Effects of oral fructose and glucose on plasma GLP-1 and appetite in normal subjects

Kong, Marie‐France; Chapman, Ian; Goble, Elizabeth A.; Wishart, Judith M.; Wittert, Gary; Morris, Howard A.; Horowitz, Michael

doi:10.1016/s0196-9781(99)00006-6

Cited by 84 publications

(79 citation statements)

References 39 publications

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“…Accordingly, although we did not observe differences in the magnitude of the delay in gastric emptying when equivalent doses of monosaccharides were given intravenously, this does not exclude a difference following oral administration, particularly because ingested fructose is absorbed from the intestine much more slowly (via glucose transporter 5) than glucose and, hence, results in lower plasma concentrations than oral glucose (via sodium-glucose cotransporter 1) (30,53). It should be recognized that we studied only a relatively small number of subjects, and the possibility that there are modest differences in the effects of intravenous fructose and glucose, which may potentially contribute to the slightly more rapid gastric emptying of oral fructose compared with oral glucose, cannot be excluded (11,17,24,45,52) although this may well be explicable by the differential effects on gut hormone release, particularly GLP-1 (33,47,57). Four subjects experienced transient, mild epigastric discomfort during intravenous fructose infusion.…”

Section: Discussionmentioning

confidence: 96%

“…Fructose is used widely in the type 2 diabetic diet and has largely replaced sucrose in a number of processed foods, particularly beverages (15,57). The glycemic response to fructose is also substantially less than to glucose (4,9,24,33,57). There are also substantial differences in the effects of oral glucose and fructose on the release of gastrointestinal hormones, including insulin (57) and the "incretin" hormones glucagon-like peptide (GLP)-1 (33,55,57) and glucose-dependent insulinotropic-polypeptide (GIP) (57).…”

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confidence: 99%

“…The glycemic response to fructose is also substantially less than to glucose (4,9,24,33,57). There are also substantial differences in the effects of oral glucose and fructose on the release of gastrointestinal hormones, including insulin (57) and the "incretin" hormones glucagon-like peptide (GLP)-1 (33,55,57) and glucose-dependent insulinotropic-polypeptide (GIP) (57). Fructose-induced insulin release is glucose dependent in that insulin secretion following intravenous (10) and oral (48) fructose is greater during hyper-than during euglycemia.…”

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confidence: 99%

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Effects of intravenous fructose on gastric emptying and antropyloroduodenal motility in healthy subjects

Stevens

Doran²,

Russo³

et al. 2009

American Journal of Physiology-Gastrointestinal and Liver Physi

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KL. Effects of intravenous fructose on gastric emptying and antropyloroduodenal motility in healthy subjects. Am J Physiol Gastrointest Liver Physiol 297: G1274-G1280, 2009. First published October 1, 2009 doi:10.1152/ajpgi.00214.2009.-Gastric emptying (GE) of glucose is regulated closely, not only as a result of inhibitory feedback arising from the small intestine, but also because of the resulting hyperglycemia. Fructose is used widely in the diabetic diet and is known to empty from the stomach slightly faster than glucose but substantially slower than water. The aims of this study were to determine whether intravenous (iv) fructose affects GE and antropyloroduodenal motility and how any effects compare to those induced by iv glucose. Six healthy males (age: 26.7 Ϯ 3.8 yr) underwent concurrent measurements of GE of a solid meal (100 g ground beef labeled with 20 MBq 99m Tc-sulfur colloid) and antropyloroduodenal motility on three separate days in randomized order during iv infusion of either fructose (0.5 g/kg), glucose (0.5 g/kg), or isotonic saline for 20 min. GE (scintigraphy), antropyloroduodenal motility (manometry), and blood glucose (glucometer) were measured for 120 min. There was a rise in blood glucose (P Ͻ 0.001) after iv glucose (peak 16.4 Ϯ 0.6 mmol/l) but not after fructose or saline. Intravenous glucose and fructose both slowed GE substantially (P Ͻ 0.005 for both), without any significant difference between them. Between t ϭ 0 and 30 min, the number of antral pressure waves was less after both glucose and fructose (P Ͻ 0.002 for both) than saline, and there were more isolated pyloric pressure waves during iv glucose (P ϭ 0.003) compared with fructose and saline (P ϭ NS for both) infusions. In conclusion, iv fructose slows GE and modulates gastric motility in healthy subjects, and the magnitude of slowing of GE is comparable to that induced by iv glucose. glucose; glycemia scintigraphy; manometry IT IS GENERALLY RECOGNIZED that, in health, gastric emptying is regulated tightly, primarily as a result of feedback inhibition generated by interaction of nutrients with the small intestine, the magnitude of which is dependent on the length and region of small intestine exposed to nutrient (36, 37), so that the overall rate of entry of nutrients into the small intestine approximates ϳ2 kcal/min in healthy subjects (5,28,36,45). The motor correlates of the slowing of gastric emptying induced by the presence of nutrients in the small intestine include relaxation of the proximal stomach (2), suppression of antral motility (22), and stimulation of phasic and tonic pyloric contractions (23). Monosaccharides empty from the stomach more slowly than water or isotonic saline because of small intestinal feedback (17), but there may be subtle differences between them. In particular, fructose, when given as intragastric loads to monkeys (45), empties more rapidly than glucose. The slightly more rapid rate of emptying of oral fructose compared with oral glucose has also been demonstrated in humans (11,17,24,52).In ...

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Section: Discussionmentioning

confidence: 96%

mentioning

confidence: 99%

mentioning

confidence: 99%

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Effects of intravenous fructose on gastric emptying and antropyloroduodenal motility in healthy subjects

Stevens

Doran²,

Russo³

et al. 2009

American Journal of Physiology-Gastrointestinal and Liver Physi

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“…Oral fructose was found to be less satiating than fructose delivered in the intestine. 21,22 The presence of free fructose in soft drinks thus has a great influence on appetite and subsequent weight gain. It has also been argued that fructose leads to reduced levels of leptin, an important satiety signal.…”

Section: Type Of Carbohydrate Decides Feeding Behaviourmentioning

confidence: 99%

The effect of low carbohydrate on energy metabolism

Erlanson–Albertsson

Mei

2005

Int J Obes

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OBJECTIVE: To investigate whether low-carbohydrate diets are efficient for reduction of body weight and through which mechanism. DESIGN: A couple of studies using low-carbohydrate diets in the treatment of obesity are reviewed. Mechanisms for explaining the reduced appetite are described in relation to knowledge on regulation of appetite for fat and carbohydrate. RESULTS: Studies with low-carbohydrate diets demonstrate a rapid weight loss, being more pronounced after 3 and 6 months compared to low-fat diets. After 12 months there is no difference between the low-carbohydrate and the conventional low-fat diet on weight loss. Both diets lead to improvements in risk factors for coronary heart disease, the low-carbohydrate diet leading to a greater decrease in serum triglycerides and increase in HDL cholesterol compared to the low-fat diet. Blood pressure, insulin sensitivity and LDL cholesterol were improved to a similar degree by the two diets. The mechanism for the rapid weight loss with the low-carbohydrate diet is a suppressed appetite, first through the high-protein content of the diet, second through the ketogenic nature of the diet with satiety signals for fat being active and third through the absence of hunger-promoting carbohydrate components like sucrose and/or fructose. CONCLUSION: A rapid initial weight loss occurs with a low-carbohydrate diet due to a suppressed appetite. There is as yet no indication of an increased metabolic rate and an increased thermogenesis by the low-carbohydrate diet. The safety and efficacy of low-carbohydrate diets have to await further studies.

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“…For example, differences in ad libitum food intake between treatments have been observed previously with no reported effect of treatments on appetite. 51 Unfortunately, the HI and NI subjects differed in many baseline characteristics including BMI and fasting plasma lipids and cholesterol in the present study (Table 1) as this study was originally designed to answer a different question. 20 Therefore, to remove the influence of BMI, a covariate analysis was run with only BMI included in the model for the following two reasons.…”

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confidence: 97%

Enhanced food intake regulatory responses after a glucose drink in hyperinsulinemic men

2007

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Objective: To determine the effect of hyperinsulinemia on food intake and plasma concentrations of glucose and food intake regulatory hormones in men after a glucose drink. Design: Cross-sectional clinical intervention study of the effect of a glucose drink on food intake regulation. Subjects: Thirty-three normoinsulinemic (NI) (body mass index (BMI) ¼ 25.370.6; age ¼ 41.472.4) and 32 hyperinsulinemic (HI) men (BMI ¼ 29.570.6; age ¼ 43.472.6). Measurements: Food intake was measured from a pizza meal 1 h after subjects consumed either a noncaloric sweetened drink or a glucose-containing drink (75g/300 ml) in random order on two occasions. On another occasion, blood samples were taken every 30 min for 2 h after the glucose drink. Results: Fasting insulin in the HI and NI men was 6573 (mean7s.e.m.) and 2671.5 pmol/l, respectively. Food intake at the pizza meal was reduced by the glucose drink (Po0.01), but more so in HI (À9.774.1 %) than NI men (À5.473.4 %) (P ¼ 0.06). The increase in plasma insulin and cholecystokinin (CCK) after the glucose drink was greater and the plasma concentrations of leptin were higher, and ghrelin and adiponectin were lower in HI men than in NI men (Po0.05). Conclusion: These results support epidemiological data suggesting that hyperinsulinemia, at least in the early stages, may provide resistance to weight gain, possibly through physiological mechanisms of food intake control.

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Effects of oral fructose and glucose on plasma GLP-1 and appetite in normal subjects

Cited by 84 publications

References 39 publications

Effects of intravenous fructose on gastric emptying and antropyloroduodenal motility in healthy subjects

Effects of intravenous fructose on gastric emptying and antropyloroduodenal motility in healthy subjects

The effect of low carbohydrate on energy metabolism

Enhanced food intake regulatory responses after a glucose drink in hyperinsulinemic men

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