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Y F Liu

Publications and source records attributed to Y F Liu.

At least 37 records · Page 2Linked to original sources
PubMed2000

Activation of MLK2-mediated signaling cascades by polyglutamine-expanded huntingtin.

We previously reported that expression of polyglutamine-expanded huntingtin induces apoptosis via c-Jun amino-terminal kinase (JNK) activation in HN33 cells (Liu, Y. F. (1998) J. Biol. Chem. 273, 28873-28822). Extending this study, we now demonstrate a role of mixed-lineage kinase 2 (MLK2), a JNK activator, in polyglutamine-expanded huntingtin-mediated neuronal toxicity. We find that normal huntingtin interacts with MLK2, whereas the polyglutamine expansion interferes with this interaction. Similar to the expression of polyglutamine-expanded huntingtin, expression of MLK2 also induces JNK activation and apoptosis in HN33 cells. Co-expression of dominant negative MLK2 significantly attenuates neuronal apoptosis induced by the mutated huntingtin. Furthermore, over-expression of the N terminus of normal huntingtin partially rescues the neuronal toxicity induced by MLK2. Our results suggest that activation of MLK2-mediated signaling cascades may be partially involved in neuronal death induced by polyglutamine-expanded huntingtin.

Animals↗
PubMed2000

[Extramedullary plasmacytoma of the head and neck: a clinicopathologic, immunohistochemistry study].

OBJECTIVE: To investigate the relation between histopathological feature, clinical behavior characters, immunoglobulin (Ig) secretory function and prognosis of the extramedullary plasmacytoma (EMP) of the head and neck. METHOD: 12 cases of EMP in the head and neck region were studied retrospectively. The clinicopathological records from January, 1977 to December, 1996 were reviewed. Immunohistochemical (IHC) stains for detecting intracytoplasmic immunoglobulin kappa (IgG kappa) and lambda (IgG lambda) were carried out. RESULT: 10 cases of the patients were male and 2 female; Their ages ranged from 32 to 67 years with an average of 57 years. The tumors were located in the nasosinus (6), nasopharynx (2), Larynx (3) and ear (1). Low-(I), intermediate (II) and high-grade (III) tumors were 3, 3 and 6 cases respectively. Two patients with EMP of nasopharynx were treated with radiotherapy, in others radiotherapy was administered after complete surgical resection. Follow-up time ranged from 10 to 76 months. IHC showed monoclonality of the plasma cell and was positive for IgG lambda (6 cases) and IgG kappa (6 cases, conferming the identical clonal origin of the plasma cells. The 5-year survival for grade I, II and III were 75.0%, 62.0% and 37.6%, 37.5% and 68.50% for IgG lambda positive and IgG kappa positive cases, respectively. There are statistically significance between them (P < 0.01). CONCLUSION: EMP in head and neck region are rare plasma cell tumors. IHC play an important role in differential diagnosis. The combination of surgery and radiotherapy proved to be an adequate and effective treatment. The grading and IgG secretory function may be valuable for predicting the prognosis of EMP.

Adult↗
PubMed1999

Phosphorylation of insulin receptor substrate-1 (IRS-1) by protein kinase B positively regulates IRS-1 function.

Incubation of cells with insulin leads to a transient rise in Tyr phosphorylation of insulin receptor substrate (IRS) proteins, accompanied by elevation in their Ser(P)/Thr(P) content and their dissociation from the insulin receptor (IR). Wortmannin, a phosphatidylinositol 3-kinase inhibitor, selectively prevented the increase in Ser(P)/Thr(P) content of IRS-1, its dissociation from IR, and the decrease in its Tyr(P) content following 60 min of insulin treatment. Four conserved phosphorylation sites within the phosphotyrosine binding/SAIN domains of IRS-1 and IRS-2 served as in vitro substrates for protein kinase B (PKB), a Ser/Thr kinase downstream of phosphatidylinositol 3-kinase. Furthermore, PKB and IRS-1 formed stable complexes in vivo, and overexpression of PKB enhanced Ser phosphorylation of IRS-1. Overexpression of PKB did not affect the acute Tyr phosphorylation of IRS-1; however, it significantly attenuated its rate of Tyr dephosphorylation following 60 min of treatment with insulin. Accordingly, overexpression of IRS-1(4A), lacking the four potential PKB phosphorylation sites, markedly enhanced the rate of Tyr dephosphorylation of IRS-1, while inclusion of vanadate reversed this effect. These results implicate a wortmannin-sensitive Ser/Thr kinase, different from PKB, as the kinase that phosphorylates IRS-1 and acts as the feedback control regulator that turns off insulin signals by inducting the dissociation of IRS proteins from IR. In contrast, insulin-stimulated PKB-mediated phosphorylation of Ser residues within the phosphotyrosine binding/SAIN domain of IRS-1 protects IRS-1 from the rapid action of protein-tyrosine phosphatases and enables it to maintain its Tyr-phosphorylated active conformation. These findings implicate PKB as a positive regulator of IRS-1 functions.

Androstadienes↗
PubMed1999

Stimulation of cAMP synthesis by Gi-coupled receptors upon ablation of distinct Galphai protein expression. Gi subtype specificity of the 5-HT1A receptor.

The three Galphai subunits were independently depleted from rat pituitary GH4C1 cells by stable transfection of each Galphai antisense rat cDNA construct. Depletion of any Galphai subunit eliminated receptor-induced inhibition of basal cAMP production, indicating that all Galphai subunits are required for this response. By contrast, receptor-mediated inhibition of vasoactive intestinal peptide (VIP)-stimulated cAMP production was blocked by selective depletions for responses induced by the transfected serotonin 1A (5-HT1A) (Galphai2 or Galphai3) or endogenous muscarinic-M4 (Galphai1 or Galphai2) receptors. Strikingly, receptor activation in Galphai1-depleted clones (for the 5-HT1A receptor) or Galphai3-depleted clones (for the muscarinic receptor) induced a pertussis toxin-sensitive increase in basal cAMP production, whereas the inhibitory action on VIP-stimulated cAMP synthesis remained. Finally, in Galphai2-depleted clones, activation of 5-HT1A receptors increased VIP-stimulated cAMP synthesis. Thus, 5-HT1A and muscarinic M4 receptor may couple dominantly to Galphai1 and Galphai3, respectively, to inhibit cAMP production. Upon removal of these Galphai subunits to reduce inhibitory coupling, stimulatory receptor coupling is revealed that may involve Gbetagamma-induced activation of adenylyl cyclase II, a Gi-stimulated cyclase that is predominantly expressed in GH4C1 cells. Thus Gi-coupled receptor activation involves integration of both inhibitory and stimulatory outputs that can be modulated by specific changes in alphai subunit expression level.

Adenylate Cyclase Toxin↗
PubMed1999

[Determination of bentazon and 2,4-D butyl in mixture formulation by HPLC].

Bentazon and 2,4-D butyl(the active ingredients of Cao Di) were determined by reversed phase HPLC aimultancously using methanol/acetonitrile/citrate buffer(pH 3.1) as a mobile phase on Shim-pack clc-CN column. Results showed that the linear correlation and recovery of 2,4-D butyl were 1.000 and (100.2 +/- 0.8)% respectively, and those of bentazon were 1.000 and (98.6 +/- 0.9)% respectively. The coefficients of variation for bentazon and 2,4-D butyl were all was 0.37%.

2,4-Dichlorophenoxyacetic Acid↗
PubMed1998

Expression of polyglutamine-expanded Huntingtin activates the SEK1-JNK pathway and induces apoptosis in a hippocampal neuronal cell line.

Huntington's disease is one of a growing number of hereditary neurodegenerative disorders caused by expansion of a polyglutamine stretch at the NH2 terminus of huntingtin. To explore whether polyglutamine-expanded huntingtin induces neuronal toxicity, I examined the expression of the full-length of huntingtin with 16, 48, or 89 polyglutamine repeats in a rat hippocampal neuronal cell (HN33). Expression of mutated huntingtin with 48 or 89 polyglutamine repeats stimulated c-Jun amino-terminal kinases (JNKs) activity and induced apoptotic cell death in HN33 cells while expression of normal huntingtin with 16 polyglutamine repeats had no toxic effect. The JNK activation precedes apoptotic cell death and co-expression of a dominant negative mutant form of stress-signaling kinase (SEK1) nearly completely blocked activation of JNKs and neuronal apoptosis mediated by mutated huntingtin. Taken together, my studies demonstrate that expression of polyglutamine-expanded huntingtin induces neuronal apoptosis via activation of the SEK1-JNK pathway.

Animals↗
PubMed1998

BCL-6 gene mutations in posttransplantation lymphoproliferative disorders predict response to therapy and clinical outcome.

Posttransplantation lymphoproliferative disorders (PT-LPDs) represent a heterogeneous group of Epstein-Barr virus-associated lymphoid proliferations that arise in immunosuppressed transplant recipients. Some of these lesions regress after a reduction in immunosuppressive therapy, whereas some progress despite aggressive therapy. Morphological, immunophenotypic, and immunogenotypic criteria have not been useful in predicting clinical outcome. Although structural alterations in oncogenes and/or tumor suppressor genes identified in some PT-LPDs correlate with a poor clinical outcome, the presence of these alterations has not been a consistently useful predictor of lesion regression after reduction of immunosuppression. We examined 57 PT-LPD lesions obtained from 36 solid organ transplant recipients for the presence of mutations in the BCL-6 proto-oncogene using single-strand conformation polymorphism and sequence analysis, followed by correlation with histopathologic classification and clinical outcome, which was known in 33 patients. BCL-6 gene mutations were identified in 44% of the specimens and in 44% of the patients; none were identified in the cases classified as plasmacytic hyperplasia. However, mutations were present in 43% of the polymorphic lesions and 90% of the PT-LPDs diagnosed as non-Hodgkin's lymphoma or multiple myeloma. BCL-6 gene mutations predicted shorter survival and refractoriness to reduced immunosuppression and/or surgical excision. Our results suggest that the BCL-6 gene structure is a reliable indicator for the division of PT-LPDs into the biological categories of hyperplasia and malignant lymphoma, of which only the former can regress on immune reconstitution. The presence of BCL-6 gene mutations may be a useful clinical marker to determine whether reduction in immunosuppression should be attempted or more aggressive therapy should be instituted.

Cell Transformation, Neoplastic↗
PubMed1997

Kaposi's sarcoma-associated herpesvirus sequences in benign lymphoid proliferations not associated with human immunodeficiency virus.

BACKGROUND: Kaposi's sarcoma-associated herpesvirus (KSHV) DNA sequences have been identified in approximately 95% of Kaposi's sarcoma (KS) lesions and primary effusion lymphomas (PELs), suggesting a pathogenetic role for this virus in these lesions. However, KSHV has also been identified in a variety of specimens, including lymph nodes, peripheral blood B cells, semen, and prostate tissue, with varying frequencies. This suggests that KSHV, like Epstein-Barr virus, may be ubiquitously distributed. To evaluate further the clinical spectrum of KSHV infection and define better the prevalence of this virus in lymphoid tissues in the general population, the authors examined a wide spectrum of benign lymphoid proliferations occurring in human immunodeficiency virus (HIV)-negative individuals. METHODS: One hundred eight lymphoid lesions were examined for the presence of KSHV by polymerase chain reaction (PCR) amplification using primers to open reading frame (ORF) 26. Positive cases were confirmed by Southern blot hybridization using an internal oligonucleotide probe and by PCR amplification using primers to ORF 74 and ORF 75 of the virus. RESULTS: Only 4 (4%) of 108 specimens were KSHV positive. Three positive lymph node specimens were taken from patients with multicentric Castleman's disease (3 of 11 total cases of Castleman's disease; 3 of 5 total cases of multicentric Castleman's disease). The remaining case was a lymph node showing paracortical hyperplasia, taken from a patient with systemic lupus erythematosus. CONCLUSIONS: KSHV is not detectable by PCR technology in a wide range of lymphoid proliferations occurring outside of HIV infection. These studies further support the contention that KSHV is preferentially associated with KS, PEL, and some cases of multicentric Castleman's disease.

Adolescent↗
PubMed1997

SH3 domain-dependent association of huntingtin with epidermal growth factor receptor signaling complexes.

Based on the presence of multiple proline-rich motifs in the huntingtin sequence, we tested its possible association with epidermal growth factor (EGF) receptor signaling complexes through SH3 domain-containing modules. We found that huntingtin is associated with Grb2, RasGAP, and tyrosine-phosphorylated EGF receptor. These associations are regulated by activation of the EGF receptor, suggesting that they may be part of EGF receptor-mediated cellular signaling cascade. In vitro binding studies indicate that SH3 domains of Grb2 or RasGAP are required for their binding to huntingtin. Our results suggest that huntingtin may be a unique adapter protein for EGF receptor-mediated signaling and may be involved in the regulation of Ras-dependent signaling pathways.

Adaptor Proteins, Signal Transducing↗
PubMed1997

Molecular characterization of IgA- and/or IgG-switched chronic lymphocytic leukemia B cells.

The immunoglobulin (Ig) variable region (V) genes expressed by IgM chronic lymphocytic leukemia (CLL) B cells display little or no somatic mutations. However, preliminary findings have shown that Ig V genes of IgA and IgG CLLs may be somatically mutated, suggesting that isotype-switched CLLs may represent a "subtype" of the disease. To investigate the degree and nature of somatic mutations and the role of antigen (Ag) in the clonal selection and expansion of isotype-switched CLLs, and to determine whether specific oncogene or tumor suppressor gene mutations are associated with isotype-switched CLLs, we analyzed the expressed Ig VH gene, bcl-1 and bcl-2 proto-oncogene, and p53 tumor suppressor gene configurations of 3 IgA-, 1 IgG-, and 1 IgA/ IgG-expressing CLLs. These isotype-switched CLL B cells expressed surface HLA-DR, CD19, CD23, and CD5, and displayed no alterations of the bcl-1 and bcl-2 oncogenes and the p53 tumor-suppressor gene. The cDNA VH-D-JH gene sequence was joined with that of the C alpha gene in the B cells of the three IgA CLLs, and with that of the C gamma gene in the IgG CLL B cells. In the IgA/IgG-coexpressing CLL B cells, identical VH-D-JH cDNA sequences were spliced to either C alpha or C gamma genes. In all five CLLs, the pattern of C mu DNA probe hybridization to the digested genomic DNAs was consistent with deletion of the C mu exon from the rearranged Ig gene locus, suggesting that these CLL B cells had undergone DNA switch recombination. In one IgA CLL, the expressed VH gene was unmutated. In all other class-switched CLLs, the Ig VH segment gene was mutated, but the point mutations were not associated with intraclonal diversification. In one IgA and in the IgA/IgG-coexpressing CLL, the nature and distribution of the mutations were consistent with Ag selection. These findings suggest that IgA- and/or IgG-expressing CLLs represent, in their VH gene structure, transformants of B cells at different stages of ontogeny. They also suggest that Ag may play a role in the clonal selection of some of these isotype-switched leukemic cells, but bcl-1 and bcl-2 oncogene rearrangements and p53 tumor suppressor gene mutation are not associated with the pathogenesis of isotype-switched CLLs.

Amino Acid Sequence↗
PubMed1997

Regulation of thyroid hormones in the secretion of insulin and gastric inhibitory polypeptide in male rats.

The effect of thyroid hormones on glucose-induced secretion of gastric inhibitory polypeptide (GIP) and insulin was studied. Male rats were thyroidectomized (Tx) or sham Tx. Sham Tx rats were injected with either propylthiouracil ([PTU] 20 mg/kg intraperitoneally) or saline for 2 weeks. In addition, thyroid-intact rats were injected intravenously with triiodothyronine ([T3]5 microg/kg) or saline 10 minutes before an oral glucose load (3.2 g/kg). Blood samples were collected from each animal via a jugular catheter at 0, 10, 20, 30,45, 60, and 90 minutes following glucose ingestion. Plasma levels of GIP and insulin were measured by specific radioimmunoassays (RIAs). Thyroidectomy-induced hypothyroidism increased the basal level of plasma GIP, but decreased that of insulin. Insulin levels at 10, 20, and 30 minutes following oral glucose were lower in hypothyroid rats than in euthyroid rats. Conversely, GIP levels at 60 and 90 minutes following glucose ingestion in PTU-induced hypothyroid rats were higher than those in euthyroid rats. Furthermore, glucose-stimulated insulin secretion was unaltered by pretreatment with T3, whereas the glucose-induced increase in plasma GIP was completely abolished by preinjection of T3 in thyroid-intact rats. These results suggest that thyroid functions are involved in the regulation of insulin and GIP secretion in rats.

Animals↗
PubMed1997

Acipimox attenuates hypertriglyceridemia in dyslipidemic noninsulin dependent diabetes mellitus patients without perturbation of insulin sensitivity and glycemic control.

Hyperlipidemia, hypertriglyceridemia in particular, is a common feature in patients with noninsulin dependent diabetes mellitus (NIDDM) and may associate with insulin insensitivity. Acipimox, being widely prescribed for treating hypertriglyceridemia, is also used in NIDDM patients for their dyslipidemia. In the present study, we evaluated the effect of acipimox in Chinese NIDDM patients with hypertriglyceridemia. A total of 16 patients enrolled in a double-blind, randomized, placebo-controlled and two-period crossover study. After an 8 week run-in period, patients were randomly assigned into two groups receiving either acipimox (250 mg, twice daily) or placebo treatment. A total of 12 weeks later, these two groups switched their treatment for an additional 12 weeks. Blood samples were collected at the end of the run-in period and then at 4-week intervals in the whole study for lipid profile. A modified insulin suppression test was performed at the ends of the run-in period, 12-week and 24-week treatment to assess changes in insulin sensitivity. Our results showed that acipimox significantly lowered serum total triglyceride while compared to those by placebo. However, no difference was observed in serum non-esterified fatty acid, low-density lipoprotein cholesterol, total cholesterol (TC), high density lipoprotein-cholesterol (HDL-C) and HDL-C/ TC ratio between the two groups. Furthermore, glycemic indices and insulin sensitivity were similar during the base-line, placebo or acipimox periods. Taken together, our data suggest that acipimox significantly lowered TG without perturbation of insulin sensitivity in hypertriglyceridemic NIDDM patients.

Adult↗
PubMed1997

Mechanism for inhibition of deoxyribonuclease activity by antisera.

The activity of bovine DNase, but not that of porcine DNase, is inhibited by antisera against bovine DNase, and vice versa. Inhibition of DNase is found in the immunoglobulin G-containing fractions, as shown by ion exchange chromatography. Inactive DNase, carboxymethylated specifically at the active site His134, competes with active DNase and reverses the antisera inhibition of DNase, suggesting that the epitode responsible for inhibition does not contain the active site His134. Alignment of the sequences of DNase of these two species shows that the greatest variation occurs between residues 153 and 163, within which are three consecutive peptide bonds, Lys-Trp-His-Leu, that are readily cleaved by trypsin, chymotrypsin, or thermolysin. The 8-hr digest of DNase by each of these three proteases has lost the ability to reverse antisera inhibition. The degree of antisera inhibition varies with the metal ion used as the activator for DNase-catalyzed reactions. When Mn2+, Co2+, or Mg2+ plus Ca2+ are used as activators, inhibition is approximately 50%. When pBR322 plasmid is used as substrate, gel electrophoresis shows that the DNase-catalyzed DNA hydrolysis produces a significant amount of double-strand cuts with Mn2+, Co2+, or Mg2+ plus Ca2+ as activators and antisera inhibit DNase action only on double-strand cuts. With only Mg2+ as the activator no double-strand cuts are observed, either in the presence or absence of antisera, and the DNase activity is not significantly inhibited. We conclude that antisera inhibition is due to antibody binding of the DNase polypeptide chain within residues 153 and 163. These residues are not crucial for catalysis, but are required for DNA binding, which results in double-strand cuts.

Animals↗
PubMed1997

Effect of lead ingestion on concentrations of lead in tissues and eggs of laying Tsaiya ducks in Taiwan.

This experiment was conducted to investigate Pb concentrations in soft tissues and eggs from laying Tsaiya ducks (Anas platyrhynchos var. domestica), dosed via gelatin capsule with 10 or 20 mg Pb/kg BW daily for 3 mo. Body weights of ducks were not influenced by Pb treatment. In addition, no clinical syndromes involving Pb intoxication were found throughout the experiment. The two levels of Pb consistently resulted in increases in the Pb content of blood, kidney, liver, and gizzard, whereas only 20 mg Pb/kg BW per d of dose additionally increased the Pb in femoral muscle. More Pb was deposited in the kidney and liver after Pb exposure than in the gizzard or femoral muscle. Lead residues in yolk and eggshell from Pb-dosed ducks were significantly higher than in controls; however, Pb in albumen was generally low and was not influenced by Pb treatment.

Administration, Oral↗
PubMed1997

[Effect of zuogui wan on the contents of hypothalamic monoaminic transmitters and body weight in rats treated with monosodium glutamate neonatally].

OBJECTIVE: To evaluate the interrelationship between the traditional Chinese medicine the Kidney-Yin Deficiency Syndrome and the metabolism of hypothalamic monoaminic neurotransmitters after the lesion of arcuate nucleus (ARC). METHODS: Rats were injected with monosodium glutamate (MSG, at 2, 4, 6, 8, 10 days after born. 4 mg/g body weight, s.c.) during the neonatal period, then the contents of hypothalamic monoaminic transmitters were determined with HPLC and the changes of increase of body weight were observed. RESULTS: Decreases in levels of norepinephrine (NE), dopamine (DA) associated with its metabolite, 3,4-dihydroxyphenyl acetic acid (DOPAC) were observed, while vanillylmandelic acid (VMA), metabolite of NE, serotonin (5-HT) and 5-hydroxyindole acetic acid (5-HIAA) were unchanged. Furthermore, adult rats with neonatal MSG treatment also demonstrated growth retardation, obesity but lower body weight, and shorter length of naso-anal. Zuogui Wan, classical drugs of nourishing and recuperating the Kidney-Yin, relieved the disorder of the metabolism of hypothalamic monoaminic transmitter in MSG-rats. CONCLUSION: The metabolic disorders of the central monoaminic transmitters may be related with the Deficiency of the Kidney-Yin.

Animals↗
PubMed1997

Cutaneous infection by Scedosporium apiospermum and its successful treatment with itraconazole.

We report the case of a 42-year-old man with a 13-year history of bilateral faciocervical infiltrative erythema, which had been misdiagnosed as tuberculoderma and which had failed to respond to treatment with adrenal corticosteroids and antituberculotics. On admission to the department, Scedosporium apiospermum was identified on lesion biopsies and fungus cultures as the causative agent and a diagnosis of cutaneous infection by S. apiospermum was made. This is the first report of chronic skin granuloma caused by S. apiospermum in China. Treatment with oral itraconazole (100-400 mg/day) led to clinical cure within 4 months.

Adult↗
PubMed1996

Coordination of biliary and upper gastrointestinal motility in the fasted conscious pig.

A chronic pig model was developed which permits the simultaneous measurement of integrated biliary motility as resistance to flow (CBD inflow), gallbladder, duodenal and gastric motility in addition to collection of venous blood samples for gut hormones estimations. Animals displayed a duodenal interdigestive cycle of 55.4 +/- 3.4 min (mean +/- SEM, n = 6), consisting of phase I, II and III (21.2 +/- 2.1, 70.5 +/- 2.0, 8.7 +/- 0.5% of the cycle, respectively). A gastric interdigestive cycle of 60.2 +/- 6.5 min (n = 4) was similarly demonstrated consisting of three phases which corresponded to the three duodenal phases. The gastric phases I, II and III comprised 26.3 +/- 3.0, 71.2 +/- 2.7 and 2.5 +/- 0.8% of the cycle, respectively. The gastric phase III immediately preceded the onset of the duodenal phase III. The gallbladder likewise displayed an interdigestive cycle of 54.5 +/- 7.2 min (n = 6) consisting of a quiescent period (37.2 +/- 3.7% of the cycle) corresponding temporally to duodenal phase III and phase I. This quiescent phase was followed by a period of rhythmic contractions (64.5 +/- 4.1% of the cycle) which corresponded temporally to duodenal phase II. The onset of the gallbladder quiescent period coincided with the onset of duodenal phase III. The CBD inflow similarly demonstrated an interdigestive cycle of 53.4 +/- 9.6 min (n = 4) duration, consisting of three phases. The initial phase was evident as a period of rapid inflow, the onset of which coincided with the onset of duodenal phase III and the gallbladder quiescent period, and occupied 12.0 +/- 0.8% of the cycle. The second phase which occupied 18.0 +/- 7.4% of the cycle, was typified as a period of declining inflow which reached a relatively stable level at a time corresponding to the end of duodenal phase I. The third phase consisted of the maintenance of the inflow rate achieved at the end of the previous phase (60% of maximum inflow), corresponding in onset and duration with duodenal phase II and occupied 70.0 +/- 8.6% of the cycle. Plasma motilin levels fluctuated in relation to the duodenal interdigestive cycle, peaking during phase III relative to phase I (36.9 +/- 8.5 vs 25.4 +/- 7.7 pg mL-1, respectively, n = 5, P < 0.05). Cholecystokinin levels did not fluctuate, remaining low (2.3 +/- 2.1 pM cholecystokinin octapeptide equivalents, n = 5) throughout the duodenal interdigestive cycle, but increased about two fold after ingestion of solid food. Feeding disrupted the gastric, duodenal, gallbladder and CBD inflow cycles.

Animals↗