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Biomedical subjects

J Hansky

Publications and source records attributed to J Hansky.

At least 19 recordsLinked to original sources
PubMed1992

Relationship of satiety to postprandial glycaemic, insulin and cholecystokinin responses.

The effect of plasma glucose on satiety and the capacity of carbohydrates to stimulate cholecystokinin (CCK) remain unclear. The aim of this study was to test the hypothesis that the magnitude of the postprandial plasma glucose and insulin response is inversely related to the CCK response and to subjective satiety. Seven healthy, male volunteers consumed equal carbohydrate portions (0.5 g/kg body weight) of six test meals (Rice Bubbles, Sustain, Vita-Brits, All-Bran, porridge and white bread) in random order after an overnight fast. An egg and bacon meal was consumed as a non-carbohydrate control providing 0.5 g protein/kg body weight. Serum CCK, plasma glucose and insulin and subjective satiety (measured by a rating scale) were assessed over 3 h and quantified using the glycaemic index (GI), insulin index (II), the peak satiety score and area under the incremental curve (AUC). The observed GIs (mean +/- SE) ranged from 42.5 +/- 2.6 for All-Bran to 116.2 +/- 11.4 for Rice Bubbles, using white bread as the reference food (GI = 100). Peak satiety scores varied eightfold from 0.21 +/- 0.4 for Sustain to 1.64 +/- 0.4 for All-Bran. Significant inverse relationships were observed between the peak satiety score and both the glycaemic and insulin index of the seven meals (r = -0.916, p less than 0.001 and r = -0.926, p less than 0.001). A direct relationship was observed between satiety (AUC) and the CCK response (AUC) (r = 0.73 p less than 0.01). The results suggest that glycaemic and insulin responses to carbohydrate foods are inversely proportional to the CCK response and satiety.

Adult↗
PubMed1992

Potential regulators of feeding behavior in anorexia nervosa.

We recruited 10 patients with anorexia nervosa and 6 age- and height-matched control subjects. Basal and postprandial concentrations of glucose, insulin, cholesterol, amino acids, gastrin, and pancreatic polypeptide (PP) were measured in response to a standard mixed meal. The only satiety signal that was significantly different between the anorectic group and the control group was PP (P less than 0.001). Tryptophan-LNAA and tyrosine-LNAA ratios were not significantly different in the two groups; however, there was a trend toward a lower tryptophan-LNAA ratio in the anorectic group. Gastrin concentrations were significantly decreased in the anorectic group (P less than 0.001) as were basal insulin concentrations (P less than 0.05). Decreased gastrin concentrations may play a role in the gastric symptoms associated with anorexia nervosa. Previous findings that PP release is diminished in obesity, together with the present findings of PP increase in anorexia nervosa, suggest that this peptide may play a role in appetite control mechanisms.

Adolescent↗
PubMed1989

Campylobacter pylori--a role in non-ulcer dyspepsia?

Non-ulcer dyspepsia (NUD) is a common complaint in which no systematic illness or organic proximal alimentary tract disease can be identified. The pathophysiology of NUD is probably heterogeneous. Eighty-two subjects with NUD were studied in a prospective randomized placebo-controlled study to assess the efficacy of colloidal bismuth subcitrate (CBS) chewable tablets at a dose of four tablets daily for 1 month. The role of Campylobacter pylori and associated histological gastritis was evaluated. Sixty-one percent of NUD patients had C. pylori in the gastric antrum compared with 25% of age-matched controls. C. pylori was associated with acute and chronic inflammation (P less than 0.001) in the antrum. C. pylori was cleared in 59% of CBS-treated subjects compared with only 4% placebo (P less than 0.05). Both acute and chronic inflammation improved in subjects cleared of bacteria. Clearance of C. pylori and histological improvement was associated with a significant decrease in symptoms. In C. pylori negative subjects improvement in symptoms occurred in both the placebo and active treatment groups. This study would suggest that C. pylori and associated histological gastritis may play a role in non-ulcer dyspepsia.

Adult↗
PubMed1979

Mortality in patients with haematemesis and melaena: a prospective study.

In a prospective study of death in 817 patients with haematemesis and melaena admitted on 894 occasions, the protocol included admission of all patients to a defined unit, early endoscopy and resuscitation, and planned management. Over the three consecutive two-year periods of the study mortality significantly decreased from 9% to 2.4%. Although the operative rate remained the same, the operative mortality fell from 16% to 1.6%. The fall in mortality was greatest in patients with bleeding gastric ulcers. These results suggest that prospective studies with a defined policy can influence the mortality in patients with upper gastrointestinal bleeding.

Adolescent↗
PubMed1979

Bleeding duodenal ulcer: reduction in mortality with a planned approach.

In a 6-year prospective study from 1972 to 1978 266 patients were admitted to a haematemesis and melaena unit with bleeding duodenal ulcer. There were 13 deaths, a mortality of 5 per cent. A comparison between the three consecutive 2-year periods of study showed an initial mortality of 6 per cent for the first 4 years falling to 2 per cent for the 93 admissions during the final 2 years of experience. Of the 120 patients treated surgically, 10 died in hospital, giving an operative mortality of 8 per cent. The trend in operative mortality was from 13 per cent for the initial 2-year period to 8 per cent for the second period and to 3 per cent for the final 2 years. The operative rate was consecutively 45, 50 and 34 per cent. There was 1 death in conservatively treated patients during each 2-year period of study. Three types of operation were performed: vagotomy, pyloroplasty and oversewing of the ulcer; Polya gastrectomy; and vagotomy and antrectomy. There was no difference in morbidity and mortality between these operations. At a mean follow-up of 3.1 years, 90 per cent of the patients had a good result from their operation. It is concluded that a prospective system of management with an active policy of early endoscopy, surgery and regular audit reduces the mortality from bleeding duodenal ulcer.

Adult↗
PubMed1979

Long-term cimetidine in duodenal ulcer disease.

Forty patients with chronic duodenal ulcer who had healed endoscopically with a 6-week course of cimetidine were randomized double blind to 1 year of either placebo or cimetidine tablets 400 mg bid (20 patients in each group). Patients were seen at monthly intervals, and endoscopy was performed at clinical relapse or on completion of 1 year. One of 20 patients on active cimetidine relapsed clinically and endoscopically at 3 months; 16 of 20 patients on placebo relapsed clinically and endoscopically within 9 months, the majority within 3 months, and 2 were shown to have asymptomatic chronic ulcers at routine 12-month endoscopy. None of the 19 patients on active cimetidine routinely endoscoped at 12 months showed evidence of ulceration. This study confirms a high relapse rate when short-term cimetidine is ceased and indicates that maintenance treatment with cimetidine prevents relapse.

Alcohol Drinking↗
PubMed1979

Effects of long-term cimetidine on serum gastrin in duodenal ulcer.

Basal and food-stimulated gastrin were measured in 16 patients with duodenal ulcer before and during long-term maintenance therapy with 400 mg cimetidine twice daily. Basal gastrin (mean +/- SE) rose significantly from 27.5 +/- 3.1 pmol/liter precimetidine to 32.8 +/- 2.1, 37.2 +/- 2.6, and 38.5 +/- 3.3 pmol/liter at 1, 3, and 6 months, respectively. The total integrated gastrin response to a protein meal was 1.67 +/- 0.18 nmol/liter/120 min pre-, and 2.54 +/- 0.35, 3.29 +/- 0.3, and 4.36 +/- 0.4 nmol/liter/120 min at 1, 3, and 6 months, respectively. These increases were significantly higher at each time period. This study has thus demonstrated a progressive increase in both basal and food-stimulated gastrin during cimetidine therapy, and this increase could theoretically lead to an increase in gastric acid secretion following cessation of cimetidine.

Aged↗
PubMed1979

Radioimmunoassay of secretin in serum.

A radioimmunoassay for the measurement of immunoreactive secretin has been developed. The assay is specific and sensitive so that 2.8 fmol/ml can be measured. Basal secretin levels in man are generally undetectable and a protein-rich meal does not elicit a secretin response. However, the intraduodenal instillation of HCl leads to a prompt rise in circulating immunoreactive secretin and exogenous secretin administered intravenously is easily and accurately measured.

Animals↗
PubMed1979

Cholecystokinin-like peptides in brain and intestine of obese-hyperglycaemic mice.

Cholecystokinin-(CCK) like peptides have been measured in the brain and small intestine of ob/ob hyperglycaemic mice and lean littermates. CCK-like peptides were measured by radioimmunoassay employing an antiserum to CCK octapeptide (CCK 8) and gastrin 17 I125 label. Although this antiserum detects gastrin with equal affinity to CCK, concomitant assay of tissue extracts with a gastrin specific antibody failed to reveal any detectable gastrin. Extracts of brain and small intestine showed levels of CCK of 96 +/- 12.6 pmol g-1 and 45 +/- 6.1 pmol g-1 in the obese mice; 101 +/- 8.7 pmol g-1 and 36 +/- 2.5 pmol g-1 in the lean mice. These were not significantly different. It has been suggested that CCK may be a satiety factor and it has been reported that there is less CCK in brain of obese mice compared with lean mice. This study has failed to confirm the previous finding and indicates that, in this animal model, tissue levels of CCK probably do not modulate appetite.

Animals↗
PubMed1979

The Mallory-Weiss lesion as a cause of upper gastrointestinal bleeding.

A prospective study of patients with upper gastrointestinal bleeding admitted to a haematemesis and melaena unit has revealed an incidence of Mallory-Weiss tears of 8% (59 of 762 patients undergoing endoscopy). Prior vomiting was present in 60% and an associated upper gastrointestinal lesion in 44 percent. The majority of patients had a recent ingestion of alcohol and/or analgesics, whilst 34% had chronic heavy alcohol intake. Approximately 50% of patients required no blood transfusion, while 37% had over three units of blood. No patient in the group required surgical intervention, and one patient died because of general debility. This study suggests that the Mallory-Weiss tear accounts for a significant proportion of patients admitted with upper gastrointestinal bleeding, but that the mortality and morbidity are low.

Adolescent↗
PubMed1979

Bleeding stomal ulceration.

In a prospective study of patients with haematemesis and melaena, there were 22 admissions of patients with bleeding stomal ulceration, representing 2.5% of total admissions to the Unit. In 16 patients the bleeding was from superficial stomal lesions. These lesions, endoscopically and histologically, resembled alkaline reflux gastritis, a recently defined cause of postgastrectomy bile vomiting. Five patients presented with chronic ulceration following inadequate gastric surgery. One patient was admitted on two occasions. Nine patients received more than five units of blood and came to operation for continued bleeding. In seven of the surgical cases, the bleeding was from superficial stomal lesions. Our experience suggests that truncal vagotomy is necessary to control the bleeding in these patients. One patient presented with superficial stomal ulceration and carcinomatous change. This patient died. It is important to subject these lesions to biopsy, and biopsy with extension of a previous gastrectomy is indicated to control bleeding, and to exclude malignancy.

Adult↗
PubMed1979

The protective effect of cimetidine on stress-induced acute gastric ulceration in the rat.

The effect of intraperitoneal cimetidine, an H2 receptorantagonist, has been assessed on the development of cold-restraint induced acute gastric ulcers in rats. Cimetidine in doses ranging from 20-100 mg per kg body weight significantly reduced the incidence of acute gastric ulceration compared with saline controls in this model. The protective effect of cimetidine suggests a prophylactic role for this agent in stress-induced gastric or duodenal ulceration in man.

Animals↗
PubMed1979

The effect of cimetidine on gastrin release in ulcer disease.

The effect of a single dose of 400 mg of the H2-receptor antagonist cimetidine on protein meal stimulated immunoreactive gastrin was assessed in ten patients with gastric ulcer and ten patients with duodenal ulcer. In gastric ulcer patients, serum gastrin (mean +/- SE) rose from 34 +/- 2.2 pmol.l-1 to a peak of 80 +/- 5.0 pmol.l-1 at 45 minutes without and from 36 +/- 2.2 to 107 +/- 8.0 pmol.l-1 at 60 minutes with cimetidine; in duodenal ulcer it rose from 26 +/- 3.0 to 47 +/- 5.1 pmol.l-1 at 45 minutes without and 26 +/- 3.2 to 52 +/- 5.1 pmol.l-1 at 60 minutes with cimetidine. Integrated gastrin responses in gastric ulcer were 4900 +/- 800 pmol.l-1 120 minutes without and 7000 +/- 900 pmol.l-1 120 minutes with cimetidine and 1560 +/- 300 pmol.l-1 120 minutes without and 2620 +/- 400 pmol.l-1 120 minutes with cimetidine in duodenal ulcer patients. These gastrin increases after cimetidine are comparable to those achieved with continuous intragastric neutralisation with alkali.

Adult↗
PubMed1979

Serum gastrin after 12 months' continuous cimetidine therapy for duodenal ulcer.

Serum immunoreactive gastrin was measured in 14 patients with duodenal ulcer before and during a 12-month course of cimetidine 400 mg bd. All patients were symptomatically well during the cimetidine therapy and both basal gastrin and that in response to a protein rich meal were assessed before, at six months and at 12 months during therapy. The basal and post-prandial gastrin were significantly higher at six and 12 months on cimetidine than before cimetidine but the six and 12 month levels were similar. This study thus shows that the progressive increase in serum gastrin during six months of continuous cimetidine therapy does not occur beyond this time period.

Adult↗
PubMed1979

Evidence that the cholinergic enteropancreatic reflex may be independent of cholecystokinin release.

Studies were performed in four dogs with chronic gastric and pancreatic fistulas following intraduodenal perfusion with 10 mmole hr-1 of sodium oleate for 30 minutes. Radioimmunoassay (RIA) of plasma CCK LI was undertaken by an RIA method using labeled, desulfated CCK 8 I125 and an antiserum raised to CCK 8. The detection limit for the assay was 0.25 to 0.5 fmole and the lowest detectable plasma level was 5 to 10 fmoles ml-1. Since there was equal cross-reactivity to gastrin, a gastrin-specific assay also was employed to evaluate any changes in gastrin levels. After oleate infusion the plasma CCK increment above basal was 50 +/- 11 fmoles ml-1, with return to basal levels after 60 minutes. Administration of atropine significantly (P less than 0.01) inhibited the release of CCK in the first 20 minutes. Thereafter CCK release was not reduced. Plasma gastrin values did not change before and after oleate perfusion. Pancreatic protein output increased from 72 +/- 12 to 420 +/- 55 mg/10 min-1 after oleate administration. However, after atropinization the rise in pancreatic protein output was significantly lower (152 +/- 36 mg/10 min-1) (P less than 0.01). We have shown that, using our RIA method, there is a measurable rise in plasma CCK LI after intraduodenal oleate. After atropinization the CCK response was decreased significantly during the first 30 minutes, but was virtually unchanged during the second 30 minutes, when the fall in pancreatic protein output was most marked. We conclude that the cholinergic mechanism which plays a role in the endogenous stimulation of pancreatic protein secretion by intraduodenal oleate cannot be explained simply be decreased CCK release. This mechanism may be hormonal, distinct from secretin, or neural possibly, via activation of an enteropancreatic reflex.

Animals↗