Effect of intravenous fat on cholecystokinin secretion and gallbladder motility in man.

During total parenteral nutrition (TPN) gallbladder bile stasis and hypomotility have been well documented. Little is known, however, about the effect of the separate components of TPN on gallbladder motor function. Inasmuch as fat, administered intraduodenally, is a potent stimulus of cholecystokinin (CCK) secretion and gallbladder contraction we have investigated whether intravenous (IV) fat affects gallbladder motility. Six healthy volunteers were studied on two separate occasions, during infusion of Intralipid 10%, 200 mL/h or saline infusion (control) for 3 hours, to evaluate the effect of IV infusion of fat on (1) plasma CCK concentration and gallbladder volume and (2) CCK-induced gallbladder emptying. Intravenous infusion of Intralipid resulted in significant increases in serum triglycerides from 0.9 +/- 0.1 to 5.1 +/- 1.3 mmol/L (at 90 min). During fat infusion no significant changes in plasma CCK and gallbladder volume were noted when compared with basal values or to the control experiment. During IV fat, concomitant infusion of 0.25, 0.5, and 1.0 Ivy dog unit (IDU) per kilogram per hour of CCK-33 resulted in a significant reduction in gallbladder volume from 26 +/- 6 cm3 (basal) to 15 +/- 4 cm3 (p less than .05), 6 +/- 2 cm3 (p less than .05) and 2.5 +/- 1 cm3 (p less than .05), respectively. No significant differences in CCK-induced gallbladder emptying were observed between IV fat and saline infusion (control). It is concluded that, in contrast to intraduodenal fat, IV infusion of fat does not affect (1) basal plasma CCK and gallbladder volume and (2) CCK-induced gallbladder contraction.     

Impact of enteral and parenteral nutrition on hepatic and muscle glucose metabolism

Liver and muscle metabolism were assessed in dogs adapted to long-term total parenteral (TPN) and enteral (TEN) nutrition. Studies were done in 13 conscious long-term catheterized dogs in which sampling (artery, portal and hepatic vein, and iliac vein), infusion catheters (inferior vena cava, duodenum), and transonic flow probes (hepatic artery, portal vein, and iliac artery) were implanted. Fourteen days after surgery dogs were grouped to receive TPN or TEN. After 5 days of TPN/TEN, substrate balances across the liver and limb were assessed. The liver was a marked net consumer of glucose in both groups (23.6 +/- 3.3 vs 22.6 +/- 2.8 micromol x kg(-1) x min(-1), TPN vs TEN) despite near normoglycemia (6.5 +/- 0.3 vs 6.7 +/- 0.2 mmol/L). Arterial insulin levels were higher during TEN (96 +/- 6 vs 144 +/- 30 pmol/L; p < .05). The majority (79 +/- 13 vs 76% +/- 7%) of the glucose taken up by the liver was released as lactate. Despite higher insulin levels during TEN the nonsplanchnic tissues consumed a lessor quantity of glucose (25.9 +/- 3.3 vs 16.1 +/- 3.9 micro x mol x kg(-1) x min(-1)). In summary, the liver undergoes a profound adaptation to TPN and TEN making it a major site of glucose uptake and conversion to lactate irrespective of the route of nutrient delivery. However, the insulin requirements are higher with TEN possibly secondary to impaired peripheral glucose removal.     

Effect of serum zinc level on amount of collagen-hydroxyproline in the healing gut during total parenteral nutrition: an experimental study

Changes of serum zinc level in dogs receiving either a zinc-free solution or a zinc-supplement solution during total parenteral nutrition (TPN) and the influence of variety of serum-zinc level on serum albumin and collagen-hydroxyproline (C-Hyp) in the incised intestine were investigated. The serum zinc level of zinc-free dogs that was 126.0 +/- 34.3 micrograms per deciliter at the initiation of TPN decreased significantly to 80.0 +/- 15.0 micrograms per deciliter during the one week of TPN, whereas that of zinc-supplement dogs did not decrease during the same period of TPN. Lowering of the serum albumin value was more evident in zinc-free dogs than in zinc-supplement dogs. The amount of C-Hyp in the incised area of the intestine of zinc-free dogs was 2.63 +/- 0.66 micrograms per milligram and that of zinc-supplement dogs was 4.26 +/- 1.04 micrograms per milligram and this difference was significant. It was found that serum zinc level during TPN sharply reflects a supplement of zinc, and C-Hyp in the incised gut and serum albumin of zinc-free dogs are lower than those of zinc-supplement dogs.     

Duodenal motor response to continuous enteral feeding is impaired in mechanically ventilated critically ill patients

In order to investigate the duodenal motor response to continuous enteral feeding during critical illness, we recorded the duodenal contractions of 12 mechanically ventilated critically ill patients during a 4 h fasting period immediately followed by another 4 h period of continuous (100 kcal/h) nasogastric feeding with a polymeric diet. Duodenal motility was recorded by manometry (perfused catheter technique) and the migrating motor complexes (MMC) were identified by their activity front (period of high frequency, regular contractions). The incidence and the mean duration of activity fronts as well as the mean duration of the MMC (time interval separating two successive activity fronts) recorded during both periods were compared. The incidence of activity fronts (fasting: median: 2.5, interquartile range: 5.5; feeding: median: 2, interquartile range: 3.5), their duration (fasting: 6.2 +/- 1.6 min; feeding: 5.8 +/- 1.6 min), and the mean duration of the MMC (fasting: 50.9 +/- 24.7 min; feeding: 49.1 +/- 20.3 min) were similar during both periods. We conclude that in these patients, the fasting pattern of motility is not interrupted by the continuous nasogastric administration of a polymeric diet. Since the activity fronts of the MMCs are highly propulsive, we suggest that their abnormal persistence during feeding may play a role in the pathophysiology of unexplained diarrhoea in some critically ill patients.     

Differences in cholecystokinin release and gallbladder contraction between emulsified and nonemulsified long-chain triglycerides.

BACKGROUND: Fat is a potent stimulus of cholecystokinin (CCK) release. Apart from lipolysis, fatty acid chain length, and saturation, emulsification may also determine the magnitude of CCK release. METHODS: We have studied the effect of emulsification of soybean oil on CCK and pancreatic polypeptide (PP) release (radioimmunoassay [RIA]) and gallbladder motility (ultrasonography). Six healthy subjects were studied on three separate occasions in random order during (1) intraduodenal administration of emulsified long-chain triglycerides (LCT) (6 mmol/h for 120 minutes); (2) equimolar amounts of nonemulsified LCT with addition of emulsifier; and (3) saline with emulsifier (control). RESULTS: Intraduodenal administration of both nonemulsified LCT and emulsified LCT induced significant (p < .05) increases in plasma CCK and PP levels and reductions in gallbladder volume. However, compared with nonemulsified LCT, emulsified LCT resulted in a readier and significantly stronger CCK release (212+/-62 pmol/L per 120 minutes vs 36+/-7 pmol/L per 120 minutes; p < .05); PP release (2034+/-461 pmol/L per 120 minutes vs 671+/-106 pmol/L per 120 minutes; p < .05); and gallbladder contraction (77%+/-2% vs 41%+/-7%; p < .05). No significant alterations were observed in plasma CCK or PP levels and gallbladder volume during administration of saline with emulsifier. CONCLUSIONS: Intraduodenal administration of a low-dose emulsified LCT more potently stimulates CCK and PP release and gallbladder contraction in comparison to equimolar amounts of nonemulsified LCT. These findings point to an important role for solubilization of LCT in determining the magnitude of CCK release from the intestine.     

Different effects of long-chain and medium-chain triglycerides on glucose oxidation during total parenteral nutrition.

This study was undertaken to clarify differences in the effects of lipid emulsions containing either long-chain or medium-chain triglycerides (MCT) on glucose metabolism during total parenteral nutrition (TPN). Glucose kinetics were assessed in beagle dogs using primed, constant infusions of [14C]- and [6-3H]glucose. The rate of appearance of glucose, the percent of VCO2 derived from the oxidation of glucose, the rate of glucose oxidation, and the percent of glucose uptake oxidized were measured at the end of 72 hours of each of the two TPN regimens, ie, TPN in which soybean oil served as long-chain triglyceride comprising 40% of nonprotein calories (L-TPN), and TPN in which tricaprylin emulsion served as MCT (M-TPN). Glucose intake was 5.9 +/- 0.5 mg/kg per minute in L-TPN and 5.8 +/- 0.2 mg/kg per minute in M-TPN. There was no significant difference in the rate of glucose appearance between L-TPN and M-TPN. The rate of glucose oxidation was higher with M-TPN than with L-TPN (p < .05). Not only the percent of VCO2 derived from the oxidation of glucose but also the percent of glucose uptake oxidized tended to be higher during M-TPN than during L-TPN. These findings suggest that the glucose metabolism of dogs receiving L-TPN is different from that of dogs receiving M-TPN.     

The Effect of Intravenous Fat and Total Parenteral Nutrition on Biliary Physiology

Patients on long-term total parenteral nutrition (TPN) have an increased incidence of gallstones. To determine the pathophysiologic mechanisms responsible for gallstone formation in these patients, we fed three groups of prairie dogs intravenously for 10 days with continuous infusions of isocaloric, isovolemic, and isonitrogenous solutions with either 0, 25, or 50% of nonprotein calories provided as Intralipid. A fourth group of prairie dogs was hyperalimented with the 25% solution for 28 days. Control animals were fed Purina rat Chow ad libitum. Each animal's bile salt pool was labeled with iv ³H-cholic acid 16 hr prior to collecting gallbladder and hepatic bile specimens. The ratio of gallbladder to hepatic bile ³H-cholic acid specific activity (dpm/mol of bile acid), an index of gallbladder stasis, was significantly (p <0.05) lower in TPN animals (<0.65 ± 0.19) compared to controls (1.07 ± 0.11).This finding indicates that gallbladder stasis developed in all animals fed by TPN. TPN did not alter gallbladder or hepatic bile lithogenic index. Two of five 28-day TPN animals developed biliary sludge, and one of these animals formed pigment gallstones. TPN without lipid decreased serum cholesterol concentration. As the lipid concentration of the TPN solution was increased, serum cholesterol increased. These data indicate that TPN induces gallbladder stasis regardless of caloric source but does not increase bile lithogenic index despite a dose-related rise in serum cholesterol as the percent of calories provided as lipid is increased. We conclude that TPN-induced gallbladder disease results from gallbladder stasis and not from increased bile cholesterol saturation. (Journal of Parenteral and Enteral Nutrition 8 :263–268, 1984)     

Total body potassium, fat and water during total parenteral nutrition in Crohn's disease

The body composition was studied by measurement of body weight (BW) and total body potassium (TBK), fat and water in 13 patients with Crohn's disease (CD), who were given altogether 18 courses of total parenteral nutrition (TPN) with nil by mouth each lasting at least 3 weeks. At the start of TPN, one group of steroid-free patients displayed intracellular potassium depletion, as reflected by the ratio TBK/lean body mass (LBM) (group 1). Another group of steroid-free patients showed no depletion of intracellular potassium (group 2). The patients given prednisolone all showed intracellular potassium depletion and were assigned to a separate group (group 3). During the initial 19-44 days of TPN, TBK, LBM and BW increased in group 1. All patients with intracellular potassium depletion (groups 1 + 3) showed an increase in TBK and TBK/LBM during the initial 19-51 days of TPN. For steroid-free patients (groups 1 + 2) there were linear relationships between the rate of energy supply per kg LBM and the 24 h change in BW during the third and fourth weeks of TPN (r = 0.79) and between the 24 h change inBW and LBM during the first 19-44 days of TPN (r = 0.59). A steady state in BW was found on administering 53 kcal/kg LBM/24 h. It is concluded that CD patients with intracellular potassium depletion are likely to be improved in terms of TBK and TBK/LBM by at least 3 weeks of TPN as given in the present study. Steroid-free CD patients with intracellular potassium depletion are, moreover, likely to show an improvement in LBM by at least 3 weeks of TPN, and an increase in their BW during the initial 3-6 weeks of TPN will probably reflect an increase in LBM. The pre-TPN TBK/LBM ratio may be a predictor of the repletion rate of the LBM compartment during TPN of steroid-free wasted CD patients.     

Treatment effects of parenteral vitamins in total parenteral nutrition patients

To determine the prevalence of abnormal vitamin levels in an adult hospitalized population requiring total parenteral nutrition (TPN) and to assess the effect of routine parenteral vitamin therapy on vitamin levels, we studied 35 general surgical patients. Assays for 12 vitamins were performed both before and after a standard 10-day course of TPN. Patients were given nothing by mouth. The first 25 patients received a daily parenteral vitamin mixture tailored to the recommendations of the Nutrition Advisory Group of The American Medical Association (maintenance dose). The final 10 patients were given a parenteral multivitamin dose providing substantially greater amounts of most vitamins (repletion dose). Only 58% (190/324) of pre-TPN vitamin levels were normal, 25% were low, and 17% were high. No patient had fewer than two abnormal baseline levels. Vitamin levels did not correlate with serum albumin, body weight, or nitrogen balance. After 10 days of treatment, only 39% of low pre-TPN vitamin levels improved; most (45/62) of the low posttreatment levels were low at baseline. The higher repletion dose resulted in a significantly (p less than 0.01) greater percent increase in vitamin A, C, and pyridoxine levels. The prevalence of abnormal vitamin levels in this population is high (42%). Standard parenteral vitamin therapy leads to marginal improvement in abnormally low pre-TPN vitamin levels.     

Long-term parenteral nutrition in unrestrained nonhuman primates: an experimental model

A freely mobile jacket and tether system was developed for the investigation of total parenteral nutrition (TPN)-induced metabolic bone disease and complications of prolonged TPN in 12 Macaca fascicularis nonhuman primates. The animals received TPN for 49 +/- 7 d (means +/- SEM), providing 82 +/- 2 kcal.kg-1.d-1. Serum glucose increased from 3.6 +/- 0.2 mmol/L at baseline to 8.3 +/- 1.9 mmol/L (p less than 0.01) during TPN, and serum albumin decreased from 38 +/- 1 g/L at baseline to 29 +/- 1 g/L (p less than 0.001) during 2.75% amino acid TPN and 30 +/- 2 g/L (p less than 0.01) during 5% amino acid TPN infusion. No significant changes were seen in serum prealbumin, total protein, bilirubin, alanine aminotransferase, and 5'-nucleotidase during TPN infusion. Major complications included catheter sepsis, hyperglycemia, diarrhea, and premature death in six animals. Thus, metabolic complications of prolonged TPN support may be investigated in a freely mobile nonhuman primate.     

Successful pregnancy outcome using total parenteral nutrition from the first trimester of pregnancy

A 27-yr-old gravida 3, para 2 was supported from the 8th week of pregnancy by intermittent daily total parenteral nutrition (TPN) following the loss of her small bowel. Nutrient intake was adjusted by monitoring nitrogen balance and the rate of increase in fetal cranial enlargement. Maternal calcium balance proved difficult to maintain, since massive urinary Ca+2 losses occurred during infusion of nutrients (576 +/- 2 mg/12 hr on TPN compared to 47 +/- 12 mg/12 hr off). This increase in urine Ca+2 was due to depressed Ca+2 reabsorption by the kidney (87.1 +/- .7 vs 98.1 +/- .3%) and increased filtered load (4623 +/- 241 mg/12 hr vs 2591 +/- 329). Initially calcium balance was -180 mg/day. Nitrogen balance assessed by total stool and urine nitrogen was 1.1 g/24 hr, which was judged to be suboptimal. Deficits were corrected by increasing nitrogen intake, lengthening the duration of infusion and the oral administration of elemental calcium during periods off infusion. A normal fetus was delivered vaginally without complications at 351/2 weeks. This patient demonstrates that normal fetal growth and development as well as appropriate maternal weight gain and nitrogen balance can be maintained throughout pregnancy, including the first trimester, by intermittent daily TPN.     

Metabolic and thermogenic response to continuous and cyclic total parenteral nutrition in traumatised and infected patients

16 traumatised or infected patients on mechanical ventilation were randomised to continuous TPN or to cyclic TPN after a 24-h period of glucose infusion (1.25 kJ x kg BW(-1) x h(-1)). Energy supply was equivalent to 1.3 x baseline energy expenditure. Glucose, fat and amino acids were administered at a constant rate over 24 h in the continuous TPN group and over 12 h, followed by glucose (1.25 kJ x kg BW(-1) x h(-1)), in the cyclic TPN group. Nutrient-induced thermogenesis was lower during continuous than during cyclic TPN (5 +/- 4 vs. 12 +/- 7%, mean +/- SD, p < 0.05), as was the increase in CO(2) elimination (13 +/- 11 vs. 30 +/- 7%, respectively, p < 0.01). Energy balance was more positive during continuous TPN. In both groups, energy expenditure reached a plateau during the first 12 h of TPN infusion. The lower nutrient-induced thermogenesis and more positive energy balance, indicates a more efficient utilisation of nutrients during continuous than during cyclic TPN. The lower CO(2) production during continuous TPN, may be advantageous when respiratory function is compromised. The plateau in energy expenditure in response to TPN infusion may be useful as a guideline for nutritional therapy.     

The effect of artificial feeding on cholestasis, gallbladder sludge and lithiasis in infants: correlation with plasma cholecystokinin levels

The occurrence of hepatic cholestatis (judged by fasting serum bile acid levels), gallbladder sludge formation and lithiasis (ultrasonography) and their correlation with plasma cholecystokinin (CCK) levels was studied in a group of children on continuous total parenteral nutrition (TPN) (n = 95), and later in 40 of these children on cyclic TPN (cTPN). After resumption of oral feeding, 75 were studied on partial oral feeding (2-4 meals) and 40 on constant rate enteral nutrition (CREN) then 45 on total oral feeding (4-6 meals). Gallbladder sludge occurred in 23% of the children on TPN for 1 month and 32% of those on cTPN for 3 months. On CREN, the sludge rate was unchanged, but dropped significantly (17%) on partial oral feeding, and disappeared in children on total oral feeding. Serum bile acids were abnormal in 80% of children on TPN or cTPN and diminished significantly on total oral feeding only. Plasma CCK levels on TPN, cTPN and CREN were identical to fasting levels of children on total oral feeding. Plasma CCK levels increased significantly 1 h post-prandially during both partial (p < 0.02) and total oral feeding (p < 0.001). There was a significant negative correlation between the gallbladder sludge rate and CCK levels for all methods of feeding. This study demonstrates the frequent occurrence of hepatic cholestasis in infants, and the much lower frequency of gallbladder sludge in children compared to adults on TPN. Plasma CCK levels obtained during the different methods of feeding could explain the reduction and eventual disappearance of sludge following stimulation of CCK secretion by discontinuous feeding.     

Effect of age on substrate oxidation during total parenteral nutrition

OBJECTIVE: Parenteral nutrition is increasingly used in the elderly. Aging is accompanied by metabolic changes that can modify substrate use. We compared substrate oxidation during cyclic total parenteral nutrition (TPN) in elderly and middle-aged patients. METHODS: Twelve elderly patients (eight women, four men; 72 +/- 5 y) and 12 middle-aged patients (nine women, three men; 39 +/- 13 y) who were on cyclic TPN for intestinal failure were investigated while in stable condition after at least 15 d of TPN. No patient was diabetic. Indirect calorimetry was performed during fasting and every 30 min during the 3 h of TPN infusion and 3 h after infusion, allowing the measurement of nutrient oxidation. Blood samples were obtained every hour for the measurement of glucose, insulin, triacylglycerols, and free fatty acids. RESULTS: In the fasting state, resting energy expenditure was significantly higher in the elderly patients than in the middle-aged patients (39.3 +/- 8.1 versus 31.9 +/- 4.3 kcal/kg of fat-free mass per day, P = 0.008). During TPN, lipid oxidation was significantly higher in the elderly patients than in the middle-aged patients (1.09 +/- 0.17 versus 0.84 +/- 0.27 mg x kg(-1) x min(-1), P = 0.011); glucose oxidation was significantly lower in the elderly patients than in the middle-aged patients (2.19 +/- 0.93 versus 3.22 +/- 1.54 mg x kg(-1) x min(-1), P = 0.038). Areas under the curves of glycemia and free fatty acids were significantly higher in the elderly patients. CONCLUSION: In the elderly, TPN was associated with significantly higher lipid oxidation and lower glucose oxidation than in younger patients. TPN formulas and flow rates should therefore be adapted in the elderly.     

Serum levels of coenzyme Q10 and lipids in patients during total parenteral nutrition

Serum levels of coenzyme Q10 (CoQ10) as well as lipids were determined in patients during total parenteral nutrition (TPN). The mean CoQ10 levels (M +/- SD) were 0.77 +/- 0.30 microgram/ml for 108 normal subjects and 0.59 +/- 0.35 microgram/ml for 95 patients before TPN. The mean CoQ10 level of the patients decreased significantly to 0.35 +/- 0.23 microgram/ml one week after the start of TPN, and then remained almost unchanged during TPN for up to 6 weeks. When the patients receiving TPN (TPN patients) were grouped according to their clinical diagnoses, the mean CoQ10 level of patients with cancer was significantly lower than that of the other patients without cancer in 4 week therapy, but there was no difference in the levels between the patients with and without diseases of the gastrointestinal tract. Serum levels of total cholesterol (T-Chol) and esterified cholesterol in TPN patients also declined below their respective normal ranges, but not to the same extent in comparison to CoQ10. The levels of triglycerides (TG), phospholipids (PL), non-esterified fatty acids, low density lipoproteins, very low density lipoproteins, chylomicrons, and cholesterol in the high density lipoprotein fraction in serum of TPN patients were within their normal ranges. The levels of CoQ10 in TPN patients were correlative to those of T-Chol, TG, and PL, and decreased rapidly prior to the latter levels.     

Total parenteral nutrition energy composition affects small intestinal disaccharidase activity in the newborn miniature pig

Total parenteral nutrition (TPN) decreases disaccharidase activity in the small intestine of humans and miniature piglets. The possibility, however, that specific components of TPN (eg, the energy mix) will increase disaccharidase activity has largely been unexplored. The identification of such components would be particularly useful in the treatment of premature infants with immature gastrointestinal tracts and patients with small intestinal mucosal disease associated with decreased disaccharidase activity. To determine whether the TPN energy composition affects small intestinal disaccharidase activity, 7-day-old miniature piglet littermates were randomized to receive TPN containing either glucose (group G) or glucose and fat (group G/F) as the nonnitrogen energy source(s). The TPN regimens were isonitrogenous and isoenergetic. The piglets were not allowed oral intake during the 7 days they were maintained on TPN. At 14 days of age the piglets were killed and the small intestines analyzed for weight, protein, DNA, and disaccharidase activity. Body weight was similar between groups at both the beginning and end of the study. The TPN regimen did not affect small intestinal weight of protein and DNA content. However, jejunal and ileal sucrase and ileal maltase activities (mumol/min.kg body wt +/- SD) were greater in group G than those in group G/F (28 +/- 9 vs 19 +/- 11, p = 0.04; 13 +/- 7 vs 7 +/- 4, p = 0.037; and 31 +/- 8 vs 19 +/- 10, p = 0.0088, respectively). No differences in lactase activity were noted between groups.(ABSTRACT TRUNCATED AT 250 WORDS)     

Serum carnitine levels in bone marrow transplant recipients

This study investigated plasma carnitine levels in patients undergoing allogenic bone marrow transplantation. The patients received fat-based TPN (50% fat, 50% CHO; calorie: nitrogen ratio 125:1) for an average of 33 +/- 7.5 days. TPN was started before transplantation and stopped when patients were able to eat. Caloric needs were estimated using the Harris-Benedict equation; 150% of the estimated BEE was given for the first two weeks after transplantation. The amount of TPN was gradually decreased as patients resumed their oral intake. All patients had low-normal serum carnitine levels before transplantation. There was no significant change in total or free serum carnitine levels during the course of TPN. However, in patients who had symptoms of graft vs. host reaction (GVH), the highest carnitine values during GVH (total 72.3 +/- 6.5 and free 61.2 +/- 12.4 mumol/l) were significantly higher (p < 0.001) than the baseline values (total 27.1 +/- 9.3 and free 24.9 +/- 9.6 mumol/l) or the highest non GVH values after transplantation (total 32.0 +/- 10.7 and free 29.0 +/- 10.7 mumol/l, respectively). The serum triglyceride, total cholesterol, and HDL cholesterol remained within normal range. In conclusion, bone marrow transplant patients receiving fat-based TPN have normal circulating levels of carnitine. GVH reaction caused an increase in the carnitine levels, which was probably due to increased tissue catabolism.     

Acetate and hypercalciuria during total parenteral nutrition

Hypercalciuria and negative calcium balance are complications of total parenteral nutrition (TPN). Because metabolism of the TPN formula generates an acid load that can induce hypercalciuria, we evaluated the effect of supplementing the formula with acetate. In a randomized crossover study six patients on continuous and six on cyclic TPN received no added acetate or 160 mmol acetate/d replacing 160 mmol chloride/d for 3 d each. Blood and urine measurements were obtained on day 3 of each formula. Acetate, which is metabolized to bicarbonate, increased blood pH and decreased renal acid excretion. Urinary Ca decreased in every patient from 422 +/- 63 to 240 +/- 46 mg/d (10.5 +/- 1.6 to 6.0 +/- 1.4 mmol/d) and from 468 +/- 68 to 285 +/- 54 mg/d (11.7 +/- 1.7 to 7.1 +/- 1.3 mmol/d) during continuous and cyclic TPN, respectively. Filtered Ca load decreased slightly whereas renal tubular Ca reabsorption increased significantly with acetate. Serum parathyroid hormone, 25-hydroxyvitamin D, 1,25-dihydroxyvitamin D, and urinary cyclic AMP were not different.     

Platelet glutathione peroxidase activity in long-term total parenteral nutrition with and without selenium supplementation.

Selenium (Se) is not routinely included in total parenteral nutrition (TPN) solution; thus, patients receiving long-term TPN may be at risk of Se deficiency, which may cause fatal cardiomyopathy. Platelet glutathione peroxidase (GSH-Px) activity, as well as Se levels and GSH-Px activity in plasma and erythrocytes during prolonged TPN, was measured in six patients with chronic gastrointestinal disease. During the time course of TPN, Se administration was discontinued for 12 weeks, and then resupplemented for another 12 weeks. Before the study period, all Se indices had been maintained within the normal range. After discontinuation of Se supplementation, a significant decrease in platelet GSH-Px activity was observed after 1 week (from 64 +/- 7 [mean +/- SD] to 39 +/- 5 U/g of protein). After resupplementation, it increased after 1 week (from 44 +/- 9 to 65 +/- 10 U/g of protein). Plasma Se indices significantly changed within 3 weeks after withdrawal and reintroduction of Se (Se: from 136 +/- 28 to 75 +/- 14 and from 61 +/- 22 to 125 +/- 33 micrograms/L; GSH-Px: from 236 +/- 50 to 140 +/- 36 and from 128 +/- 32 to 220 +/- 64 U/L). Erythrocyte Se indices showed no significant changes during the study period. The results demonstrate that platelet GSH-Px activity is the most sensitive index of Se status in TPN patients.     

Tissue storage of vitamins A and E in rats drinking or infused with total parenteral nutrition solutions

The total parenteral nutrition (TPN) rat and its sham-operated control were used as a model to compare the metabolism and storage of vitamins A and E when they are administered intravenously or orally. Male Fisher rats were depleted of both vitamins for several months with a diet free of vitamins A or E, but containing retinoic acid for growth. TPN solutions containing aqueous dispersions of retinol, retinyl palmitate and dl-alpha-tocopheryl acetate were infused at 2.3 ml/h into the jugular veins of 10 TPN rats. Eight sham-operated control rats drank similar volumes from food cups. TPN rats received 115.3 +/- 4.5 (mean +/- SEM) micrograms of retinol equivalents and 2.2 +/- 0.2 mg of alpha-tocopherol equivalents per day; controls received 146.4 +/- 16.5 micrograms and 2.1 +/- 0.3 mg, respectively. After 7 days the animals were fasted overnight and killed. Plasma levels of retinol were 27.8 +/- 1.5 micrograms/dl for TPN rats, and 27.4 +/- 1.2 for controls. Plasma alpha-tocopherol was 1909 +/- 183 micrograms/dl for TPN rats and 1063 +/- 77 for controls. The only forms of the vitamins found in plasma after overnight fasting were unesterified retinol and unesterified alpha-tocopherol. Sham-operated control rats stored amounts of vitamins A and E similar to values reported in the literature for fed animals. TPN rats stored more of both vitamins than controls in liver, heart, and spleen, but not in testes. The enhanced liver vitamin storage by TPN rats did not appear to be due to a slight increase in lipid content. The results indicate that both vitamins A and E infused in TPN solutions maintain blood levels and are stored in tissues.