0.107

0.108

EFFECTS OF ENTERAL NUTRITION ON EXOCRINE PANCREATIC SECRETION IN DOGS E. Klein, S. Schneibaum, G. Ben-Ari (Department of Surgery C, The Chaim Sheba Medical Center, Tel-Hashomer, Israel)

Various pancreatic pathological states may involve nutritional deterioration. Total parenteral nutrition (TPN) has been advocated as part of the management in these cases. We studied the effects of intraintestinal nutrition, using separate components of TPN, on the exocrine pancreatic secretion in dogs. Eight dogs were surgically prepared with a Tery-Vela fistula (using an isolated proximal jejunal segment) and a Thomas cannula inserted in the duodenum opposite the main pancreatic papilla. The exocrine pancreatic secretion was collected by means of a cannula inserted into the papilla and analyzed for volume output, bicarbonate, electrolytes and amylase concentration. Continuous drip of separate TPN components (Intralipid, 25% glucose and amino acids solution), was then instituted through the isolated jejunal loop and the effects upon the exocrine pan- creatic secretion observed. Hypertonic glucose significantly reduced (40%)* pancreatic volume output while fat emulsion caused an increase (35%). Amino-acids solution did not effect pancreatic volume flow. Fat caused significant increase in bicarbonate output (40%) while amino- acids and glucose did not cause any significant change. Amylase levels significantly increased (250%) during fat emulsion drip, and decreased (50%) while hypertonic glucose was administered. No change was observed with amino- acid treatment. The electrolytes remained within normal range throughout the observa- tion. Our results demonstratethatintraintestinal hypertonic glucose has a depressing effect, while fat has a stimulating effect upon exocrine pancreatic secretion. These observations suggest that in considering nutritional assistance in various patho- logical states in which pancreatic output depression is desired, high glucose, high protein with low fat components would be the suggested formula for the treatment. *percent of control values

EFFECT OF ENTERAL FEEDING WITH PECTIN ON LIPOGENESIS R. Rolandelli, M Koruda, G.

Settle, K. Pourier, P. Stein, J. Rombeau (Department of Surgery, University of Pennsyl- vania and Medical Research Service, Philadelphia Veterans Administration Medical Center, U.S.A.)

Certain dietary fibers, such as pectin, are completely fermented by bacteria in the colon. Short chain fatty acids (SCFAS) produced by the fermentation of these fibers may be absorbed, providing an additional caloric source which may in turn affect fat metabolism. To determine the effect of pectin fermentation on lipogenesis, we fed 3 groups of rats (275-300 g) a liquid diet (LD) providing 1.0 gN/kg/d as free amino acids (Aminosyn) and 250 kcal/kg/d as glucose polymers (Polycose). The LD was administered via gastrostomy for 6 days. CONTROLS received the LD alone; PECTINS, LD with the addi- tion of 1% pectin; and NEOMYCINs, LD with 1% pectin and neomycin (80 mg/kg/d). On the fifth day, all diets included 12.5% D20. After the infusion of labelled diets for 24 hours, animals were sacrificed and the total content, by gas chromatography, and deuterium incorporation, by mass spectroscopy, of palmitate, stearate and oleate in the liver were determined. The amount of each fatty acid synthesized by the liver was calculated.

Palmitate l:?~?$b c -p- -+ PECTINa + -p- + NEOMYCINa

Stearate .Ol 33.7 0.7 .Ol 21.1 0.7 c

Oleate ;.;I;.;{ .Ol I j 10.7 0.4 .03 5.6 0.4 c t 1

. . .002 9.4(0.3) .002 4.1(0.2)c a N=6/group; bMean(SD), mg/liver/24 hr.; 'p>.3 vs CONTROLS

The pectin supplemented fat-free diet led to a significant increase in the synthesis of fatty acids in the liver. This effect of pectin was not observed when colonic bacterial activity was reduced with the administration of the antibiotic neomycin. Pectin's effect on lipogenesis likely results from the absorption of SCFAs produced by bacterial fermentation. These data are consistent with the hypothesis that pectin provides an additional energy source for the host when fermented by colonic bacteria.

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