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Biomedical subjects

J Ardill

Publications and source records attributed to J Ardill.

At least 19 recordsLinked to original sources
PubMed2006

Development of a disease-specific Quality of Life questionnaire module for patients with gastrointestinal neuroendocrine tumours.

Quality of life (QoL) measurements are increasingly being used as an end point in cancer clinical trials. Standard generic QoL questionnaires may not assess symptoms produced by neuroendocrine tumours. Here we report the development of a disease-specific quality of life score questionnaire for patients with neuroendocrine tumours of the gut to supplement the EORTC core cancer questionnaire, the QLQ-C30. Phases 1-3 of the EORTC quality of life group guidelines for module development were used to design the new questionnaire. Forty-one relevant issues (questions) were generated after an extensive literature search. Following interviews of 15 health care workers and 35 patients, a 35 question provisional questionnaire was constructed. This was translated into seven European languages and pre-tested in 180 patients resulting in a 21-item module that will be validated in an international clinical trial. The EORTC QLQ-NET21 provides a site-specific module to supplement the QLQ-C30 for patients with neuroendocrine tumours.

Adolescent↗
PubMed2005

Inhibition of dipeptidyl peptidase IV activity by oral metformin in Type 2 diabetes.

AIMS: Glucagon-like peptide-1 (GLP-1) and gastric inhibitory polypeptide (GIP) are important insulinotropic hormones that enhance the insulin secretory response to feeding. Their potential for treating Type 2 diabetes is limited by short biological half-life owing to degradation by dipeptidyl peptidase IV (DPP IV). We investigated the acute effects of metformin on DPP IV activity in Type 2 diabetes to elucidate inhibition of DPP IV as a possible mechanism of action. METHODS: Eight fasting subjects with Type 2 diabetes (5M/3F, age 53.1+/-4.2 years, BMI 36.8+/-1.8 kg/m2, glucose 8.9+/-1.2 mmol/l, HbA1c 7.8+/-0.6%) received placebo or metformin 1 g orally 1 week apart in a random, crossover design. RESULTS: Following metformin, DPP IV activity was suppressed compared with placebo (AUC0-6 h 3230+/-373 vs. 5764+/-504 nmol ml/l, respectively, P=0.001). Circulating glucose, insulin and total GLP-1 were unchanged. Metformin also concentration-dependently inhibited endogenous DPP IV activity in vitro in plasma from Type 2 diabetic subjects. CONCLUSION: Oral metformin effectively inhibits DPP IV activity in Type 2 diabetic patients, suggesting that the drug may have potential for future combination therapy with incretin hormones.

Administration, Oral↗
PubMed2001

Plasma somatostatin and gastrointestinal peptides in Alzheimer's disease and vascular dementia.

Few markers distinguish between different dementia types. As dementia affects many body systems outside the central nervous system, we investigated gastrointestinal regulatory peptides as possible disease markers in Alzheimer's Disease (AD) and vascular dementia (VaD). Subjects with mild-to-moderate dementia were diagnosed as probable AD and VaD according to defined criteria. Gastrointestinal peptides were stimulated using a standardized meal test, administered after an overnight fast to 58 dementia patients (40 AD, 18 VaD) and 47 controls matched for age and sex. Blood samples were taken at designated time intervals, and basal and stimulated plasma concentrations of eleven peptides were determined by radio-immunoassay. Results were analysed using the Kruskal-Wallis one-way analysis of variance; the Mann-Whitney U test was used in post hoc analysis where appropriate. There were significant differences in somatostatin levels but in none of the other peptides. Basal somatostatin was significantly increased in VaD compared to controls (p<0.05), and AD (p<0.005). Maximum stimulated levels were significantly elevated in VaD compared to AD (p<0.01). Median basal and stimulated levels of somatostatin were increased in VaD compared to AD, but the overlap in individual values between the groups makes it unlikely to be useful in distinguishing the two types of dementia.

Aged↗
PubMed2001

Gastrin, somatostatin and infantile hypertrophic pyloric stenosis.

UNLABELLED: Despite multiple and often contradictory research, no firm conclusions regarding the role of hypergastrinaemia in infantile hypertrophic pyloric stenosis (IHPS) have been established. Evaluation of somatostatin, the main physiological antagonist of gastrin, has not been assessed in previous studies. Long-term evaluation following pyloromyotomy suggests persistent abnormalities in gastrin and somatostatin in IHPS. The objective of this case-controlled study was to compare fasting serum gastrin and somatostatin levels in IHPS. Serum sample were collected from 39 children with IHPS at the time of pyloromyotomy and 20 age-matched controls with no evidence of gastrointestinal disease. Standard radioimmunoassay techniques were used to detect circulating levels of the hormones. A two-tailed t-test was used for statistical analysis. The levels of the two hormones (mean +/- SEM) revealed that there was no evidence of hypergastrinaemia in IHPS compared with controls (75.6 +/- 16.1 and 68.1 +/- 7.8 ng l(-1), respectively), but that the level of somatostatin was significantly elevated (38.9 +/- 6.4 and 30.5 +/- 5.8 ng l(-1), p = 0.016). An inverse trend in the gastrin/somatostatin levels could not be identified in IHPS. CONCLUSION: Somatostatin but not gastrin is raised in IHPS. Somatostatin is known to inhibit the actions of inhibitory neurotransmitters in the pylorus and may explain the development of pylorospasm, which is believed to be important in the development of pyloric tumours. These results do not agree with a previous long-term follow-up study, but reflect the hormonal imbalance at the time of pyloric hypertrophy.

Biomarkers↗
PubMed1986

Absence of evidence for a role of calcitonin in the etiology of femoral neck fracture.

Twenty elderly women with fracture of the femoral neck were compared with 10 age-matched women undergoing elective hip surgery. In spite of an equivalent calcium response to intravenous calcium, neither basal nor stimulated calcitonin levels were significantly different between the groups. Parathormone, 25OHD, and 1,25(OHD)2 showed no significant differences between the femoral neck fracture group and control subjects. It is thus unlikely that calcitonin has an important role in the etiology of postmenopausal osteoporosis associated with femoral neck fracture.

Aged↗
PubMed1986

Effect of calcium and stanozolol on calcitonin secretion in patients with femoral neck fracture.

The role of calcitonin in the aetiology of postmenopausal osteoporosis remains uncertain. Oestrogen, an established therapy for postmenopausal osteoporosis, has been shown to enhance calcitonin secretion. In order to assess whether two other osteoporotic drug treatments, oral calcium and stanozolol (an anabolic steroid), may also affect calcitonin secretion, 20 elderly women with femoral neck fracture were randomly selected to receive either 880 mg calcium or 5 mg stanozolol daily for 12 weeks. Basal calcitonin and serum calcium were not altered significantly by either treatment. The calcitonin response to a 10 min infusion of calcium was enhanced following treatment with oral calcium but not stanozolol. This suggests one possible mechanism of action whereby calcium may exert its antiresorptive effect on bone and supports the use of oral calcium in the treatment of postmenopausal osteoporosis.

Aged↗
PubMed1984

Suppression of somatostatin release by duodenogastric reflux in dogs.

The effect of duodenogastric reflux on systemic and portal venous blood concentrations of somatostatin has been studied in the dog. Duodenogastric reflux suppressed somatostatin concentrations in both systemic and portal venous blood, but this did not occur when bile alone was diverted into the stomach. The suppression was also much less marked when truncal vagotomy accompanied the reflux. These findings suggest that altered somatostatin activity may play a part in the production of the pathophysiological changes occurring in clinical conditions such as peptic ulceration, in which there is an increase in duodenogastric reflux.

Animals↗
PubMed1984

The hormonal changes produced by duodenogastric reflux.

Serum systemic and portal venous blood levels of secretin, vasoactive intestinal polypeptide (VIP), gastric inhibitory peptide (GIP), somatostatin, insulin and pancreatic polypeptide (PP) have been examined in dogs with and without surgically produced duodenogastric reflux. Serum levels of secretin, VIP, insulin and PP showed no change, but reflux caused a significant elevation of GIP levels and a suppression of somatostatin levels in both systemic and portal venous blood.

Animals↗
PubMed1983

Vasoactive intestinal polypeptide in obesity.

Twenty-six patients who were more than 35 per cent above their ideal weight were examined before the introduction of a weight reduction programme. At the end of a three-month period, seven patients had lost more than 10 per cent of their body weight. These patients had significantly lower triglyceride levels, fasting gastric inhibitory polypeptide levels (GIP) and prolactin levels. Fasting vasoactive intestinal polypeptide levels (VIP) before commencing diet were raised in six of the 19 patients who subsequently did not lose weight whereas the seven patients who lost weight had normal VIP levels (X2 = 3.07, P less than 0.05). Patients with high VIP levels had higher triglyceride levels, higher mean C-terminal glucagon-like immunoreactivity (C-GLI) and higher post glucose infusion secretin levels. There was a significant correlation between triglycerides and VIP. The significance of abnormally high VIP levels in obesity and the inability of these patients to lose weight is discussed.

Adult↗
PubMed1982

Glucose tolerance in the elderly: the role of insulin and its receptor.

Oral glucose tolerance tests were performed in young and elderly subjects with minimal risk factors for diabetes mellitus. Compared to the normal glucose tolerance in the young there was a 45% rate of impaired tolerance in the elderly. Fasting insulin levels were significantly lower in the elderly but post-glucose insulin responses in the first hour were similar in young and elderly subjects. Peripheral insulin action was assessed in terms of the 125 monoiodoinsulin binding to specific insulin receptor sites on circulating lymphocytes in the young, the elderly and a group of age and sex matched obese maturity-onset diabetics. Specific insulin binding was not significantly different in the elderly than in the young but was significantly lower in the diabetics than the young and the elderly. The results suggest that neither defective insulin binding are major causative factors in the reduced glucose tolerance of the elderly.

Adult↗
PubMed1980

The effect of metformin treatment on gastric acid secretion and gastrointestinal hormone levels in normal subjects.

Gastric acid secretion and gastrointestinal hormone levels were measured in healthy non-diabetic subjects after metformin treatment (1.5 g/day). The maximum acid output was increased from 15.7 +/- 3.9 mmol/h (mean +/- SEM) to 30.0 +/- 7.1 mmol/h (p < 0.05) and the peak acid output was increased from 16.4 +/- 4.1 mmol/h to 31.7 +/- 7.2 mmol/h (p < 0.05) after two weeks treatment. Serum insulin, gastric inhibitory polypeptide and secretin levels were normal. After treatment for one week, however, there was a significant increase in fasting vasoactive intestinal peptide (VIP) from 83 +/- 6 ng/1 to 102 +/- 9 ng/1 (p < 0.02) and in stimulated VIP from 58 +/- 5 ng/1 to 79 +/- 5 ng/1 (p < 0.05). Stimulated glucagon-like immunoreactivity (GLI) was also increased from 82 +/- 10 ng/1 to 174 +/- 24 ng/1 (p < 0.01) after one week's treatment. It is suggested that metformin acts as a weak histamine agonist.

Adult↗
PubMed1978

Effect of catecholamines on gastrin release.

In vivo and in vitro techniques have been used to study the effect of catecholamines on gastrin release. The i.v. infusion of epinephrine in dogs produced a significant rise in plasma gastrin concentration. This response was prevented by the administration of propranolol to block beta-adrenergic receptors. The infusion of isoproterenol, a beta-adrenergic agonist, produced a significant rise in gastrin levels, while phenylephrine, an alpha-adrenergic agonist, had no effect. In in vitro studies using isolated pieces of rat antrum, isoproterenol stimulated acute phase release of gastrin, whereas phenylephrine was again without effect. The studies indicate that catecholamines directly influence G cell function.

Animals↗
PubMed1978

On the relationship between gastrin, gastric secretion, and adjuvant arthritis in rats.

The elevation of plasma immunoreactive gastrin known to occur during the induction of adjuvant-induced arthritis (Rooney et al., 1973) has been shown to be maximal at 7 days after injection. Gastrin administered exogenously accelerated and exacerbated the inflammatory joint disease. Some evidence has been presented that the endogenous immunoreactive gastrin had biological activity in terms of gastric acid secretion.

Animals↗
PubMed1978

Elevations of gastrointestinal hormones in chronic renal failure.

Fasting levels of 5 gut hormones were studied in 30 patients with advanced uraemia (CRF), 40 undergoing regular dialysis (RD) and 555 renal transplant patients (RT). Mean values of gastrin and total glucagon were markedly elevated in CRF and RD patients compared with 20 normal subjects; there were lesser elevations in pancreatic glucagon, insulin and vasoactive intestinal peptide (VIP). Secretin levels were unchanged. In RT patients, fasting levels of VIP and pancreatic glucagon had returned to normal, while levels of gastrin, total glucagon and insulin remained slightly elevated compared with controls. Food stimulated hormone levels were measured in 18 RD patients and compared with 18 controls. After eating, RD patients failed to show the late increase in total glucagon, or the suppression of VIP and secretin seen in normal subjects; the pattern of gastrin and insulin response was similar to controls, but after the initial increase plasma levels in RD patients tended to show a slower decline. Thus involvement of the gastrointestinal tract in uraemia is associated with functional disturbance of the endocrine system of the gut.

Gastrins↗