Gastric Sensor Research Articles

Dynamic Monitoring of Systemic Biomarkers with Gastric Sensors.

Continuous monitoring in the intensive care setting has transformed the capacity to rapidly respond with interventions for patients in extremis. Noninvasive monitoring has generally been limited to transdermal or intravascular systems coupled to transducers including oxygen saturation or pressure. Here it is hypothesized that gastric fluid (GF) and gases, accessible through nasogastric (NG) tubes, commonly found in intensive care settings, can provide continuous access to a broad range of biomarkers. A broad characterization of biomarkers in swine GF coupled to time‐matched serum is conducted . The relationship and kinetics of GF‐derived analyte level dynamics is established by correlating these to serum levels in an acute renal failure and an inducible stress model performed in swine. The ability to monitor ketone levels and an inhaled anaesthetic agent (isoflurane) in vivo is demonstrated with novel NG‐compatible sensor systems in swine. Gastric access remains a main stay in the care of the critically ill patient, and here the potential is established to harness this establishes route for analyte evaluation for clinical management.

Antidiuretic Hormone and Serum Osmolarity Physiology and Related Outcomes: What Is Old, What Is New, and What Is Unknown?

Although the physiology of sodium, water, and arginine vasopressin (AVP), also known as antidiuretic hormone, has long been known, accumulating data suggest that this system operates as a more complex network than previously thought. English-language basic science and clinical studies of AVP and osmolarity on the development of kidney and cardiovascular disease and overall outcomes. Apart from osmoreceptors and hypovolemia, AVP secretion is modified by novel factors such as tongue acid-sensing taste receptor cells and brain median preoptic nucleus neurons. Moreover, pharyngeal, esophageal, and/or gastric sensors and gut microbiota modulate AVP secretion. Evidence is accumulating that increased osmolarity, AVP, copeptin, and dehydration are all associated with worse outcomes in chronic disease states such as chronic kidney disease (CKD), diabetes, and heart failure. On the basis of these pathophysiological relationships, an AVP receptor 2 blocker is now licensed for CKD related to polycystic kidney disease. From a therapeutic perspective, fluid intake may be associated with increased AVP secretion if it is driven by loss of urine concentration capacity or with suppressed AVP if it is driven by voluntary fluid intake. In the current review, we summarize the literature on the relationship between elevated osmolarity, AVP, copeptin, and dehydration with renal and cardiovascular outcomes and underlying classical and novel pathophysiologic pathways. We also review recent unexpected and contrasting findings regarding AVP physiology in an attempt to explain and understand some of these relationships.

Modulation of gastric nesfatin by rapamycin

Nesfatin‐1, an 82 amino acid peptide mainly found in the hypothalamus and stomach, is a novel satiety hormone acting through a leptin‐independent mechanism in the hypothalamus. Mechanism by which production of nesfatin‐1 is regulated remains unknown. Here we showed the co‐localization of pS6K, the downstream target of the mammalian target of rapamycin (mTOR) in the gastric X/A like cells. Reciprocal relationship of gastric mTOR signaling and nesfatin‐1 was observed during changes in energy status. Both mTOR activity and gastric nesfatin‐1 were down‐regulated by fasting, and returned to near basal level by re‐feeding. In high fat diet induced obese mice, gastric mTOR signaling and nesfatin‐1 were enhanced. Inhibition of the gastric mTOR signaling by rapamycin attenuated the expression of gastric nesfatin‐1 mRNA and protein in both lean and obese mice. Attenuation of mTOR activity by rapamycin or over‐expression of TSC1 or TSC2 reduced the expression of nesfatin in Min‐6 cells, suggesting a direct effect of mTOR signaling. In conclusion, gastric mTOR is a gastric sensor whose activity is linked to the regulation of gastric nesfatin‐1.

Regulation of gastric hormones by systemic rapamycin

The mammalian target of rapamycin (mTOR), an evolutionarily conserved serine–threonine kinase, is an intracellular fuel sensor critical for cellular energy homeostasis. Gastrointestinal endocrine cells play a vital role in the regulation of energy balance by secreting hormones that inform the brain about energy supply. Here we showed the localization of mTOR signaling molecules in more than 90% of gastric ghrelin cells and 36 ± 3% of gastrin cells, while no somatostatin-positive cell showed phospho-S6K1 immunoreactivity. Inhibition of mTOR significantly stimulated expression of gastric ghrelin mRNA and protein, and the concentration of plasma ghrelin (2.06 ± 0.34 ng/ml vs. 12.53 ± 3.9 ng/ml, p < 0.05), inhibited gastrin synthesis and secretion (75.01 ± 6.71 pg/ml vs. 54.04 ± 3.65 pg/ml, p < 0.05), but had no effect on somatostatin production (165.2 ± 25.07 pg/ml vs. 178.9 ± 29.14 pg/ml, p = 0.73). Gastric mTOR is a gastric sensor whose activity is linked to the differential regulation of gastric hormone production and release.