Biomedical subjects

J M Beety

Publications and source records attributed to J M Beety.

4 recordsLinked to original sources

PubMed2001

Nutrient regulation of post-heparin lipoprotein lipase activity in obese subjects.

This study examines the immediate effect of ingestion of oral carbohydrate and fat on lipoprotein lipase (LPL) activity post-heparin in six lean and six obese age-matched women. Subjects were given, on two separate occasions, 340 kcal carbohydrate or an equicaloric amount of fat, both in 300 ml of water. Post-heparin LPL activity (10,000 U) was measured on each occasion 120 minutes after ingestion of the meal. Following oral carbohydrate postprandial plasma insulin levels were significantly higher in obese subjects than in lean (p < 0.01). Impaired glucose tolerance was seen in the obese group. GIP secretion was similar in lean and obese subjects both during oral fat and carbohydrate ingestion. GLP-1 secretion post-carbohydrate was lower in obese subjects. Total LPL activity unadjusted for body weight was similar in the two groups after carbohydrate administration but was significantly lower when adjusted per kg body weight. Total LPL activity was lower in the lean group at 130 minutes after fat administration (p < 0.02). Fasting serum triglycerides were higher in the obese group and were inversely related to the post-carbohydrate LPL activity (r = - 0.65, p < 0.02). Intraluminal lipoprotein lipase activity is not increased in established obesity. Fat and carbohydrate nutrients may affect LPL activity differently in lean and obese subjects.

Adult↗

PubMed1999

Inhibition of insulin, glucose-dependent insulinotropic polypeptide (GIP) and glucagon-like peptide-1 (GLP-1) secretion by octreotide has no effect on post-heparin plasma lipoprotein lipase activity.

This study examines the immediate effect of modulating postprandial insulin and insulinotropic hormone (glucose-dependent insulinotropic polypeptide, GIP; glucagon-like peptide-1, GLP-1) secretion on the activation of lipoprotein lipase (LPL) in six lean and six obese age-matched women. Subjects were given, on two separate occasions, 340 kcal of carbohydrate alone or combined with an IV infusion of octreotide, (100 microg infusion from 30 min before the meal for 150 min). Post-heparin LPL activity (10,000 U) was measured on each occasion 120 minutes post-carbohydrate. Following oral carbohydrate postprandial plasma insulin levels were significantly higher in obese subjects than in lean (p < 0.01). Glucose tolerance was slightly impaired in obese subjects. Insulin, GIP and GLP-1 secretion post-carbohydrate was markedly reduced by octreotide in lean and obese subjects. LPL activity was similar in the two groups after carbohydrate administration and was unaffected by octreotide. Inhibition of postprandial insulin, GIP and GLP-1 secretion acutely did not reduce post-heparin LPL activity either in lean or obese subjects.

Adult↗

PubMed1996

Attenuated GLP-1 secretion in obesity: cause or consequence?

BACKGROUND: Hypersecretion of insulinotropic factors such as glucose dependent insulinotropic polypeptide (GIP) and glucagon-like peptide-1(7-36)amide (GLP-1) have been postulated to account for the hyperinsulinaemia of obesity. AIMS: To examine the role of GLP-1 and GIP in obese women and matched controls. SUBJECTS: Six lean and six obese women subjects matched for age. METHODS: The gut hormone, plasma glucose, and serum triglyceride responses were studied over 180 minutes after oral carbohydrate and fat meals. Heparin (10,000 units) was given intravenously at 120 minutes. RESULTS: There was pronounced attenuation of plasma GLP-1 secretion to oral carbohydrate in the obese compared with lean subjects but no such difference in response to oral fat load. There were no differences in the plasma GIP responses to carbohydrate or fat feeding. There was an apparent fall in plasma GLP-1 values in all subjects after administration of heparin. CONCLUSION: Postprandial GLP-1 secretion in response to oral carbohydrate is considerably attenuated in obese subjects. The cause of this attenuation of GLP-1 secretion is not known although we suggest that both this fall and the overall reduction in GLP-1 values in obese subjects may be related to an increase in plasma non-esterified fatty acids.

Adult↗

PubMed1994

The effects of dietary sugar-beet fibre and guar gum on lipid metabolism in Wistar rats.

This study investigates the mechanisms of action for the hypocholesterolaemic effects of sugar-beet fibre (SBF) and guar gum. Four groups of ten male Wistar rats were fed ad lib. on test diets containing either 100 g SBF or guar/kg, or control diets containing 100 g cellulose or wheat bran/kg for 28 d. Food intake, weight gain and food consumption ratios were unaffected by the diets. Circulating cholesterol and hepatic cholesterol concentrations were significantly lower in both SBF- and guar-fed groups compared with either cellulose- or bran-fed animals. Circulating triacylglycerol concentrations were significantly lower in SBF- and guar-fed animals, but total hepatic lipid concentrations and hepatic and adipose tissue lipogenesis rates were unaffected by the diets. Hepatic cholesterol-7 alpha-hydroxylase (EC 1.14.13.17) activities were significantly higher in the guar-fed animals compared with cellulose or bran control groups. Hepatic 3-hydroxy-3-methylglutaryl-CoA reductase (EC 1.1.1.88) activities were unaffected. Circulating bile acid concentrations were significantly lower in SBF- and guar-fed animals and faecal bile acid output was significantly higher in the guar-fed group compared with bran- or cellulose-fed groups. This study supports the hypothesis that guar exerts its hypocholesterolaemic effect via intraluminal bile acid binding and loss of cholesterol from increased faecal bile acid excretion. The mechanism of action for the hypocholesterolaemic effect of SBF is less clear; the results of the present study point to a mechanism involving disruption of the enterohepatic bile acid circulation, possibly via changes in the rate of absorption of dietary lipid.

Adipose Tissue↗