[Current nutrition supporting programs of the population in the USA]. / Wspólczesne programy dozywiania ludnosci w Stanach Zjednoczonych.

In this work main programs of nutrition-supporting in the USA were presented as a part of national and local social and health policy. Following programs were reviewed namely: FSP (The Food Stamp Program), NSLP (The National School Lunch Program), SBP (School Breakfast Program), SMP (The Special Milk Program), WIC Program (The Special Supplemental Food For Women, Infants and Children), SFSP (The Summer Food Service Program). The level of monthly income per person (no more than 130% of poverty line) is the condition for participation in every program. Some programs (e.g. FSP) are addressed to all citizens, who are fulfilling income criteria, whereas other (e.g. WIC, SBP) are available to selected population groups only. Assistance within these programs may occur in various forms (e.g. food stamps for family, possibilities in using of low cost meals, free of cost milk for school children). Authors suggest to utilize some of US experience in nutrition-supporting programs also in Poland.

Comparison of organ uptake and disappearance half-time of human epidermal growth factor and insulin.

Epidermal growth factor (EGF), which was originally identified in salivary glands and saliva, has been also found in the kidney and urine, suggesting that the kidney may be an alternate source of this peptide. Liver was considered as the major site of the degradation of EGF but the involvement of other organs has been little studied. Therefore, we carried out comparative studies on the organ uptake and the disappearance half-time of EGF and insulin (having similar molecular size) in the same model of anesthetized dog with arterial (from aorta) and venous (from mesenteric, portal, hepatic, renal, femoral and jugular veins) blood sampling from various organs. Basal plasma level of EGF (1.32 +/- 0.33 pmol/l) and insulin (62.1 +/- 13.8 pmol/l) in the aorta was not significantly different from that recorded at various sampling sites. During i.v. infusion of EGF at 41.6 and 166.6 pmol/kg/h, the respective arterial EGF concentrations averaged 103 +/- 21 and 240 +/- 49 pmol/kg/h and the percent reduction in plasma EGF after passage through the head, leg, intestines and liver was about 30-50% and that after passage through the kidney was about 95%. During insulin (6.9 pmol/kg/h) infusion, the arterial hormone level averaged 227 +/- 21 pmol/l and this level was significantly reduced (by 23-42%) after passage through the head, leg, intestine, liver and kidney but no significant difference was found between various venous sampling sites. EGF and insulin appearing in the urine during EGF or insulin infusion accounted for about 40 and 7% of the difference between the entering and leaving renal masses of the peptide. Mean disappearance half time on stopping of EGF and insulin infusion was, respectively, 2.32 +/- 0.58 and 6.88 +/- 1.25 min. We conclude that unlike insulin, which is removed to similar extent by various organs including the kidney and the liver, EGF is taken up mainly by kidney and EGF present in urine originates mainly from renal clearance of peptide.

Comparison of ranitidine and cimetidine in the inhibition of histamine, sham-feeding, and meal-induced gastric secretion in duodenal ulcer patients.

The effects of ranitidine, a new H2-receptor antagonist which does not contain an imidazole ring, and cimetidine have been determined on histamine, meal-induced gastric acid secretion, and serum gastrin levels in duodenal ulcer patients. Compared with cimetidine, ranitidine was found to be about eight times more potent an inhibitor of histamine-induced secretion and four to five times more potent an inhibitor of sham-feeding, and real feeding induced acid secretion without effecting serum gastrin levels.

Comparison of biological activity and disappearance rates of synthetic big gastrin, little gastrin and minigastrin in the dog.

Three synthetic preparations of big gastrin (G-34), little gastrin (G-17) and minigastrin (G-14) have been compared with regard to gastric acid stimulatory potency, rate of disappearance and the relation between acid secretion and the change in serum immunoreactive gastrin in gastric fistula and Heidenhain pouch dogs. Equimolar graded doses (12.5 to 200 pmol/kg-hr) of G-14, G-17 and G-34 produced similar rates of acid secretion with equal ED50 for all three gastrin peptides. Equimolar doses of G-14 and G-17 also resulted in similar increments in serum immunoreactive gastrin, but those of G-34 caused approximately two to three times greater increments in serum gastrin than did G-14 or G-17. The disappearance half-times determined by measuring serum gastrin at short intervals after discontinuation of equimolar dose (1000 pmol/kg-hr) infusions of each gastrin peptide were 1.75, 4.85 and 11.53 min for G-14, G-17 and G-34, respectively. The calculated space of distribution was similar for all three gastrin preparations and ranged from 20-30% body weight. These results indicate that the three major gastrin components differ in half-times and in relating secretory potency, in that relatively higher molar concentrations of G-34 than G-14 or G-17 were required to produce equal rates of acid secretion.

Comparison of methionine-enkephalin and morphine in the stimulation of gastric acid secretion in the dog.

In dogs with Heidenhain pouches and gastric fistulas, we studied acid secretion in response to systemic or portal infusion of methionine-enkephalin (met-enkephalin), enkephalin-analog, or morphine. All these opiate compounds caused a dose-dependent increase in acid secretion under basal conditions and resulted in a significant rise in pentagastrin- or histamine-induced acid secretion. The stimulation by opiates of gastric secretion was accompanied by an increase in the mucosal blood flow but without any significant change in serum gastrin concentration. Gastric acid stimulation by met-enkephalin and morphine was strongly inhibited not only by naloxone, an opiate antagonist, but also by blockers of H2-receptors (metiamide) or cholinergic receptors (atropine), suggesting a cooperative interaction between opiates and other stimuli of parietal cells. The gastric stimulation by met-enkephalin and its analog, but not by morphine, was markedly reduced by portal administration of these compounds, indicating a marked inactivation of opiate peptides by hepatic transit. This study shows that enkephalin and morphine stimulate gastric acid secretion by a gastrin-independent mechanism sensitive to atropine and H2-blocker and probably involving opiate receptors.

Pancreatic secretion and cyclic AMP in pancreatic tissue after intravenous infusion of secretin and vasoactive intestinal peptide in cats.

This study demonstrates that secretin and vasoactive intestinal peptide increased dose-dependently pancreatic bicarbonate secretion and cyclic AMP content in pancreatic tissue homogenates in cats. It is concluded that both hormones may act on the same receptor site in the pancreas and that their action is based on stimulation of the adenylate cyclase-cyclic AMP system.

Cephalic phase of gastric secretion in healthy subjects and duodenal ulcer patients: role of vagal innervation.

In 10 healthy subjects and 25 duodenal ulcer patients, gastric acid and pepsin and serum gastrin responses to cephalic-vagal stimulation induced by modified sham-feeding (MSF) were studied before and after vagotomy and atropinisation and compared with those to maximal stimulation with pentagastrin. When the MSF-induced peak acid output was normalised as a percentage of peak response to pentagastrin it was about 62% in healthy subjects and 66% in duodenal ulcer patients. Serum gastrin concentration was not changed significantly by modified sham-feeding either in normal subjects or in duodenal ulcer patients. Truncal vagotomy completely abolished gastric acid and pepsin responses to MSF in duodenal ulcer patients. Atropine almost completely suppressed gastric acid and pepsin responses to MSF in healthy subjects and reduced those in duodenal ulcer patients by about 62%. The combination of the modified sham-feeding and pentagastrin infusion resulted in augmentation of the acid output in duodenal ulcer patients but not in healthy subjects. This study shows that the cephalic phase results in a potent gastric acid and pepsin stimulation which is not accompanied by any change in serum gastrin concentration either in healthy subjects or duodenal ulcer patients and which is abolished by vagotomy and suppressed by atropine.

Direct inhibition of gastric secretion and mucosal blood flow by arachidonic acid.

1. Gastric acid and pepsin secretion stimulated almost maximally by i.v. infusion of histamine, the mucosal blood flow, and the immunoreactive prostaglandin E (PGE) content have been measured following arachidonic acid administration either intra-arterially or topically to the mucosa of the fundic portion of a stomach kept in a Lucite chamber. 2. Arachidonic acid administered directly to the stomach produced a marked and significant inhibition of histamine-induced gastric secretion accompanied by a reduction in mucosal microcirculation and a rise in the immunoreactive PGE content in the gastric juice. 3. These secretory and circulatory changes induced by arachidonic acid were prevented by pretreatment of the gastic mucosa with indomethacin, a potent inhibitor of the prostaglandin synthetase system. 4. Arachidonic acid infused intra-arterially in graded doses resulted in a dose-dependent reduction in gastric acid secretion, mucosal blood flow and cyclic AMP mucosal content. 5. These studies indicate that arachidonic acid applied directly to the stomach causes a marked gastric secretory inhibition, probably due at least in part to the enzymic transformation of arachidonic acid to prostaglandins and possibly other active lipids responsible for the changes in the gastric mucosal microcirculation and cyclic AMP mucosal content.

Comparison of intraduodenal and intravenous administration of amino acids on gastric secretion in healthy subjects and patients with duodenal ulcer.

The ability of an amino acid mixture given intraduodenally or intravenously to stimulate gastric secretion is compared in healthy subjects and in duodenal ulcer patients. Graded amounts of amino acids by both routes produced a similar increase in acid output in healthy subjects, reaching about 30% of the maximal response to pentagastrin. Serum gastrin concentrations remained virtually unchanged but serum alpha amino acid nitrogen levels were about twice as high with intravenous as with intraduodenal administration. Intravenously administered amino acids produced a significantly higher acid output in patients with duodenal ulcer than in healthy subjects, but did not produce a significant increase in gastric acid or pepsin secretion when combined with a pentagastrin infusion as compared with pentagastrin alone. Cimetidine (2 mg/kg/h) added to intravenous amino acid infusions caused almost complete suppression of acid secretion. This study indicates that amino acids are capable of stimulating gastric secretion after intraduodenal and after intravenous administration. The response to the latter is significantly higher in patients with duodenal ulcer than in healthy subjects, does not appear to involve gastrin release, is not affected by pentagastrin, and is strongly suppressed by histamine H2-blocker.

Effect of methylated prostaglandin E2 analogue on insulin secretion in man.

Previous studies of the effect of E series prostaglandins /PGs/ on insulin secretion gave conflicting results in animals and little information in man. This study was designed to determine the effect of methylated PGE2 analogue /15/S/- 15-methyl PGE2 methyl ester/, given orally, intraduodenally or intravenously, on insulin secretion, both under basal conditions and in response to intraduodenal or intravenous administration of glucose in 22 male volunteers. Methylated PGE2 kept basal serum insulin level unchanged, but significantly reduced insulin response by 15 +/- 6 microunits/ml to intravenous glucose pulse injection /0.1 g/kg/ or by 45 +/- 11 microunits/ml to intraduodenal glucose infusion /0.5 g/kg-hr/. Blood glucose level was unaffected in tests with intraduodenal methylated PGE2, but in tests with intravenous administration it was significantly reduced. These studies demonstrate that methylated PGE2 analogue given orally, intraduodenally or intravenously results in a potent suppression of insulin response to glucose challenge.

Effect of somatostatin on meal-induced gastric secretion in duodenal ulcer patients.

The effect of somatostatin, a growth hormone releasing-inhibiting hormone (GH-RIH) on basal and meal-, pentagastrin-, or histamine-stimulated gastric acid and pepsin secretion was studied in six duodenal ulcer patients. Intravenous GH-RIH infused in graded doses ranging from 0.62 to 5.0 microgram/kg/hr produced a dose-related inhibition of pentagastrin-induced acid secretion reaching about 15% of control level at the dose of 5.0 microgram/kg/hr. Acid inhibition was paralleled by a decrease in the pepsin output and accompanied by a dose-dependent reduction in serum growth hormone and insulin levels measured by radioimmunoassay. GH-RIH used in a single dose of 2.5 microgram/kg/hr produced about 85% inhibition of acid secretion induced by a meal (measured by intragastric titration) accompanied by a significant decrease in serum gastrin and insulin levels. The effect of GH-RIH on histamine-stimulated secretion was very modest and observed only after stopping the GH-RIH infusion. Thus GH-RIH suppressed acid and pepsin secretion induced by pentagastrin and a meal, and this effect was accompanied by a suppression of serum growth hormone and gastrin levels which may contribute to the inhibition of gastric secretion observed.

Double-blind clinical trial on gastroduodenal ulcer healing with prostaglandin E2 analogues.

Seventy-seven patients with gastroduodenal ulcer were treated with two methyl-prostaglandin E2 analogues, m-PGE2, in a double-blind clinical trial. Each of three groups was given 15 S-15 methyl PGE2 methyl ester, 15 R-15 methyl PGE2 methyl ester, and placebo, respectively. Both forms of m-PGE2 analogues appeared to reduce gastric acid secretion, to shorten ulcer healing, and also to produce some side-effects, form 'S' being the more potent. Prompt healing of the ulcer with these agents did not prevent the recurrence of the disease. As the serum gastrin response to a meal after m-PGE2 administration was not reduced, this agent seems directly to affect oxynthic cells.