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Biomedical subjects

L M Morgan

Publications and source records attributed to L M Morgan.

At least 73 records · Page 4Linked to original sources
PubMed1986

Insulin and C-peptide levels after oral and intravenous glucose. Contribution of enteroinsular axis to insulin secretion.

Peripheral venous plasma insulin and C-peptide concentrations were measured in 10 healthy volunteers, given either 100 g glucose orally or sufficient intravenous (i.v.) glucose to produce similar glucose concentrations when measured in arterialized blood. The incremental areas under both the insulin and C-peptide curves were significantly increased after oral as compared with i.v. glucose administration by 229% and 138%, respectively. Arteriovenous plasma glucose differences were higher after oral glucose administration and were positively correlated with plasma insulin concentrations. Plasma gastric inhibitory polypeptide (GIP) and insulin concentrations were measured in seven healthy volunteers given oral glucose loads ranging from 25 to 200 g. Both the magnitude and duration of the GIP and insulin responses after oral glucose ingestion were dose dependent. These results suggest that the main cause of the increase in peripheral insulin levels after large oral carbohydrate loads is augmented insulin secretion rather than reduced hepatic extraction, indicating the possibility that an enteroinsular factor does exist, in accordance with the "incretin" concept. They also emphasize the need to document both arterial and venous glucose concentrations for the correct interpretation of experiments investigating glucose homeostasis.

Administration, Oral↗
PubMed1985

The effect of guar gum on carbohydrate-, fat- and protein-stimulated gut hormone secretion: modification of postprandial gastric inhibitory polypeptide and gastrin responses.

The effect of incorporating guar gum into predominantly single-component meals of carbohydrate, fat or protein on liquid gastric emptying and on the secretion of gastric inhibitory polypeptide (GIP), gastrin and motilin, was studied in healthy human volunteers. Volunteers were given either 80 ml Hycal (carbohydrate meal), 150 g cooked lean minced beef (protein meal) or 200 ml double cream (fat meal) either with or without 5 or 6 g guar gum. Liquid gastric emptying was monitored in the fat and protein meals by taking 1.5 g paracetamol, consumed in water, with the meals and monitoring its appearance in circulation. Postprandial insulin and GIP levels were both significantly reduced by addition of guar gum to the carbohydrate meal. Postprandial GIP secretion was also reduced by addition of guar gum to the protein meal, but protein-stimulated gastrin secretion was enhanced by guar gum. There was a significant negative correlation between peak circulating gastrin levels and the corresponding GIP levels. Postprandial GIP secretion and plasma motilin levels were unaffected by addition of guar gum to the fat meal. 5 and 10 g guar gum/l solutions in water possessed buffering capacities between pH 2.75 and 5.5. Guar gum at 5 g/l caused no detectable change in liquid gastric-emptying time. The observed augmentation of gastrin secretion by guar gum following a protein meal could be due either to the buffering capacity of guar gum or to the attenuation of GIP secretion. It is possible that the chronic use of guar gum could be associated with changes in gastric acid secretion.

Adult↗
PubMed1983

Effect of pretreatment with a high fat diet on the gastric inhibitory polypeptide and insulin responses to oral triolein and glucose in rats.

Male Wistar rats were pretreated with 3 ml triolein orally for 4 days in addition to their normal diet. A similar control group were allowed free access to normal laboratory food. When given an oral fat load (1 ml triolein) plasma gastric inhibitory polypeptide (GIP) and triglyceride levels were significantly higher in the fat pretreated group. Inhibition of fat-stimulated GIP release by exogenous insulin was demonstrated in the untreated control group (plasma GIP: 663 +/- 49 versus 853 +/- 92 ng/l, mean +/- SEM p less than 0.025), but pretreatment with an oral fat load abolished this effect (plasma GIP: 1008 +/- 95 versus 1116 +/- 100 ng/l, p NS). Plasma glucose levels were significantly higher in fat pretreated rats given oral fat and intraperitoneal insulin compared with untreated controls (plasma glucose nadir 2.6 +/- 0.48 versus 1.6 +/- 0.15 mmol/l, p less than 0.05). Fat-pretreated rats showed significantly higher insulin and glucose levels compared with the untreated rats when given oral glucose (plasma insulin: 6.2 +/- 1.2 versus 2.5 +/- 0.59 micrograms/l, p less than 0.01; plasma glucose: 10.2 +/- 0.39 versus 8.9 +/- 0.41 mmol/l, p less than 0.025). Pretreatment of rats on a high fat diet causes (1) increased GIP secretion in response to an oral fat load, (2) abolition of the feed-back inhibition of exogenous insulin on fat-stimulated GIP release, and (3) some degree of insulin resistance.

Animals↗
PubMed1983

Comparison of peripheral glucose uptake after oral glucose loading and a mixed meal.

Forearm glucose uptake (FGU) and other metabolic responses were studied in six normal men for three hours after a 75-g oral glucose load and a mixed meal containing 75 g carbohydrate. After the meal the rise in arterial glucose levels was considerably less than that following the oral glucose load but the overall insulin responses from 0 to 180 minutes were not statistically different. Although the initial rise in FGU was more gradual after the meal, the subsequent elevation was more sustained and, at the termination of the study, exceeded significantly that seen after the oral glucose load. The rise in GIP levels during the first hour was similar after the meal and the oral glucose load, but thereafter concentrations following the oral glucose load fell while those after the meal continued to rise. When the incremental area (delta) is used as the index of response, the results show that while the glucose response (delta G) after the meal (19.1 +/- 5.3 units) was only 26% of that after oral glucose loading (72.7 +/- 7.0 units), the corresponding increase in FGU (delta FGU) reached 62% (55.0 +/- 12.8 units after the meal, 89.2 +/- 20.0 units after the oral glucose load). Thus, the increase in peripheral glucose uptake relative to the glycemic response (delta FGU/delta G) was significantly greater after the meal than following the oral glucose load alone (P less than 0.05). In conclusion, relative to the rise in arterial glucose levels, peripheral glucose uptake is greater after a meal than after glucose loading with an equivalent carbohydrate challenge. Furthermore, the present data support previous studies emphasizing the failure of GIP alone to explain the entero insular axis.

Administration, Oral↗
PubMed1983

Immunohistochemical studies of the GABA system in the pancreas.

gamma-Amino butyric acid (GABA) is a major inhibitory neurotransmitter in the mammalian brain. In the present study the indirect immunofluorescence technique was employed to localize the GABA-synthesizing enzyme glutamate decarboxylase, and the GABA-metabolizing enzyme GABA-transaminase within the rat pancreas. Both enzymes were found to occur only in the beta-cells of the islets of Langerhans. The other endocrine cell types, the exocrine tissue and the nervous elements in the pancreas did not contain either enzyme. Animals treated with the beta-cell toxins streptozotocin or alloxan showed a loss of immunoreactive cells in the islets. The results provide morphological evidence of the coexistence of GABA and insulin in the beta-cells of the endocrine pancreas.

4-Aminobutyrate Transaminase↗
PubMed1981

Correlation of endogenous somatostatin, gastric inhibitory polypeptide, glucagon and insulin with gastric function in the conscious calf.

Levels of endogenous somatostatin, gastric inhibitory polypeptide (GIP), glucagon and insulin were measured during gastric (abomasal) emptying in the conscious calf. Isotonic NaHCO3 infused into the duodenum increased rates of emptying of a saline test meal and of gastric acid secretion, but had no effect on basal levels of blood glucose, somatostatin, GIP, insulin or glucagon. By contrast, intraduodenal infusion of 60 mM-HCl caused complete inhibition of gastric emptying, reduction of acid secretion, and an immediate increase in plasma somatostatin from 121.3 +/- 9.4 (S.E.M.) to 286.3 +/- 16.3 pg/ml (P less 0.01) but levels of GIP, insulin, glucagon and glucose were unaltered. Intravenous injection of somatostatin (0.5 microgram/kg) suppressed the antral electromyographic recording and gastri efflux so long as plasma somatostatin levels remained above approx. 200pg/ml. This suggest that somatostatin can be released by intraduodenal acidification and that it inhibits gastric function by an endocrine effect. Since somatostatin retards gastric emptying it may therefore have an indirect role in nutrient homeostasis by limiting discharge of gastric chyme to the duodenum.

Animals↗
PubMed1980

Introduction of computer facilities to a clinical chemistry laboratory.

A clinical chemistry laboratory information system based on MUMPS is described, together with the problems associated with its implementation. Tabular displays and cusum charts as well as cumulative records are available on a real-time basis. Data capture is by both on-line and off-line techniques. After 18 months' live running the management of information within the laboratory has been significantly improved.

Chemistry, Clinical↗
PubMed1980

Evidence for preferential stimulation of gastric inhibitory polypeptide secretion in the rat by actively transported carbohydrates and their analogues.

A rat intestinal perfusion technique has been used to assess the ability of a number of monosaccharides, monosaccharide analogues and disaccharides to stimulate intestinal release of immunoreactive gastric inhibitory polypeptide (GIP). Perfusates containing glucose, sucrose, galactose, maltose, 3-O-methylglucose or alpha- or beta- methylglucoside at concentrations of 100 mmol/l in Krebs-Ringer phosphate buffer (KRP) produced significant stimulation of GIP release compared with the control perfusions with KRP alone (P less than 0.02). Mannose, 6-deoxygalactose, 2-deoxyglucose, myoinositol, fructose or lactose (100 mmol/l of each) did not stimulate GIP release compared with controls. There was no significant difference in the ability of sucrose, maltose or beta-methylglucoside (100 mmol/l of ach) to release GIP compared with 100 mmol glucose/l, but galactose, 3-O-methylglucose and alpha-methylglucoside (100 mmol/l of each) produced significantly lower GIP responses than did glucose (P less than 0.02). Addition of 5 mmol phloridzin/l to a perfusate containing 50 mmol glucose/l prevented intestinal absorption of glucose and abolished the GIP response. The molecular configuration of monosaccharides which have the ability to stimulate GIP release agreed well with the structural requirements for active transport by the sodium-dependent hexose pathway.

Animals↗
PubMed1979

The effect of oral galactose on GIP and insulin secretion in man.

The insulinotropic effect of 50 g galactose given orally to 5 normal volunteers on two occasions--once with and once without a period of hyperglycaemia produced by an intravenous glucose infusion--was studied. Oral galactose caused a rise in plasma GIP from fasting levels of 260 +/- 50 ng/l (mean +/- S.E.M.) to a maximum of 900 +/- 65 ng/l 30 min after ingestion, but in the presence of induced hyperglycaemia the GIP response was significantly diminished and delayed (maximum plasma GIP levels 595 +/- 110 ng/l at 45 min, p less than 0.05). The insulin response to galactose was greatly enhanced by IV glucose (mean area under plasma insulin curve with galactose alone 236.5 +/- 66.0, with galactose + IV glucose 451.9 +/- 81.6, p less than 0.025). The mean rise in plasma galactose was significantly lower in the presence of IV glucose (mean peak level 1.97 +/- 0.28 mmol/l with galactose alone, 0.69 +/- 0.16 mmol/l galactose + IV glucose, p less than 0.025). Oral galactose caused the release of GIP, which is powerfully insulinotropic in the presence of moderate hyperglycaemia. The lower plasma GIP and galactose levels observed following oral galactose in the presence of IV glucose may be accounted for either by postulating that insulin inhibits the absorption of oral galactose, or that insulin exerts a negative feed-back control on GIP release and accelerates galactose disposition in the body.

Administration, Oral↗
PubMed1979

The effect of unabsorbable carbohydrate on gut hormones. Modification of post-prandial GIP secretion by guar.

Five healthy volunteers and 6 diabetics were given a mixed test meal on two occasions--once with and once without 10 g guar flour. Addition of guar caused a 47% decrease in maximum post-prandial GIP levels, a 48% decrease in blood glucose and a 48% decrease in plasma insulin in normal subjects. In diabetics, addition of guar caused a 30% reduction in maximum post-prandial GIP and 58% decrease in blood glucose. Four normal and 6 diabetic subjects were given a predominantly carbohydrate meal, again with and without 10 g guar. Addition of guar caused a 78% decrease in blood glucose and a 59% decrease in plasma insulin in normal subjects. In diabetics addition of guar caused a 71% decrease in maximum post-prandial plasma GIP and a 68% decrease in blood glucose. Lowering of post-prandial blood glucose, plasma insulin and GIP levels by guar was statistically significant in every case. Addition of guar to the predominantly carbohydrate meal caused a decrease in total plasma GLI in both normal and diabetic subjects but reached statistical significance only in the normal subjects. There was a highly significant correlation (r = 0.83; p less than 0.0005) between peak post-prandial insulin levels in normal subjects and the corresponding plasma GIP concentration. The reduction of GIP or GLI secretion may, therefore, be partly responsible for the smaller rise in plasma insulin observed in normal volunteers when guar is added to meals.

Adult↗
PubMed1978

Radioimmunoassay of gastric inhibitory polypeptide.

A radioimmunoassay for the measurement of gastric inhibitory polypeptide (GIP) in unextracted plasma in man has been developed using a rabbit antiserum raised against porcine GIP. Porcine GIP was employed also as standard and to produce a 125I-labelled tracer. The assay was able to distinguish 110 pg/ml GIP from zero in plasma samples. Negligible cross-reactivity was demonstrated with cholecystokinin, insulin, pancreatic polypeptide, glucagon, secretin, and vasoactive intestinal polypeptide. The mean overnight fasting plasma GIP level in 28 normal subjects was 203 pg/ml (range: undetectable--420 pg/ml). Plasma GIP levels rose, within 45 minutes of eating a mixed meal, to a mean level of 1573 pg/ml.

Animals↗
PubMed1976

Chromosome polymorphism and banding patterns in the owl monkey (Aotus).

Diploid numbers, chromosome morphology, G- and C-banding characterisitics and pelage phenotypes were studied in 330 owl monkeys (Aotus) captured and exported from several parts of South America. Among these animals, seven distinctive karyotypes were recognized by the number of chromosomes and their individual identification by G- and C-banding methods. These seven karyotypes were distributed among four distinctive phenotypes differentiated by color patterns in the pelage. These specific phenotypes were designated in this study with capital letters (A through D) and the karyotypes by Roman numerals (I-VII), followed in parentheses by their diploid number. Specimens with phenotype A originated from Brazil and their karyotypes all conformed to a type designated karyotype I (2n=54). Animals classified as having phenotype B were exported from Colombia and their karyotypes were designated as karyotypes II (2n=54), III (2n=53), IV (2n=52), and V (2n=46). Monkeys received from Peru were designated as phenotype C and karyotype VII (2n=52). A group of owl monkeys received from Bolivia were designated as having karyotype VI (2n=50 male; 2n=49 female). Their distinctive phenotype was labeled D. All males in this sample had a diploid number of 49 and the Y-chromosome was translocated to an autosome.

Animals↗