Refeeding Research Articles

Effect of protein depletion and short-term parenteral refeeding on the host response to interleukin 1 administration.

Previous studies have demonstrated that protein malnutrition adversely affects the synthesis and release of interleukin 1 by monocytic cells. The purpose of this study was to investigate the protein and trace metal metabolism of severely protein-malnourished guinea pigs given exogenous interleukin 1 in the postabsorptive state or while concomitantly receiving total parenteral nutrition (TPN). Protein-depleted guinea pigs in the postabsorptive state failed to exhibit fever, granulocytosis, accelerated amino acid oxidation, or an acute-phase protein response after administration of interleukin 1 or endotoxin. However, a reduction in the serum concentration of zinc (P less than 0.05) and iron (P less than 0.05) was observed in the guinea pigs given interleukin 1, but not in those given endotoxin. The short-term (1 day) administration of TPN restored positive leucine balance (P less than 0.001) and reduced leucine release from protein breakdown (P less than 0.001). No other differences in the protein metabolism or trace metal response to interleukin 1 were observed as a result of short-term TPN feeding. Body temperatures of these malnourished guinea pigs given interleukin 1 and TPN became febrile or hypothermic depending on initial body temperatures. It is concluded that an attenuated capacity to synthesize interleukin 1 and a failure to mount an appropriate acute-phase protein response to exogenously administered interleukin 1 exist in this protein-malnourished animal model. Furthermore, this diminished protein response appears to be independent of short-term substrate provision because TPN for 1 day was unable to restore the full effects of the acute-phase response as mediated by interleukin 1.

Malnutrition, refeeding, and malaria

Malnutrition, refeeding, and malaria

Effects of starvation and refeeding on lung biochemistry in rats.

Adult rats received one fifth of their measured daily food consumption until they lost 40% body weight. Some of these rats were then refed until they reached their initial body weight. We measured the following in fed, starved, and refed animals: (1) disaturated phosphatidylcholine (DSPC) content of lung tissue and of lavage fluid, (2) protein content of lung tissue and of lavage return, and (3) DNA and RNA content of lung tissue. In starved lungs, tissue and lavage DSPC content, total protein and RNA contents, and RNA/DNA ratios were significantly lower than in fed rats. After refeeding, DSPC values returned completely to normal, whereas protein, DNA, and RNA contents were significantly higher than in fed rats. The RNA/DNA ratio was similar in the fed and refed groups. Changes in lavage DSPC are consistent with the increased surface elastic forces in starvation and their return to normal with refeeding reported by us previously. It appears that starvation leads to a reduction in cell size without changes in cell number and that refeeding is associated with a more significant increase in cell number than in cell size.

Effect of total parenteral nutrition on gut hormone release in humans

Prolonged absence of food from the gut is said to cause hypoplasia of the intestine and pancreas. Whether gut and pancreatic hormone secretion is correspondingly altered is not known. As total parenteral nutrition (TPN) and nil per os is now used to treat many gastrointestinal disorders, we investigated what effect intralumenal starvation of the gut, yet adequate nutritional support had on gastrointestinal and pancreatic hormonal release in humans. Gut hormone release was studied before and after a standard meal in 9 patients with Crohn's disease treated by nil per os and TPN for a mean of 25 days (range 18–52). Subsequently after a variable period of normal oral diet (mean 156 days; range 38–395), the same meal study was repeated. Fasting and peak postprandial concentrations of gastrin, motilin, GIP, secretin, pancreatic polypeptide, pancreatic glucagon, and VIP immediately after a period of nil per os and TPN (NPO-TPN) were not significantly different from the second meal study after refeeding (RF) and were equivalent to levels observed in healthy subjects. Although the postprandial rise in glucose was identical with both meals, after NPO-TPN the peak insulin response was significantly (p < 0.001) lower than the normal levels after refeeding. With both meals, basal enteroglucagon was similar, yet a significantly (p < 0.01) higher peak level occurred after NPO-TPN. To assess the effect of TPN (mean 22 days, range 18–25) on gut hormone release, we also undertook sequential hormone measurements before, during, and after TPN in 8 other patients. No significant change in plasma gastrin, motilin, pancreatic polypeptide, GIP, secretin, or enteroglucagon was observed as a consequence of TPN. Thus after TPN and nil per os in humans the fasting and postprandial gut endocrine response is well maintained. Higher postprandial levels of enteroglucagon may reflect greater ileal exposure to the nutrient load as a consequence of decreased transit time, while the diminished insulin response, yet identical, glucose levels may point to peripheral insulin hypersensitivity after TPN.

Suppression of infection by famine and its activation by refeeding--a paradox?

Suppression of infection by famine and its activation by refeeding--a paradox?

Effects of fasting and refeeding. II. Tubular sites of sodium reabsorption and effects of oral carbohydrate on potassium, calcium and phosphate excretion.

Effects of fasting and refeeding. II. Tubular sites of sodium reabsorption and effects of oral carbohydrate on potassium, calcium and phosphate excretion.