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.

The addition of soybean phosphatidylcholine to triglyceride increases suppressive effects on food intake and gastric emptying in rats.

Nishimukai M, Hara H, Aoyama Y.

Division of Applied Bioscience, Graduate School of Agriculture, Hokkaido University, Sapporo 060-8589, Japan.

The physiologic roles of dietary lecithin have not yet been clearly defined. We examined the effects of soybean lecithin on gastric emptying (Experiments 1 and 2) and food intake (Experiment 3) in rats. Male Wistar rats were fed 2 g of a 20 g lipid/100 g diet containing various levels of lecithin after 24 h of food deprivation; gastric contents were collected 3 h after feeding (Experiment 1). In Experiment 2, the effects of lecithin and a CCK-A receptor antagonist on gastric emptying were examined using a modified phenol red recovery technique. In Experiment 3, their effects on food intake were examined after an intraduodenal infusion of an oil emulsion containing 50 mg soybean oil (SO) or SO partially replaced by lecithin (14-50%). Gastric emptying rates of the lipid and protein in the test diet (Experiment 1) or of phenol red (Experiment 2) were lower in the groups administered lecithin. Food intake for 60 min was lower in rats infused with the oil emulsion containing lecithin (25, 50%) than in rats not administered lecithin. The suppressive effects of lecithin on gastric emptying and food intake were largely reduced by devazepide. These results demonstrate that oil containing lecithin inhibits gastric emptying and food intake, and the effects are associated in part with CCK release.

Cholecystokinin-A Receptors Are Involved in Food Intake Suppression in Rats after Intake of all Fats and Carbohydrates Tested.

Bellissimo N, Anderson GH.

Department of Nutritional Sciences, Faculty of Medicine, UniversityofToronto,Toronto,ON,Canada M5S 3E2.

The hypothesis of these studies was that all fats and carbohydrates suppress food intake, at least in part, via cholecystokinin-A receptors (CCKAR). Fat (coconut oil, beef tallow, olive and safflower oil) and carbohydrate (cornstarch, sucrose, glucose and fructose) preloads were given intragastrically (1 g/4 mL) 30 min before feeding. Devazepide (0.25 mg/kg), a CCKAR antagonist, was given intraperitoneally at 60 or 30 min before or with each of the macronutrient preloads. Devazepide reversed food intake suppression caused by all fat and carbohydrate sources, but the effect was not consistently related to the time of devazepide administration or to any specific feeding interval. Among the fats, coconut and olive oil were most responsive to devazepide. The effect of all carbohydrates on food intake was decreased by devazepide. We conclude that CCKAR play a role in food intake suppression caused by all fats and carbohydrates, but their role is dependent upon the composition of the fat or carbohydrate.
PMID: 12840200 [PubMed - in process]

Predicting cardiovascular risk factors from plasma cortisol measured during oral glucose tolerance tests.
Reynolds RM, Syddall HE, Walker BR, Wood PJ, Phillips DI.

Medical Research Council Environmental Epidemiology Unit, University of Southampton, Southampton,UK.

Increasing evidence suggests that activation of the hypothalamic-pituitary-adrenal (HPA) axis may contribute to the pathogenesis of the metabolic syndrome and obesity. The mechanisms are unknown but may involve alterations in the metabolic responses to feeding that interact with the HPA axis. As it is known that plasma cortisol falls during an oral glucose tolerance test (OGTT), changes in cortisol measured during an OGTT may be altered in the metabolic syndrome. We measured changes in plasma cortisol during OGTTs in a large study of 593 men and women to determine correlates of changes in cortisol with features of the metabolic syndrome and the extent to which these relationships are confounded by obesity. In men and women, higher cortisol area under the curve (AUC) during the OGTT was associated with higher glucose AUC and higher systolic blood pressure. Higher cortisol AUC was associated with reduced insulin increment in men, but higher 2-hour insulin and insulin AUC in women. However, the decline in plasma cortisol after glucose administration was poorly predictive of features of the metabolic syndrome. Obesity was associated with lower cortisol AUC but not with percentage decline in cortisol. Plasma cortisol and obesity had independent effects on plasma glucose and were the strongest predictors of plasma glucose in multiple regression analysis. Measurements of plasma cortisol during the OGTT reinforce the previously observed relationships of activation of the HPA axis in the metabolic syndrome. However, the altered HPA response to feeding does not appear to be primarily responsible for HPA activation in subjects with the metabolic syndrome.

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