and processing selection to match individual needs to minimize colonic putrefaction and, thus, optimize gut health.

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Section: Consumers Differ In Digestive Capacitymentioning

confidence: 99%

Section: Consumers Differ In Digestive Capacitymentioning

confidence: 99%

Section: Consumers Differ In Digestive Capacitymentioning

confidence: 99%

See 1 more Smart Citation

Personalizing protein nourishment

Dallas

Sanctuary

et al. 2017

Critical Reviews in Food Science and Nutrition

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“…A recent genomic characterization of the gastric flora yielded 128 different strains of bacteria, 13 of which have not been characterized in vivo [110]. There is a relationship between gastric luminal pH and the number of organisms in diseases with reduced acid secretion [111,112,113] and during acid-suppression therapy [114,115,116,117]. This change seems to be dependent on the amount of gastric acid suppression as the increase in bacteria is greater with PPI than with H 2 -RA [118,119,120].…”

Section: Gastric Acid Gi Flora and Infectionmentioning

confidence: 99%

“…Surprisingly, no similar experiments or observations have been reported in humans. What is established in humans is that underweight, malnourished patients have low levels of gastric acid secretion, whereas obese patients have a raised maximal secretory capacity (peak acid output) but normal basal acid output [117, 173, 174]. Studies in patients having had gastric banding surgery for morbid obesity have shown that peak acid output is significantly reduced following weight loss, whereas basal acid output is unchanged [175].…”

Section: Gastric Acid and Hunger Satiation And Moodmentioning

confidence: 99%

Do We Need Gastric Acid?

et al. 2008

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Evidence from comparative anatomy and physiology studies indicates that gastric acid secretion developed during the evolution of vertebrates approximately 350 million years ago. The cellular mechanisms that produce gastric acid have been conserved over the millennia and therefore proton pump inhibitors have pharmacological effects in almost all relevant species. These observations suggest that gastric acid provides an important selective advantage; however, in modern-day humans the need for gastric acid can be questioned in light of the widespread use of safe and effective pharmacologic acid suppression. The Kandahar Working Group addressed questions concerning the need, production and effects of gastric acid, specifically: (1) motility in the upper gastrointestinal (GI) tract; (2) neuroendocrine factors; (3) digestive and mucosal processes; (4) microbiology, and (5) central processes and psychological involvement. We addressed each topic with the individual models available to answer our questions including animal versus human studies, pharmacologic, surgical as well as pathophysiologic states of acid suppression.

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