Effects of fish oil on metabolic responses to oral fructose and glucose loads in healthy humans

Delarue, Jacques; Couet, Charles; Cohen, Richard A.; Bréchot, Jean-François; Antoine, Jean Michel; Lamisse, F

doi:10.1152/ajpendo.1996.270.2.e353

Cited by 60 publications

(69 citation statements)

References 29 publications

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“…Furthermore, a 35% increase in the cumulated net lipid oxidation has been previously reported in ®ve of these six subjects during the 6 h following a fructose and a glucose load (1 g kg 71 body weight). 29 The reduced basal (present study) and postprandial plasma insulin concentrations 29 might contribute to the facilitation of lipid oxidation during the ®sh oil period. In addition, ®sh oil has been shown to enhance carnitine palmitoyltransferase I activity in rats, 30 mice 31 and Syrian hamsters, 32 and to decrease the sensitivity of carnitine palmitoyltransferase I to malonyl-CoA inhibition in liver mitochondria 33 even in rats fed ®sh oil at a level as low as 0.2% of the diet.…”

Section: Discussionmentioning

confidence: 71%

Effect of dietary fish oil on body fat mass and basal fat oxidation in healthy adults

et al. 1997

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OBJECTIVE: To investigate whether the substitution of ®sh oil for visible fats in a control diet (52% carbohydrates, 16% protein, 32% fat; P:S 0.2) in¯uences body fat mass and substrate oxidation in healthy adults. DESIGN: Six volunteers (5 men; 23 AE 2 y; BMI: 21.9 AE 1.6) were fed a control diet (C) ad libitum during a period of three weeks and, 10±12 weeks later, the same diet where 6 g/d of visible fat were replaced by 6 g/d of ®sh oil (FO) for another three weeks. RESULTS: Energy intakes (IKA-calorimeter) were unchanged. Body fat mass (Dual-energy X-ray absorptiometry) decreased with FO (70.88 AE 0.16 vs 70.3 AE 0.34 kg; FO vs C; P`0.05). When adjusted for lean body mass (Ancova), resting metabolic rate (indirect calorimetry) was unchanged. Basal respiratory quotient decreased with FO (0.815 AE 0.02 vs 0.834 AE 0.02; P`0.05) and basal lipid oxidation increased with FO (1.06 AE 0.17 vs 0.87 AE 0.13 mg kg 71 min 71 ; P`0.05). CONCLUSION: Dietary FO reduces body fat mass and stimulates lipid oxidation in healthy adults.

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Section: Discussionmentioning

confidence: 71%

Effect of dietary fish oil on body fat mass and basal fat oxidation in healthy adults

et al. 1997

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“…We observed [47] that a dietary substitution of 6 g·d -1 of fish oil (1.1 g EPA + 0.7 g DHA·d -1 ) over 3 weeks in healthy young adults studied for 6 h after a 1 g·kg -1 oral glucose load induced a 40% decrease in insulinaemic response without alteration of the glycaemic response. Plasma glucose utilization and endogenous glucose production were not modified by fish oil but whole body carbohydrate oxidation was 35% decreased, fat oxidation was 35% increased and glycogen storage 100% increased.…”

Section: Healthy Subjectsmentioning

confidence: 85%

n-3 long chain polyunsaturated fatty acids: a nutritional tool to prevent insulin resistance associated to type 2 diabetes and obesity?

Delarue¹,

Foll²,

Corporeau³

et al. 2004

Reprod. Nutr. Dev.

185

122

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“…Despite intensive work, the fate of oral glucose remains surprisingly controversial. Reports of the cumulative appearance of oral glucose in plasma have varied from about 70% (34,35) to nearly 100% (36,37), and the maximal rates of glucose appearance have varied about 2-fold. Livesey et al (36) reported a study of glucose kinetics in 12-h fasted humans after an oral glucose load, using stable isotopes and mass spectrometry to detect gastric absorption of [ 13 C 6 ]glucose oral glucose.…”

Section: Discussionmentioning

confidence: 99%

Increased Hepatic Fructose 2,6-Bisphosphate after an Oral Glucose Load Does Not Affect Gluconeogenesis

Jin

Uyeda

Kawaguchi

et al. 2003

Journal of Biological Chemistry

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The generally accepted metabolic concept that fructose 2,6-bisphosphate (Fru-2,6-P 2 ) inhibits gluconeogenesis by directly inhibiting fructose 1,6-bisphosphatase is based entirely on in vitro observations. To establish whether gluconeogenesis is indeed inhibited by Fru-2,6-P 2 in intact animals, a novel NMR method was developed using [U-13 C]glucose and 2 H 2 O as tracers. The method was used to estimate the sources of plasma glucose from gastric absorption of oral [U-13 C]glucose, from gluconeogenesis, and from glycogen in 24-h fasted rats. Liver Fru-2,6-P 2 increased ϳ10-fold shortly after the glucose load, reached a maximum at 60 min, and then dropped to base-line levels by 150 min. The gastric contribution to plasma glucose reached ϳ50% at 30 min after the glucose load and gradually decreased thereafter. Although the contribution of glycogen to plasma glucose was small, glucose formed from gluconeogenesis was substantial throughout the study period even when liver Fru-2,6-P 2 was high. Liver glycogen repletion was also brisk throughout the study period, reaching ϳ30 mol/g at 3 h. These data demonstrate that Fru-2,6-P 2 does not inhibit gluconeogenesis significantly in vivo.Plasma glucose is preserved by gluconeogenesis after exhaustion of glycogen stores during a moderate fast. Following an oral glucose load, gluconeogenesis is thought to be modulated by allosteric regulation of fructose-1,6-bisphosphatase (1). This is an eminently satisfying model because a key regulatory site in glycolysis and gluconeogenesis occurs at level of fructose-6-P and fructose-1,6-P 2 (Fig. 1). Phosphofructokinase-1, the glycolytic enzyme, is potently activated by fructose-2,6-P 2 , whereas fructose-1,6-bisphosphatase, the gluconeogenic enzyme, is thought to be inhibited by this same effector molecule (2, 3). Thus, by regulating the activities of phosphofructo-1-kinase and fructose-1,6-bisphosphatase in a reciprocal manner, Fru-2,6-P 2 is thought to serve as an elegant regulator of glucose usage/production by the liver after an oral glucose load. This generally accepted model is based on kinetic analysis of fructose-1,6-bisphosphatase in vitro, which shows that Fru-2,6-P 2 competes with Fru-1,6-P 2 for the active site of fructose-1,6-bisphosphatase and that both molecules have similar affinity constants, 1-5 M (4 -6). However, the in vivo concentrations of Fru-1,6-P 2 in fasted and fed livers are 20 and 35 M, respectively, whereas those of Fru-2,6-P 2 are 1 and 8 M, respectively (7-9). This suggests that it would be difficult for Fru-2,6-P 2 to have a significant direct effect on fructose-1,6-bisphosphatase activity in vivo based simply upon concentration differences. Some evidence has been presented that suggests Fru-2,6-P 2 is not a potent inhibitor of gluconeogenesis in intact animals. For example, Kuwajima et al. (10) reported continual production of liver glycogen in sucrose-fed rats despite high levels of Fru-2,6-P 2 , and Hue and Bartrons (11) observed stimulated glucose production by glucagon in isolated hepatocytes reg...

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Effects of fish oil on metabolic responses to oral fructose and glucose loads in healthy humans

Cited by 60 publications

References 29 publications

Effect of dietary fish oil on body fat mass and basal fat oxidation in healthy adults

Effect of dietary fish oil on body fat mass and basal fat oxidation in healthy adults

n-3 long chain polyunsaturated fatty acids: a nutritional tool to prevent insulin resistance associated to type 2 diabetes and obesity?

Increased Hepatic Fructose 2,6-Bisphosphate after an Oral Glucose Load Does Not Affect Gluconeogenesis

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