Effect of Exogenous or Endogenous Gastric Inhibitory Polypeptide (GIP) on Plasma Triglyceride Responses in Rats
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We examined the effects of exogenous and endogenous GIP on plasma triglyceride levels in rats, pretreated with a fat-enriched diet, during intraduodenal infusion of a lipid test meal (Lipomul, 8 ml/h). Following the fat load the plasma triglyceride levels increased nearly linearly from a fasting value of 0.621 ± 0.031 mmol/l to 3.32 ± 0.403 mmol/l at 150 min. Simultaneously, the plasma GIP levels rose from 47.1 ± 5.1 at fasting to a peak value of 268.4 ± 32.2 pmol/l at 120 min. When porcine GIP was infused intravenously during the fat load, the plasma triglyceride increments were significantly smaller (control 1.64 ± 0.264 mmol/l versus 0.949 ± 0.114 mmol/l during GIP infusion at 60 min; p < 0.002). GIP infusion in the absence of the fat load did not change fasting triglyceride levels.Keywords:
Gastric inhibitory polypeptide
The majority of the studies that have found a lowering effect of exercise on postprandial lipaemia have employed exercise 12-18 h before a test meal of exaggerated fat content (over 60 % total energy). The aim of the present study was to investigate whether this effect is manifest when exercise is performed immediately before a test meal of moderate fat content. Eleven healthy young men cycled for 45 min at 62 % maximal heart rate or rested, and, immediately afterwards, consumed a meal of moderate fat content (35 % total energy, 0.65 g/kg body mass) in a random counterbalanced design. Blood samples were drawn before exercise, before the meal, and for 8 h postprandially. No significant differences were observed in plasma triacylglycerol concentrations and areas under the triacylglycerol concentration v. time curves between exercise and rest, although exercise reduced the postprandial lipaemic response by 17 %. Non-esterified fatty acids, glucose, and insulin did not differ significantly between the trials. In conclusion, moderate exercise performed immediately before a meal of a fat content typical to the Western diet had only a modest effect on postprandial lipaemia.
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PURPOSE: Since relatively little research is available to assess how strategies that differentially time meal consumption relative to exercise influence the degree of postprandial lipemia (PPL), the goal of this study was to compare postprandial responses to a standardized high fat meal consumed alone (M) versus the same meal consumed in conjunction with exercise (60% of VO2max for 50 min) performed either immediately prior to (EM) or two hours after (ME) meal ingestion. METHODS: Twelve young, healthy male volunteers performed the three trials in random order. Blood samples were drawn after fasting and 1, 3, 5 and 7 hours after the test meal to determine plasma concentrations of triglycerides (TG), glucose and insulin. Blood was also obtained after exercise for the EM trial. RESULTS: The area under the curve (AUC) for TG was 33% lower (p<0.05) for the EM trial in comparison to M, but no difference was detected between ME and M. The glucose AUC for M was significantly (p<0.05) higher for M than both ME and EM. No differences in AUC were detected among trials for insulin responses. CONCLUSIONS: These data suggest that exercise performed prior to a meal is more effective in reducing PPL than exercise performed 2 hours after the meal and that exercise either immediately before or 2 hours after exercise can diminish overall glucose responses. Strategies that optimally influence PPL should be explored to allow for the most beneficial management of triglyceride metabolism.
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The effect of strenuous physical exercise on postprandial gastric acid secretion and gastric emptying was evaluated in untrained healthy volunteers. Subjects exercised for 45 min on a stationary bicycle at 50 or 70% of their maximal work load, beginning 45 min after a steak meal. Compared with a control study during which subjects sat on the bicycle without exercising, exercise had no significant effect on the gastric acid secretory response to the meal (control, 31.9 +/- 8.3 mmol/120 min; exercise, 32.2 +/- 7.8 mmol/120 min) or on the amount of nonabsorbable meal marker that emptied from the stomach in 120 min (control, 88 +/- 3%; exercise, 87 +/- 4%). Increases in serum triglyceride levels after the meal were also unaffected by exercise, suggesting that absorption of dietary lipid was unimpaired by exercise. These studies indicate that strenuous exercise shortly after a meal has little effect on postprandial gastric secretory or motor function in humans.
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Purpose of review In this review we discuss the postprandial pathophysiological mechanisms that promote vascular disease, the evidence for a role of postprandial lipaemia (PPL) in vascular disease and the effect of modifiable and nonmodifiable factors in PPL. Recent findings PPL refers to the dynamic changes in serum lipids and lipoproteins (mainly in serum triglycerides) that occur after a fat load or a meal. Recent data indicate that postprandial or nonfasting triglyceride levels are better predictors of cardiovascular risk, suggesting that efficiency of postprandial handling of triglyceride-rich lipoproteins plays a role in the causation of vascular disease. Summary The recent finding that postprandial serum triglyceride levels are even better than fasting serum triglyceride levels as predictors of vascular disease indicate that it is better to measure an index of triglyceride-rich lipoproteins (in most cases serum triglyceride levels) in the postprandial period than in the postabsorptive fasting state. Moreover, by the time the postabsorptive state is reached, some of these proatherogenic triglyceride-rich lipoprotein changes may be missed in the measurement.
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Triglycerides are an important risk factor for coronary heart disease in Type 2 (non-insulin-dependent) diabetes mellitus. Although Type 2 diabetic patients have an exaggerated postprandial triglyceride response to a fat meal test, little is known about the variability of triglyceride concentrations in day-to-day life. We have studied the variability in triglyceride concentrations in 24 Type 2 diabetic patients over 6 months by having them record fasting and postprandial triglyceride concentrations at home using a Reflotron dry chemistry analyser. All patients were able to use the analyser effectively, with a correlation of 0.97 between patients' monthly Reflotron readings and those recorded by the laboratory. Over 1600 measurements were performed. The results demonstrate a large variation in both fasting (median 1.95 mmol l−1, range 0.8–6.7 mmol l−1) and postprandial triglyceride concentrations (median 2.68 mmol l−1, range 0.8–6.7 mmol l−1). This variation was accounted for by both a large intra- and inter-individual variation. Although there was a strong correlation overall between fasting and postprandial triglyceride concentrations r = 0.925 (p < 0.001), this did not apply on an individual basis. In conclusion, the large variability in triglyceride concentrations should be considered before introducing pharmacological therapy for hypertriglyceridaemia in Type 2 diabetes mellitus.
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Emerging evidence has shown that an abnormal postprandial accumulation of dietary fat is atherogenic. However, there is a lack of data describing the mechanisms for accumulation of triacylglycerol (TAG) in the postprandial period. There is therefore a need to establish a specific measure of the kinetics of endogenous and exogenous TAG in the postprandial period.
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Interdigestive motor activity has been studied extensively both in the human and canine small intestine. The more irregular postprandial pattern, however, has rarely been studied. In particular, physiological studies in humans are lacking. Thus it is unknown whether the physical state of a meal affects the duration of the postprandial motor activity or contractile activity during the postprandial period. 8 healthy male volunteers, aged 19-38 years, underwent a single ambulatory 24-hour manometry study. During the study, volunteers had two physiological meals. The solid meal consisted of pasta with vegetables, and the liquid meal was a vanilla milk drink. The two meals were both palatable, isocaloric (660 kcal) and had an identical fat content (32%). Recordings were analyzed visually for phase III of the migrating motor complex and a validated computer program calculated the mean frequency and amplitude of contractions as well as the mean area under the curve (AUC). The postprandial period was significantly shorter after the liquid meal compared to the solid meal (196 ± 43 vs. 298 ± 23 min; p < 0.04). During the postprandial period, the mean incidence of contractions (2.0 ± 0.5 vs. 3.7 ± 0.4 min-1; p < 0.02) and the mean AUC (132 ± 32 vs. 236 ± 27 mm Hg × s × min-1; p < 0.02) were significantly lower after the liquid meal. The mean amplitude of contractions during the total postprandial period, however, was not significantly different between the two test meals (19.3 ± 0.6 vs. 18.6 ± 0.8 mm Hg). We conclude that human small bowel motor activity differs markedly between solid and liquid meals. Thus the postprandial pattern persists longer after solid meals, and this may have been due to the slower gastric emptying of solids as opposed to liquids. Furthermore the small bowel contracts far more frequently after solid meals.
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Abstract An attempt was made to elucidate the mechanism whereby exercise facilitates postprandial lipid clearance. Two separate experiments examined the effects of mild and strenuous pre-meal exercise on postprandial lipemia among human male subjects. In each case, a high fat meal was consumed after a fasting blood sample was taken. Additional samples were drawn 3, 5, and 7 hr. following the meal on both a control and an experimental day. Optical density was employed as a measure of serum turbidity. Data were analyzed through analysis of variance. Strenuous pre-meal exercise appeared to hasten postprandial lipid clearance without affecting the magnitude of lipemia. Mild pre-meal exercise was seen to reduce the magnitude and duration of postprandial lipemia. These observations tend to negate the concept that exercise influences postprandial lipemia via digestive and/or absorptive mechanisms. It is hypothesized that gross differences in response to the high fat meal witnessed between the two experimental populations may be due to the variance in the mean ages of the groups.
Physical exercise
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Triglycerides are an important risk factor for coronary heart disease in Type 2 (non-insulin-dependent) diabetes mellitus. Although Type 2 diabetic patients have an exaggerated postprandial triglyceride response to a fat meal test, little is known about the variability of triglyceride concentrations in day-to-day life. We have studied the variability in triglyceride concentrations in 24 Type 2 diabetic patients over 6 months by having them record fasting and postprandial triglyceride concentrations at home using a Reflotron dry chemistry analyser. All patients were able to use the analyser effectively, with a correlation of 0.97 between patients' monthly Reflotron readings and those recorded by the laboratory. Over 1600 measurements were performed. The results demonstrate a large variation in both fasting (median 1.95 mmol l−1, range 0.8–6.7 mmol l−1) and postprandial triglyceride concentrations (median 2.68 mmol l−1, range 0.8–6.7 mmol l−1). This variation was accounted for by both a large intra- and inter-individual variation. Although there was a strong correlation overall between fasting and postprandial triglyceride concentrations r = 0.925 (p < 0.001), this did not apply on an individual basis. In conclusion, the large variability in triglyceride concentrations should be considered before introducing pharmacological therapy for hypertriglyceridaemia in Type 2 diabetes mellitus.
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