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Arterial hypertension due to fructose ingestion: model based on intermittent osmotic fluid trapping in the small bowel

DOI: 10.1186/1742-4682-7-27

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Abstract:

In normal digestion of hyperosmolar fluids, also in cases of postprandial hypotension and in patients having the "dumping" syndrome after gastric surgery, any hyperosmolar intestinal content is diluted by water taken from circulation and being trapped in the bowel until reabsorption. High fructose corn sirup (HFCS) soft drinks are among common hyperosmolar drinks. Fructose is slowly absorbed through passive carrier-mediated facilitated diffusion, along the entire small bowel, thus preventing absorption of the trapped water for several hours.Here presented interpretation is that ingestion of hyperosmolar HFCS drinks due to a transient fluid shift into the small bowel increases renin secretion and sympathetic activity, leading to rise in ADH and aldosterone secretions. Their actions spare water and sodium in the large bowel and kidneys. Alteration of colon absorption due to hormone exposure depends on cell renewal and takes days to develop, so the momentary capacity of sodium absorption in the colon depends on the average aldosterone and ADH exposure during few previous days. This inertia in modulation of the colon function can make an individual that often takes HFCS drinks prone to sodium retention, until a new balance is reached with an expanded ECF pool and arterial hypertension. In individuals with impaired fructose absorption, even a higher risk of arterial hypertension can be expected.Despite wide range of daily salt and water ingestion, sodium and fluid homeostasis is maintained through orchestrated action of aldosterone, ADH, ANP and other humoral mediators. Actions of angiotensin II and aldosterone include vasoconstriction; increased glomerular filtration with sodium reabsorption and potassium secretion in the distal tubule; increased thirst and ADH secretion [1]. Beside that, a proabsorptive trophic effect of aldosterone on the pericryptal sheath in colonic mucosa was reported [1-3] and aldosterone exposure leads to increased pericryptal sodium concentratio

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