Carbohydrate and Lipid Oxidation in Normal and Diabetic Subjects

Felber, J. P.; Magnenat, G; Castheélaz, M; Geser, C. A.; Müller-Hess, R.; Kalbermatten, N. de; Ebiner, Jérôme; Curchod, B; Pittet, Ph.; Jéquier, E

doi:10.2337/diab.26.7.693

Cited by 47 publications

(23 citation statements)

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“…The data of the present and previous studies (16,17,(53)(54)(55) indicate that 30-40% ofan oral glucose load is immediately oxidized; specifically, in the present studies 24.9 g (37%) of a 67.6-g oral load was oxidized. About 35% of this (8.9 g) could be accounted for by muscle.…”

Section: Discussionsupporting

confidence: 67%

Skeletal muscle glycolysis, oxidation, and storage of an oral glucose load.

Kelley¹,

Mitrakou²,

Marsh³

et al. 1988

J. Clin. Invest.

287

181

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Although muscle is considered to be the most important site for postprandial glucose disposal, the metabolic fate of oral glucose taken up by muscle remains unclear. We, therefore, employed the dual isotope technique (intravenous, [6-3HJ-glucose; oral, l1-'4Clglucose), indirect calorimetry, and forearm balance measurements of glucose, lactate, alanine, pyruvate, 02, and CO2 in nine normal volunteers to determine the relative importance of muscle glycogenic, glycolytic, and oxidative pathways in disposal of an oral glucose load. During the 5 h after glucose ingestion (1 g/kg), 37±3% (24.9±2.3 g) of the load was oxidized and 63±3% (42.8±2.7 g) was stored. At least 29% (19.4±1.3 g) was taken up by splanchnic tissues. Muscle took up 26% (17.9±2.9 g) of the oral glucose coincident with a 50% reduction in its oxidation of fat. 15% of the oral glucose taken up by muscle (2.5±0.9 g) was released as lactate, alanine, or pyruvate; 50% (8.9±1.4 g) was oxidized, and 35% (6.4±2.3 g) was available for storage. We conclude that muscle and splanchnic tissues take up a comparable percentage of an oral glucose load and that oxidation is the predominant fate of glucose taken up by muscle, with storage in muscle accounting for < 10% of the oral load. Thus, contrary to the prevailing view, muscle is neither the major site of storage nor the predominant site of disposal of an oral glucose load.

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Section: Discussionsupporting

confidence: 67%

Skeletal muscle glycolysis, oxidation, and storage of an oral glucose load.

Kelley¹,

Mitrakou²,

Marsh³

et al. 1988

J. Clin. Invest.

287

181

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“…The composition of plasma FFAs was unchanged over the 12-week treatment period. Plasma FFAs result from TG lipolysis of adipose tissues [4,5]; hence low-dose ω–3 PUFAs as in our study are not expected to significantly alter plasma FFA levels. The reduction of FFAs as well as plasma TG levels coincides with increased mRNA expression of enzymes involved in FA oxidation in the PBMCs of subjects receiving PPC.…”

Section: Discussionmentioning

confidence: 92%

“…FFAs have therefore been implicated as an important causative link between obesity, peripheral and hepatic insulin resistance (IR), type 2 diabetes, hyperinsulinemia, arterial hypertension and dyslipidemia, collectively referred to as the metabolic syndrome [1,2,3]. Adipose tissue lipolysis is the major source of plasma FFAs not least after an overnight fast [4,5]. An additional metabolic characteristic of hyperlipidemia is a decreased carnitine concentration in blood and tissues [6,7,8].…”

Section: Introductionmentioning

confidence: 99%

A Combination of (ω–3) Polyunsaturated Fatty Acids, Polyphenols and <i>L</i>-Carnitine Reduces the Plasma Lipid Levels and Increases the Expression of Genes Involved in Fatty Acid Oxidation in Human Peripheral Blood Mononuclear Cells and HepG2 Cells

Radler¹,

Stangl²,

Lechner³

et al. 2011

Ann Nutr Metab

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Background: Hyperlipidemia and obesity are associated with metabolic syndrome and increased risk in developing diabetes and cardiovascular disease. Nutritional supplements, e.g. L-carnitine and polyunsaturated fatty acids (PUFAs), exert lipid-lowering effects. Hence, the hypothesis that dietetic intervention reduces plasma lipid levels and metabolic enzymes in overweight hyperlipidemic subjects was tested. Subjects and Methods: In a prospective placebo-controlled double-blind study in 22 moderately hyperlipidemic obese humans consuming low-fat yoghurt enriched with a combination of low-dose PUFAs, polyphenols and L-carnitine (PPC) twice a day for 12 weeks were compared to 20 matching participants ingesting low-fat yoghurt. The effects on plasma lipids and expression of enzymes involved in regulation of fatty acid oxidation in peripheral blood mononuclear cells (PBMCs) and HepG2 cells were evaluated. Results: PPC consumption led to significantly reduced plasma free fatty acid (–29%) and triglyceride (–24%) concentrations (each p < 0.05). PPC application increased significantly peroxisome proliferator-activated receptor α (PPARα) mRNA abundances and those of PPARα target genes (carnitine palmitoyltransferases-1, CPT1A and CPT1B, carnitine acetyltransferase and organic cation transporter 2; each p < 0.05) in PBMCs. In controls, plasma lipid levels and PBMC gene expression did not change. These findings were substantiated by the results of cell culture experiments in HepG2 cells. Conclusion: Supplementation of PPC had marked lipid-lowering effects and PBMC gene expression profiles seemed to reflect nutrition-related metabolic changes.

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“…This observation suggests that the elevated plasma glucose levels in the second part of the glucose curve probably result from this defect. Deficiency in glucose oxidation in response to the toad is indeed expected to affect mostly the late phase of the glucose tolerance curve as oxidation is normally low at the beginning of the test and gradually increases to reach its maximum after 90 to 150 min [8,14].…”

Section: Discussionmentioning

confidence: 99%

“…Continuous indirect calorimetry was performed as previously, described [6,7,8], It allows determinations of both carbohydrate and lipid oxidation rates as well as calculation of the total quantity of glucose and lipid oxidized during the period of the test, the quantity of glucose oxidized at basal rate and in response to the load (suprabasal oxidation). The quantity of glucose stored during the 3 hours of the test was calculated by subtracting from the 100 g ingested glucose, the total quantity of glucose oxidized, urinary glucose loss and excess glucose remaining in the glucose space.…”

Section: C) Gas-exchange Measurementsmentioning

confidence: 99%

Glucose storage and oxidation in different degrees of human obesity measured by continuous indirect calorimetry

Felber¹,

Meyer²,

Curchod

et al. 1981

Diabetologia

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Summary. Glucose disposal of a 100 g glucose load has been determined in 26 obese compared with 10 non-obese subjects by means of a new application of continuous indirect calorimetry. The obese subjects were divided into 4 groups, according to their degree of glucose intolerance and their insulin response to the glucose load. Through this division it appeared that subjects with no glucose intolerance were moderately obese while the groups with glucose intolerance showed a higher degree of obesity, glucose intolerance increasing with age. The 10 obese subjects with no glucose intolerance (group A) presented values for glucosedisposal similar to those of the control subjects. The 4 obese subjects with impaired glucose tolerance. (group B) showed no significant changes in glucose storage and in basal oxidation, but a significant decrease in oxidation in response to the load (11 _+ 2g vs 19 _-2 lg in the control group, p <0.02). The 6 obese subjects with overt diabetes and elevated insulin response to the glucose load (group C) showed a significant decrease in glucose storage (34 _.+ 6 g vs 63 --_ I g, p < 0.001) but not in oxidation. The 6 obese subjects With overt diabetes and decreased insulin response (group D) showed a significant decrease in glucose storage (25 +4 g vs 63 -+ 1 g, p < 0.001) and oxidation (12 +__ i g, vs 19 + 1 g, p < 0.005). These observations show that in obese diabetics, glucose intolerance results primarily from decreased glucose storage and to a lesser extent from a decrease in glucose oxidation.

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Carbohydrate and Lipid Oxidation in Normal and Diabetic Subjects

Cited by 47 publications

References 0 publications

Skeletal muscle glycolysis, oxidation, and storage of an oral glucose load.

Skeletal muscle glycolysis, oxidation, and storage of an oral glucose load.

A Combination of (ω–3) Polyunsaturated Fatty Acids, Polyphenols and <i>L</i>-Carnitine Reduces the Plasma Lipid Levels and Increases the Expression of Genes Involved in Fatty Acid Oxidation in Human Peripheral Blood Mononuclear Cells and HepG2 Cells

Glucose storage and oxidation in different degrees of human obesity measured by continuous indirect calorimetry

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