hPP Concentrations Research Articles

Combination treatment of high‐pressure and CaCl2 for the reduction of sodium content in chicken meat batters: effects on physicochemical properties and sensory characteristics

SummaryA combination of high‐pressure processing (HPP, 200 MPa, 10 min) and CaCl2 (0.2%, w/w) on the cooking loss (CL), expressible moisture (EM), textural properties (hardness, springiness, cohesiveness, chewiness and firmness) and sensory attributes of reduced‐sodium (1.25% NaCl) chicken meat batters (RCMB) was investigated. The results revealed that combining HPP with CaCl2 significantly decreased EM, elevated sensory properties and acted synergistically in reducing CL and improving hardness, chewiness and firmness, which enabled RCMB to obtain quality characteristics similar to those with high salt (2.5% NaCl) content. These changes brought about by combined HPP and CaCl2 could be attributed to increased apparent viscosity and proportion of immobilised water, enhanced rheological (elastic) properties and a denser, homogeneous protein gel network with evenly dispersed small fat globules. It is interesting to take advantage of the synergy between moderate HPP and low concentrations of CaCl2 to develop meat products with reduced sodium content.

Water holding capacity of sodium‐reduced chicken breast myofibrillar protein gel as affected by combined CaCl2 and high‐pressure processing

SummaryThe water holding capacity (WHC) of sodium‐reduced (0.3 m sodium chloride, corresponding to the salt percentage (w/v) of 1.755%) myofibrillar protein (MP) gel in response to combined calcium chloride (CaCl2, 20, 60, 100 mm) and high‐pressure processing (HPP, 200 MPa, 10 min) was investigated. The results showed that 200 MPa + 20 mm CaCl2 synergistically increased the WHC of MP gel via reducing particle size of MP solutions, strengthening hydrogen‐bonding and disulphide‐bonding, promoting formation of β‐sheet and uncoiling of α‐helix, exposing tryptophan residues, enhancing hydrophobic interactions of aliphatic residues and forming a compact and continuous networked gel structure. However, high concentrations (≥60 mm) of CaCl2 could attenuate the enhancing effects of HPP on the WHC by inducing decreased hydrogen bonds, fewer tryptophan residues exposed and coarser and aggregated gel structures with large cavities. Therefore, a combined moderate HPP and low concentration of CaCl2 is a potential alternative for developing sodium‐reduced meat products.

Chemical and rheological properties of proteoglycans from Sarcandra glabra (Thunb.) Nakai.

Two proteoglycans (HPP and LPP) with different ratios of protein/polysaccharide were extracted from S. glabra. The chemical compositions, relative average molecular weights, monosaccharide compositions, FT-IR spectra, and rheological properties of the two proteoglycans were determined. The results exhibited that the two proteoglycans had pseudoplastic fluids properties and displayed shear-thinning behavior. The apparent viscosity of the two proteoglycans both increased with increasing concentrations. The temperature had different effects on the viscosity of the two proteoglycans. As temperature increased from 25 to 85 °C, the viscosity of LPP descended while the HPP's viscosity rose first and then dropped slightly. The effects of CaCl2 addition on the two samples were like that of the temperature. The viscosities of HPP and LPP had different tolerances to acidity and alkalinity. HPP solution was more sensitive to pH changes due to its high protein content. The addition of sucrose increased the viscosities of samples. The modulus G' and G″ of HPP and LPP were increased with the increase of oscillation frequency, while the crossover points of G' and G″ values decreased with the increasing concentrations of HPP and LPP. The above data presented that the two proteoglycans could be promising candidates for food industries and pharmacological applications.

Effect of harvest time on some in vitro functional properties of hop polyphenols.

Health benefits of hop polyphenols are well studied. In the present investigation, we examined the antioxidant activity, anti-nitric oxide (NO) production, and anti-adipocyte differentiation of polyphenols extracted from hops (HPP), harvested at different times for over 4years. Saaz hop variety from the Czech Republic was used in the in vitro assays. Twenty-three polyphenols were quantitatively analyzed using Orbitrap liquid chromatography-mass spectrometry (LC-MS), and their health promoting effects were assayed individually. Strong effects of low concentrations of HPP were observed in the above three assays. A significant increase in anti-adipocyte differentiation activity per unit weight of HPP was obtained in the early harvested samples. A significant difference in anti-NO production activity per unit weight of HPP was observed among the different harvest years. HPP significantly increased in early harvested samples. Our results suggest that some in vitro functional properties of hops vary with harvest time and year and are dependent on different polyphenols.

Heterogeneity of the neuropeptide Y (NPY) contractile and relaxing receptors in horse penile small arteries

The distribution of neuropeptide Y (NPY)-immunorective nerves and the receptors involved in the effects of NPY upon electrical field stimulation (EFS)- and noradrenaline (NA)-elicited contractions were investigated in horse penile small arteries. NPY-immunoreactive nerves were widely distributed in the erectile tissues with a particularly high density around penile intracavernous small arteries. In small arteries isolated from the proximal part of the corpora cavernosa, NPY (30 nM) produced a variable modest enhancement of the contractions elicited by both EFS and NA. At the same concentration, the NPY Y(1) receptor agonist, [Leu(31), Pro(34)]NPY, markedly potentiated responses to EFS and NA, whereas the NPY Y(2) receptor agonist, NPY(13-36), enhanced exogenous NA-induced contractions. In arteries precontracted with NA, NPY, peptide YY (PYY), [Leu(31), Pro(34)]NPY and the NPY Y(2) receptor agonists, N-acetyl[Leu(28,31)]NPY (24-36) and NPY(13-36), elicited concentration-dependent contractile responses. Human pancreatic polypeptide (hPP) evoked a biphasic response consisting of a relaxation followed by contraction. NPY(3-36), the compound 1229U91 (Ile-Glu-Pro-Dapa-Tyr-Arg-Leu-Arg-Tyr-NH2, cyclic(2,4')diamide) and eventually NPY(13-36) relaxed penile small arteries. The selective NPY Y(1) receptor antagonist BIBP3226 ((R)-N(2)-(diphenacetyl)-N-[(4-hydroxyphenyl)methyl]D-arginineamide) (0.3 microM) shifted to the right the concentration-response curves to both NPY and [Leu(31), Pro(34)]NPY and inhibited the contractions induced by the highest concentrations of hPP but not the relaxations observed at lower doses. In the presence of the selective NPY Y(2) receptor antagonist BIIE0246 ((S)-N2-[[1-[2-[4-[(R,S)-5,11-dihydro-6(6h)-oxodibenz[b,e]azepin-11-y1]-1-piperazinyl]-2-oxoethyl]cyclo-pentyl-N-[2-[1,2-dihydro-3,5 (4H)-dioxo-1,2-diphenyl-3H-1,2, 4-triazol-4-yl]ethyl]-argininamide) (0.3 microM), the Y(2) receptor agonists NPY(13-36) and N-acetyl[Leu(28,31)]NPY (24-36) evoked potent slow relaxations in NA-precontracted arteries, under conditions of nitric oxide (NO) synthase blockade. Mechanical removal of the endothelium markedly enhanced contractions of NPY on NA-precontracted arteries, whereas blockade of the neuronal voltage-dependent Ca(2+) channels did not alter NPY responses. These results demonstrate that NPY can elicit dual contractile/relaxing responses in penile small arteries through a heterogeneous population of postjunctional NPY receptors. Potentiation of the contractions evoked by NA involve both NPY Y(1) and NPY Y(2) receptors. An NO-independent relaxation probably mediated by an atypical endothelial NPY receptor is also shown and unmasked in the presence of selective antagonists of the NPY contractile receptors.

Two pyridinium metabolites of haloperidol are present in the brain of patients at post-mortem.

We have shown in patients taking the antipsychotic drug haloperidol (HP) that two pyridinium metabolites (HPP+ and RHPP+) are present in blood and urine in nM concentrations. These metabolites are structurally analogous to MPP+, the neurotoxic metabolite of the well-known parkinsonian-producing protoxin, MPTP. In this study we measured the concentrations of HPP+ and RHPP+ in seven regions of the brain (putamen, substantia nigra, globus pallidus, caudate, hippocampus, cerebellum and occipital cortex) obtained at post-mortem from three patients who were taking HP before death. Blood, urine, and bile from one patient were analysed as well. HPP+ was present in all regions (except for substantia nigra in one patient and globus pallidus in another); the amount/g ranged from 1.6-8.3 pMol but there was no preferential sequestration of the metabolite in dopaminergic regions. Similarly, RHPP+ was present relatively uniformly in all regions; the amount/g ranged from 1.1-7.6 pMol. The concentrations of HPP+ and RHPP+ in one patient were 24 and 13 nM in blood, 660 and 230 nM in urine, and 13.0 and 1.4 microM in bile, respectively. The presence of these pyridinums in brain adds another important piece of information to the case that, at least for HP, metabolite-induced neurotoxicity could contribute to the extrapyramidal side-effects in patients receiving long-term therapy.

Neurotoxic implications of haloperidol metabolism

A sensitive and selective method for the determination of the pyridinium metabolite (HPP+) derived from the antipsychotic drug haloperidol (HP) in brain tissue, plasma and urine using high-performance liquid chromatography with fluorescence detection is described. The HPP+ present in biological samples was extracted using a Sep-Pak C18 cartridge. Recoveries of HPP+ ranged from 78 to 90%. Final separation and quantitative estimations of HPP+ were achieved on a C18 reversed-phase column employing a mobile phase of acetonitrile—30 mM ammonium acetate (40:60, v/v) containing 10 mM triethylamine and adjusted to pH 3 with trifluoroacetic acid. The fluorescence detection utilized an excitation wavelength of 304 nm and an emission wavelength of 374 nm. Standard curves were linear in the range of 2.5–100 ng/ml for brain tissue homogenate and plasma samples and 10–500 ng/ml for urine samples. The detection limit of HPP+ was about 1 ng/ml in all biological samples. The concentrations of HPP+ in brain tissue, plasma and urine from HP-treated rats were determined using this method.

Quantitative analysis of two pyridinium metabolites of haloperidol in patients with schizophrenia

A pyridinium metabolite (HPP+) of the neuroleptic drug haloperidol has been identified in rats and in the urine of patients. The purpose of this study was to measure the steady-state blood and plasma concentrations and daily urinary excretion of HPP+ in patients treated with haloperidol. HPP+ was measured by HPLC with fluorescence detection. The chromatograms also revealed the presence of a previously unknown pyridinium species, which was identified in urine by liquid chromatography/mass spectrometry/mass spectrometry as 4-(4-chlorophenyl)-1-4-(4-fluorophenyl)-4-hydroxybutylpyridinium (RHPP+). Concentrations of RHPP+ were then measured by HPLC. The steady-state concentrations of HPP+ or RHPP+ in blood and plasma from 34 patients were virtually identical. The plasma concentrations of each metabolite were related to the daily dose of haloperidol and to its plasma concentrations. Nonlinearity in the elimination of RHPP+ was suggested by the increase in the ratio between RHPP+ and HPP+ plasma concentrations with dose or steady-state concentrations of haloperidol. The concentrations of RHPP+ in plasma and urine generally exceeded those of HPP+; the ratio between them in plasma ranged from 0.9 to 14.1. The daily urinary excretion of HPP+ and RHPP+ accounted for 0.40% +/- 0.18% and 2.3% +/- 1.4% of the haloperidol dose, respectively. The renal clearance of each species was 4.5 +/- 2.5 and 11.3 +/- 5.3 L/hr, respectively. The presence of these pyridinium species in humans raises the concern that they may be neurotoxic in a manner similar to the dopaminergic pro-neurotoxin, 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine.

Determination of the pyridinium metabolite derived from haloperidol in brain tissue, plasma and urine by high-performance liquid chromatography with fluorescence detection

A sensitive and selective method for the determination of the pyridinium metabolite (HPP +) derived from the antipsychotic drug haloperidol (HP) in brain tissue, plasma and urine using high-performance liquid chromatography with fluorescence detection is described. The HPP + present in biological samples was extracted using a Sep-Pak C 18 cartridge. Recoveries of HPP + ranged from 78 to 90%. Final separation and quantitative estimations of HPP + were achieved on a C 18 reversed-phase column employing a mobile phase of acetonitrile—30 m M ammonium acetate (40:60, v/v) containing 10 m M triethylamine and adjusted to pH 3 with trifluoroacetic acid. The fluorescence detection utilized an excitation wavelength of 304 nm and an emission wavelength of 374 nm. Standard curves were linear in the range of 2.5–100 ng/ml for brain tissue homogenate and plasma samples and 10–500 ng/ml for urine samples. The detection limit of HPP + was about 1 ng/ml in all biological samples. The concentrations of HPP + in brain tissue, plasma and urine from HP-treated rats were determined using this method.

Carbohydrate digestion and release of pancreatic polypeptide in health and diabetes mellitus.

The effects of meal volume and luminal digestion of carbohydrates on the release of pancreatic polypeptide (HPP) were investigated in eight healthy subjects and in six patients who had non-insulin dependent diabetes mellitus. On one occasion each subject ingested a placebo with 200 ml water and a starch (50 g) pudding meal (400 ml) 30 minutes later. On another occasion an amylase inhibitor that retards intraluminal starch digestion was given with the water and starch. In normal subjects, water caused a moderate rise in HPP plasma levels (16.9 (10.9) pg/ml; p less than 0.02) and ingestion of starch increased HPP in a double peaked pattern. The mean increments of the peaks were 45.0 (15.2) pg/ml (p less than 0.02) and 41.1 (17.3) pg/ml (p less than 0.05), respectively. In the diabetic subjects, the HPP concentrations did not increase in response to water. After ingestion of starch the diabetics had two peaks of HPP that were similar in magnitude, but the early postprandial peak was delayed significantly compared to normal subjects (37.5 (5.1) min v 23.4 (3.9) min; p less than 0.05). The amylase inhibitor (5 or 10 g) reduced the early postprandial HPP peak by 79% (p less than 0.05) in normal subjects and 4 g of the inhibitor reduced the early HPP peak by 58% (p less than 0.05) in the diabetics. In both groups ingestion of the amylase inhibitor abolished the late HPP peak (p less than 0.05). In conclusion, carbohydrate induced HPP release is dependent on undisturbed intraluminal starch digestion.

Effects of human pancreatic polypeptide on exocrine pancreatic function in conscious rats.

The effect of newly synthesized human pancreatic polypeptide (hPP) on pancreatic secretion stimulated by a diversion of bile-pancreatic juice (BPJ) from the intestine, and plasma hPP concentration were examined in conscious rats. Exogenous hPP infusion (1, 10 micrograms/kg/hr) inhibited pancreatic protein, bicarbonate and fluid outputs during BPJ diversion in a dose-dependent manner. During 1 and 10 micrograms/kg/hr hPP infusion plasma hPP immunoreactivity increased to 369 +/- 22.9 and 1,125 +/- 90.2 pg/ml, respectively. These results suggest that newly synthesized hPP has an inhibitory activity on exocrine function of the pancreas.

Diabetic autonomic neuropathy and impaired human pancreatic polypeptide secretion in response to food.

In normal subjects, the early human pancreatic polypeptide (hPP) increase induced by food is mainly dependent on vagal activity. Parasympathetic function and plasma hPP response to a standard mixed meal were evaluated in 10 long term insulin-dependent (type I) diabetic patients (group A), 6 age-matched newly diagnosed type I diabetic patients (group B), and 8 normal subjects. The indices of vagal function (beat to beat heart rate variation during deep breathing and the Valsalva maneuver) were uniformly altered in group A, while they were in the normal range in group B, thus excluding in these latter patients the presence of vagal damage. Plasma hPP in response to standard mixed meal was measured at 5, 15, 30, 60, and 120 min. Fasting plasma hPP concentrations (determined by RIA) in groups A and B (mean +/- SEM, 113 +/- 21 and 83 +/- 21 pg/ml, respectively) did not significantly differ from normal (59 +/- 12 pg/ml). In group A, the initial meal-induced hPP increase was significantly lower than normal (5 min, 139 +/- 12; 15 min, 173 +/- 24; 30 min, 137 +/- 17 pg/ml; P less than 0.01 vs. 5 min, 412 +/- 76; 15 min, 446 +/- 57; 30 min, 325 +/- 56 pg/ml). All group B patients had a marked early increase in the peptide, similar to that in the normal subjects. These results suggest that diabetic autonomic neuropathy is associated with dysfunction of hPP secretion, and the evaluation of hPP in response to SMM may be considered a sensitive and nonstressful method for the assessment of parasympathetic impairment in diabetes.

Effects of cisapride on the secretion of pancreatic polypeptide in healthy volunteers.

Plasma human pancreatic polypeptide (hPP) responses to intravenous injections of a new gastric and intestinal motility promoting agent, R51 619 (cisapride), were studied in healthy volunteers. The mean fasting concentrations of plasma hPP (39 +/- 5.4 pg/ml; mean +/- S.E.) were elevated significantly to the peak values of 118 +/- 25.1 pg/ml 30 min after the drug had been given in a dose of 4 mg over 5 min. However, plasma insulin (IRI), glucose and prolactin levels were not elevated. Atropine diminished the cisapride-induced hPP elevation, thereby suggesting that cisapride induced release of acetylcholine but had no antidopaminergic action.

Gastric acid and pancreatic polypeptide responses to sham feeding are impaired in diabetic subjects with autonomic neuropathy.

To assess the relationship between cardiac and extra-cardiac dysfunction in diabetic autonomic neuropathy, the gastric acid output and the pancreatic polypeptide (hPP) secretion in response to sham feeding were evaluated in diabetic patients with (group 1) and without (group 2) cardiac autonomic neuropathy (CAN), and in normal subjects (group 3). All patients assigned to the group with CAN exhibited an impaired beat-to-beat heart rate variation during deep breathing. The basal gastric acid output was comparable in the three groups (1.3 +/- 0.5, 2.8 +/- 1.5, and 3.9 +/- 1.5 mmol/h, respectively). In contrast, the gastric acid output stimulated by sham feeding was significantly lower in patients with CAN (5.3 +/- 1.3 mmol/h) than in diabetic subjects without CAN (14.0 +/- 3.5 mmol/h; P less than 0.01) and in controls (10.9 +/- 3.1; P less than 0.05). The maximal gastric acid secretion capacity, determined after pentagastrin injection, was similar in all patients. Mean basal hPP concentrations were comparable in the three groups (185 +/- 53 pg/ml, 131 +/- 29 pg/ml, and 116 +/- 19 pg/ml). In the controls and diabetic subjects without CAN, a significant mean 60% increase of the hPP levels above basal values was observed during sham feeding. In contrast, no significant hPP response occurred in the group with CAN. These data suggest that diabetic CAN is associated with dysfunctions of the vagal pathways controlling the gastric acid output and the hPP secretion. Moreover, the results demonstrate a strong association between cardiac autonomic neuropathy and gastric vagal neuropathy (P less than 0.001).

The fasting levels and the postprandial response of gastroenteropancreatic hormones before and after prolonged fasting.

The effect of a prolonged 5-day fast on the blood concentrations of vasoactive intestinal polypeptide (VIP), secretin, human pancreatic polypeptide (hPP), gastrin, and group I pepsinogens (PG I) was studied in 11 healthy subjects. During the fast there was a marked increase in the concentrations of VIP, secretin, and hPP, whereas the rise in the concentrations of gastrin and PG I was less pronounced. Refeeding suppressed the increased concentration of VIP and caused elevated postprandial concentrations of secretin and hPP, whereas starvation did not influence the postprandial release of gastrin and PG I. The study shows that prolonged starvation has a pronounced effect on gut endocrine responses.

Secretion of pancreatic polypeptide in man in response to beef ingestion is mediated in part by an extravagal cholinergic mechanism

The effect of atropine, a muscarinic cholinergic blocking agent, on the response of plasma pancreatic polypeptide (hPP) to the ingestion of beef was investigated. Six healthy subjects ingested 250 g broiled ground beef on three occasions. After beef ingestion alone, the expected biphasic plasma hPP response was observed. On the two other occasions atropine (intravenous bolus followed by infusion) was begun either at 4 or 60 min after the beginning of beef ingestion so as to coincide with the early (first) and late (second) phases of hPP response to beef ingestion. On both occasions plasma hPP concentrations returned rapidly to baseline. Mean integrated incremental hPP responses in the absence of atropine were 9.1 ± 3.4 ng min ml −1 for the first phase (0–40 min) and 29.7 ± 5.7 ng min ml −1 for the second phase (60–180 min); with atropine at 4 min, respective responses were 0.8 ± 0.9 and −1.0 ± 1.3 ng min ml −1, and with atropine at 60 min they were 10.6 ± 5.0 and 1.3 ± 1.6 ng min ml −1. After atropine administration, the half-time of disappearance of hPP from the circulation was 4–6 min, suggesting the complete cessation of stimulated hPP secretion. We conclude that the mechanisms of both the early and late phases of beef meal-stimulated release of hPP involve muscarinic cholinergic-neural transmission. The portion of the second (late) phase response which has been shown to persist after truncal vagotomy must be mediated by a cholinergic mechanism which is extravagal in character.

Sex difference in the sensitivity of the human pancreatic polypeptide cell to autonomic nervous stimulation in man.

We have examined the plasma human pancreatic polypeptide (hPP) response to beta-adrenergic (infusion of epinephrine-phentolamine), vagal cholinergic, (insulin-hypoglycemia), and extravagal cholinergic (secretion infusion) stimulation in healthy, nonobese, age-matched males and females. beta-Adrenergic stimulation caused a rise in plasma hPP concentration in males that was 6 times that of females, whereas there were no differences between the sexes in the mean responses of pulse rate, systolic and diastolic blood pressure, or in plasma concentrations of glucose, insulin, and glucagon. Extravagal cholinergic stimulation caused increases of hPP secretion that were similar in males and females. Insulin-induced hypoglycemia was the most efficacious stimulus, and caused a similar rise in hPP response in males and females. Thus, in males there is greater sensitivity of the hPP cell to beta-adrenergic stimulation than females. The plasma hPP responses appear to be a more sensitive, discriminating index of adrenergic autonomic function than cardiovascular and other pancreatic hormonal responses.

Differential metabolism of allopurinol and derivatives in Trypanosoma rangeli and T. cruzi culture forms

We have compared the metabolism of allopurinol (4-hydroxypyrazolo(3,4-d)pyrimidine; HPP), by Trypanosoma rangeli, a non-pathogenic American trypanosome, and T. cruzi, the causative agent of Chagas' disease. Our results indicate that T. rangeli was unable to animate allopurinol mononucleotide to 4-aminopyrazolopyrimidine (APP) mononucleotide. Radioactivity was located in the RNA, but not the DNA, only of T. cruzi. Substrate specificity studies showed T. cruzi succino-AMP synthetase activity being 100-fold more active on HPP mononucleotide than the T. rangeli enzyme. These results possibly explain the fact that in conventional LIT medium T. rangeli growth was resistant to high concentrations of HPP. However the incubation of this hemoflagellate in an adenine-depleted LIT medium rendered it sensitive to low concentrations of APP, while remaining resistant to HPP. In contrast, and independently of the culture medium used, T. cruzi was extremely sensitive to both pyrazolopyrimidines.

Growth hormone suppression of pancreatic polypeptide secretion.

Effects of GH treatment on human pancreatic polypeptide (hPP) secretion and glucose homeostasis were evaluated in seven GH-deficient children with chronological ages of 7–15 yr and bone ages of 5–13 yr. Both before and after long term GH therapy, blood samples were obtained for measurement of serum hPP, insulin, and glucose concentrations throughout a 24-h period during which meals were taken. In addition, serum glucose and hPP responses to insulin tolerance tests (ITT) were determined on four occasions: 1) before GH treatment, 2) 2 h after the last of three daily injections of GH, 3) 2 h after the last injection of GH (0.1 IU/kg, im), three times each week for 8 weeks), and 4) 72 h after withdrawal of GH. Fasting serum hPP concentrations were also obtained in 15 short-normal children. Mean fasting hPP concentrations were slightly but not significantly greater in the seven GH-deficient children than in the short-normal children with equivalent bone ages. In the GHdeficient children, long term GH therapy s...

Truncal vagotomy abolishes the somatostatin response to insulin-induced hypoglycemia in man.

The mechanism whereby insulin-induced hypoglycemia stimulates release of immunoreactive somatostatin (SRIF-LI) into the peripheral circulation in man is unknown. We have measured the plasma SRIF-LI response to insulin-induced hypoglycemia in 16 healthy subjects and five subjects with prior truncal vagotomy. Mean nadir of plasma glucose was similar in the two groups (37 +/- 5 and 34 +/- 2 mg/dl in the control group). Hypoglycemia induced a brisk rise in plasma pancreatic polypeptide (hPP) concentrations in healthy subjects (maximum concentration 1563 +/- 245 pg/ml) whereas in none of the postvagotomy subjects was there a significant change in hPP concentrations, indicative of completeness of the truncal vagotomy. In healthy subjects SRIF-LI concentrations rose for a basal of 168 +/- 19 pg/ml to a maximum of 254 +/- 30 at 39 +/- 4 minutes (p less than 0.005) with an incremental area of 2.8 +/- 1 ng . min/ml above basel. In vagotomized subjects, the mean basal SRIF-LI concentration of 166 +/- 22 pg/ml was not significantly different from that in healthy subjects. After insulin injection, SRIF-LI concentration fell with a net decrement of -3.2 +/- 1 ng . min /ml below the basal. It is concluded that the SRIF-LI response to insulin-induced hypoglycemia is dependent upon vagal integrity. Section of the vagus unmasks a suppressive effect of insulin action or its metabolic or hormonal consequences on the concentration of SRIF-LI in plasma.