Pathways for glucose disposal after meal ingestion in humans

2003 ◽  
Vol 284 (4) ◽  
pp. E716-E725 ◽  
Author(s):  
Hans J. Woerle ◽  
Christian Meyer ◽  
Jean M. Dostou ◽  
Niyaz R. Gosmanov ◽  
Nazmul Islam ◽  
...  
Keyword(s):  
Tritiated Water ◽  
Postprandial Glucose ◽  
Systemic Circulation ◽  
Glucose Disposal ◽  
Indirect Pathway ◽  
Postprandial Period ◽  
Glucose Storage ◽  
Meal Ingestion ◽  
And Storage ◽  
Glycogen Formation

To characterize postprandial glucose disposal more completely, we used the tritiated water technique, a triple-isotope approach (intravenous [3-H3]glucose and [14C]bicarbonate and oral [6,6-2H2]glucose) and indirect calorimetry to assess splanchnic and peripheral glucose disposal, direct and indirect glucose storage, oxidative and nonoxidative glycolysis, and the glucose entering plasma via gluconeogenesis after ingestion of a meal in 11 normal volunteers. During a 6-h postprandial period, a total of ∼98 g of glucose were disposed of. This was more than the glucose contained in the meal (∼78 g) due to persistent endogenous glucose release (∼21 g): splanchnic tissues initially took up ∼23 g, and an additional ∼75 g were removed from the systemic circulation. Direct glucose storage accounted for ∼32 g and glycolysis for ∼66 g (oxidative ∼43 g and nonoxidative ∼23 g). About 11 g of glucose appeared in plasma as a result of gluconeogenesis. If these carbons were wholly from glucose undergoing glycolysis, only ∼12 g would be available for indirect pathway glycogen formation. Our results thus indicate that glycolysis is the main initial postprandial fate of glucose, accounting for ∼66% of overall disposal; oxidation and storage each account for ∼45%. The majority of glycogen is formed via the direct pathway (∼73%).

Mechanisms for abnormal postprandial glucose metabolism in type 2 diabetes

2006 ◽  
Vol 290 (1) ◽  
pp. E67-E77 ◽  
Author(s):  
Hans J. Woerle ◽  
Ervin Szoke ◽  
Christian Meyer ◽  
Jean M. Dostou ◽  
Steven D. Wittlin ◽  
...  
Keyword(s):  
Type 2 Diabetes ◽  
Glucose Metabolism ◽  
Postprandial Glucose ◽  
Postprandial Hyperglycemia ◽  
Glucose Disposal ◽  
Glucose Release ◽  
Isotope Technique ◽  
Glucose Storage ◽  
And Storage

To assess mechanisms for postprandial hyperglycemia, we used a triple-isotope technique ([\3-3H]glucose and [14C]bicarbonate and oral [6,6-dideutero]glucose iv) and indirect calorimetry to compare components of glucose release and pathways for glucose disposal in 26 subjects with type 2 diabetes and 15 age-, weight-, and sex-matched normal volunteers after a standard meal. The results were as follows: 1) diabetic subjects had greater postprandial glucose release ( P < 0.001) because of both increased endogenous and meal-glucose release; 2) the greater endogenous glucose release ( P < 0.001) was due to increased gluconeogenesis ( P < 0.001) and glycogenolysis ( P = 0.01); 3) overall tissue glucose uptake, glycolysis, and storage were comparable in both groups ( P > 0.3); 4) glucose clearance ( P < 0.001) and oxidation ( P = 0.004) were reduced, whereas nonoxidative glycolysis was increased ( P = 0.04); and 5) net splanchnic glucose storage was reduced by ∼45% ( P = 0.008) because of increased glycogen cycling ( P = 0.03). Thus in type 2 diabetes, postprandial hyperglycemia is primarily due to increased glucose release; hyperglycemia overcomes the effects of impaired insulin secretion and sensitivity on glucose transport, but intracellular defects persist so that pathways of glucose metabolism are abnormal and glucose is shunted away from normal sites of storage (e.g., liver and muscle) into other tissues.

Impact of variable insulinemia and glycemia on in vivo glycolysis and glucose storage in dogs

1994 ◽  
Vol 266 (1) ◽  
pp. E62-E71 ◽  
Author(s):  
M. J. Christopher ◽  
C. Rantzau ◽  
G. M. Ward ◽  
F. P. Alford
Keyword(s):  
Glucose Uptake ◽  
Tritiated Water ◽  
Insulin Level ◽  
Whole Body ◽  
Glucose Disposal ◽  
Glycolytic Flux ◽  
Insulin Levels ◽  
Glucose Storage ◽  
The Impact

To determine the impact of variable plasma insulin concentrations and glycemia on the partitioning of whole body glucose metabolism between glycolysis and glucose storage, we estimated endogenous hepatic glucose production and rates of in vivo glycolytic flux (GF) and glucose storage (GS) in six normal dogs from the generation of plasma tritiated water (3H2O) and [3-3H]glucose specific activity during 150 min of somatostatin euglycemic (E) and hyperglycemic (H) clamps at hypoinsulinemic, basal, intermediate, and high insulin levels. During both E and H clamps, overall rates of GF and GS increased with the rising insulin levels, but the relative contributions to in vivo glucose disposal of GF decreased, whereas GS rose progressively with increasing insulin levels. The relative contribution of GS during H to overall glucose disposal was greater at the lower insulin level. In addition, in absolute terms, GF and GS were significantly higher (P < 0.05) during H than during E at all insulin levels. Moreover, the incremental rise in GF induced by H was equal for the low to intermediate insulin levels tested, independent of the prevailing free fatty acid (FFA) levels. However, when whole body glucose disposal rates were matched, GF and GS rates were independent of the coexisting glycemia, insulin, and/or FFA levels. We conclude that 1) insulin has a major impact on the intracellular fate of infused glucose, with a lesser but significant effect of hyperglycemia per se on these processes; 2) the magnitude of the hyperglycemia-induced increase in GF is independent of the prevailing insulin level from low to intermediate levels; and 3) in vivo GF and GS are dependent on the net rate of glucose uptake into cells but independent of absolute FFA levels or whether glucose uptake is stimulated by raised insulin or glucose levels.

Role of human liver, kidney, and skeletal muscle in postprandial glucose homeostasis

2002 ◽  
Vol 282 (2) ◽  
pp. E419-E427 ◽  
Author(s):  
Christian Meyer ◽  
Jean M. Dostou ◽  
Stephen L. Welle ◽  
John E. Gerich
Keyword(s):  
Skeletal Muscle ◽  
Glucose Homeostasis ◽  
Postprandial Glucose ◽  
Systemic Circulation ◽  
Postprandial Period ◽  
Glucose Release ◽  
Hepatic Glucose ◽  
The Difference ◽  
Hepatic Glucose Release

Recent studies indicate a role for the kidney in postabsorptive glucose homeostasis. The present studies were undertaken to evaluate the role of the kidney in postprandial glucose homeostasis and to compare its contribution to that of liver and skeletal muscle. Accordingly, we used the double isotope technique along with forearm and renal balance measurements to assess systemic, renal, and hepatic glucose release as well as glucose uptake by kidney, skeletal muscle, and splanchnic tissues in 10 normal volunteers after ingestion of 75 g of glucose. We found that, during the 4.5-h postprandial period, 22 ± 2 g (30 ± 3% of the ingested glucose) were initially extracted by splanchnic tissues. Of the remaining 53 ± 2 g that entered the systemic circulation, 19 ± 3 g were calculated to have been taken up by skeletal muscle and 7.5 ± 1.7 g by the kidney (26 ± 3 and 10 ± 2%, respectively, of the ingested glucose). Endogenous glucose release during the postprandial period (16 ± 2 g), calculated as the difference between overall systemic glucose appearance and the appearance of ingested glucose in the systemic circulation, was suppressed 61 ± 3%. Surprisingly, renal glucose release increased twofold (10.6 ± 2.5 g) and accounted for ∼60% of postprandial endogenous glucose release. Hepatic glucose release (6.7 ± 2.2 g), the difference between endogenous and renal glucose release, was suppressed 82 ± 6%. These results demonstrate a hitherto unappreciated contribution of the kidney to postprandial glucose homeostasis and indicate that postprandial suppression of hepatic glucose release is nearly twofold greater than had been calculated in previous studies (42 ± 4%), which had assumed that there was no renal glucose release. We postulate that increases in postprandial renal glucose release may play a role in facilitating efficient liver glycogen repletion by permitting substantial suppression of hepatic glucose release.

scholarly journals In Vivo Digestion of Egg Products Enriched with DHA: Effect of the Food Matrix on DHA Bioavailability

Foods ◽  
2020 ◽  
Vol 10 (1) ◽  
pp. 6
Author(s):  
Carlos Pineda-Vadillo ◽  
Françoise Nau ◽  
Catherine Guérin-Dubiard ◽  
Claire Bourlieu ◽  
Francesco Capozzi ◽  
...  
Keyword(s):  
Docosahexaenoic Acid ◽  
Venous Catheter ◽  
Systemic Circulation ◽  
Food Matrix ◽  
Postprandial Period ◽  
Egg Products ◽  
Efficient Vector

The aim of the present study was to determine to what extent the food matrix could affect the release of docosahexaenoic acid (DHA) during digestion and its incorporation into systemic circulation. In this aim, three DHA-enriched egg products having the same composition but different structure were developed: omelet, hard-boiled egg, and mousse. Then, nine pigs fitted with T-shape cannulas at duodenal level and a jugular venous catheter were fed with the DHA-enriched egg products, and duodenal effluents and plasma were collected throughout the postprandial period. Results highlighted an undeniable effect of the food matrix on digestion parameters and DHA bioavailability. The transit of DHA and protein through the duodenum was faster after the ingestion of the mousse than after the ingestion of the omelet and hard-boiled egg. While most of the DHA and protein ingested under the form of mousse had already passed through the duodenum 4.5 h after its ingestion, significantly higher quantities were still present in the case of the omelet and hard-boiled egg. In terms of bioavailability, the omelet was the most efficient vector for delivering DHA into systemic circulation. It supplied 56% and 120% more DHA than the hard-boiled egg and the mousse, respectively.

Simple validation for the hepatic venous cannula implanted chronically in conscious rats

1991 ◽  
Vol 71 (1) ◽  
pp. 359-364 ◽  
Author(s):  
M. T. Huang
Keyword(s):  
Inferior Vena Cava ◽  
Inferior Vena ◽  
Superior Vena ◽  
Tritiated Water ◽  
Vena Cava ◽  
Systemic Circulation ◽  
Tracer Injection ◽  
Conscious Rats ◽  
Tygon Tubing ◽  
Venous Cannula

A method for the detection of vena caval contamination in blood taken from hepatic venous cannulas in conscious rats was described. The procedures included 1) bolus injection of tritiated water (50 microCi) through a cannula into the abdominal inferior vena cava and 2) continuous blood sampling (less than 0.2 ml) from the hepatic venous cannula for 2 min into a 180-cm piece of Tygon tubing, starting concurrently with tracer injection. The washout of tritium was determined from samples in 15-cm sections of Tygon tubing. Because circulation from the inferior vena cava to the hepatic vein is interceded by the systemic circulation, the washout of tritium from a valid hepatic venous cannula should resemble the pattern determined elsewhere in the systemic circulation. In the current study, the reference systemic washout was determined in the superior vena cava of a group of rats similarly injected with tritiated water in the inferior vena cava. The maximum of tritium washout derived from a valid hepatic venous cannula should fall in the range encompassed by one standard deviation of the mean of the maximum of the reference (1,400 to 1,930 cpm/sample). The maximum of the washout pattern derived from the invalid cannula, which lay adjacent to the site of injection, was expected to exceed this range. On the basis of these criteria, hepatic blood flow (HBF) was determined by sulfbromophthalein (BSP) extraction in groups of rats with valid and invalid cannulas. HBF in rats with valid hepatic venous cannulas was 2.58 +/- 0.15 in the conscious state and 2.76 +/- 0.26 ml.min-1.g wet wt-1 in the ketamine-anesthetized state.(ABSTRACT TRUNCATED AT 250 WORDS)

scholarly journals Evidence for altered control of glucose disposal after total colectomy

2000 ◽  
Vol 84 (6) ◽  
pp. 813-819 ◽  
Author(s):  
M. Denise Robertson ◽  
Geoff Livesey ◽  
Shelagh M. Hampton ◽  
John C. Mathers
Keyword(s):  
Insulin Sensitivity ◽  
Insulin Resistance Syndrome ◽  
Compartment Model ◽  
Short Chain Fatty Acids ◽  
Postprandial Glucose ◽  
Insulin Concentration ◽  
Glucose Disposal ◽  
Control Group ◽  
Plasma Insulin Concentration ◽  
Steady State Kinetics

Colonic fermentation of organic matter to short-chain fatty acids has been implicated in the improvement in insulin sensitivity achieved by feeding diets rich in complex carbohydrates. The present study assessed the potential role of the colon in determining postprandial glucose kinetics. Metabolic responses to a complex-carbohydrate test meal were determined in conjunction with a primed continuous infusion of D-[6,6-2H]glucose in a group of ileostomists and sex-matched controls. Glucose disposal (GD) was computed using non-steady-state kinetics on a single compartment model. Insulin sensitivity was derived using cumulative GD as the dependent variable, and time and the integrated insulin concentration as independent variables. The ileostomist group had a significantly higher postprandial plasma insulin concentration (P=0·034) compared with the control group, but no difference in the plasma glucose concentration. Total GD was similar in each group, although the insulin-dependent GD was substantially lower in the ileostomists (0·46 v. 0·13 mg glucose/min per pmol, P=0·015). The ileostomist group also showed a 50 % lower rate of glucose oxidation in the postprandial period (P=0·005), although the rate of non-oxidative GD was not significantly affected. The present study indicates that loss of the colon is associated with several characteristics of the insulin resistance syndrome, and favours a view that the colon has a role in the control of postprandial glucose.

scholarly journals α-Tocomonoenol Is Bioavailable in Mice and May Partly Be Regulated by the Function of the Hepatic α-Tocopherol Transfer Protein

Molecules ◽  
2020 ◽  
Vol 25 (20) ◽  
pp. 4803
Author(s):  
Andrea Irías-Mata ◽  
Nadine Sus ◽  
Maria-Lena Hug ◽  
Marco Müller ◽  
Walter Vetter ◽  
...  
Keyword(s):  
Tissue Distribution ◽  
Room Temperature ◽  
Systemic Circulation ◽  
Future Research ◽  
Wild Type ◽  
Transfer Protein ◽  
In Vivo Experiments ◽  
And Storage

Tocomonoenols are vitamin E derivatives present in foods with a single double bond at carbon 11’ in the sidechain. The α-tocopherol transfer protein (TTP) is required for the maintenance of normal α-tocopherol (αT) concentrations. Its role in the tissue distribution of α-11′-tocomonoenol (αT1) is unknown. We investigated the tissue distribution of αT1 and αT in wild-type (TTP+/+) and TTP knockout (TTP−/−) mice fed diets with either αT or αT1 for two weeks. αT1 was only found in blood, not tissues. αT concentrations in TTP+/+ mice were in the order of adipose tissue > brain > heart > spleen > lungs > kidneys > small intestine > liver. Loss of TTP function depleted αT in all tissues. αT1, contrary to αT, was still present in the blood of TTP−/− mice (16% of αT1 in TTP+/+). Autoclaving and storage at room temperature reduced αT and αT1 in experimental diets. In conclusion, αT1 is bioavailable, reaches the blood in mice, and may not entirely depend on TTP function for secretion into the systemic circulation. However, due to instability of the test compounds in the experimental diets, further in vivo experiments are required to clarify the role of TTP in αT1 secretion. Future research should consider compound stability during autoclaving of rodent feed.

Impairment of glucose disposal by infusion of triglycerides in humans: role of glycemia

1989 ◽  
Vol 256 (6) ◽  
pp. E747-E752 ◽  
Author(s):  
C. P. Felley ◽  
E. M. Felley ◽  
G. D. van Melle ◽  
P. Frascarolo ◽  
E. Jequier ◽  
...  
Keyword(s):  
Glucose Oxidation ◽  
Plasma Free Fatty Acid ◽  
Regulatory Mechanisms ◽  
Glucose Disposal ◽  
Glucose Storage ◽  
Interaction Term ◽  
The Difference ◽  
Total Glucose

The present study was designed to assess the role of hyperglycemia (150 mg/dl) vs. euglycemia (90 mg/dl) on glucose metabolism in vivo during the infusion of a triglyceride emulsion (Intralipid). Seven young healthy volunteers were studied on four occasions using the hyperinsulinemic clamp technique, twice during euglycemia and twice during hyperglycemia, without or with Intralipid. Glucose oxidation (O) was calculated from continuous respiratory exchange measurements, and glucose storage (S) was obtained as the difference between total glucose disposal (M) and O. Two-way analysis of variance with interaction term demonstrated 1) a significant increase for M with hyperglycemia and a decrease with Intralipid; no interaction, and 2) in euglycemia, O/M and S/M occurred in one-to-one ratios; on the other hand, during 150-mg/dl hyperglycemia, the ratio dropped roughly to 1:2. Intralipid had no effect on the ratio, and no interaction could be observed. These results suggest the existence of physiological regulatory mechanisms by which 1) the rise in plasma free fatty acid inhibits both oxidative and nonoxidative glucose disposal, and 2) the rise in glycemia stimulates predominantly nonoxidative glucose disposal.

Effect of fasting on the intracellular metabolic partition of intravenously infused glucose in humans

1999 ◽  
Vol 277 (5) ◽  
pp. E815-E823 ◽  
Author(s):  
F. Fery ◽  
L. Plat ◽  
E. O. Balasse
Keyword(s):  
Glucose Oxidation ◽  
Glycogen Synthesis ◽  
Normal Subjects ◽  
Glucose Disposal ◽  
Indirect Pathway ◽  
Total Carbohydrate ◽  
Euglycemic Hyperinsulinemic Clamp ◽  
Direct Pathway ◽  
Group 3 ◽  
Group 2

The effects of fasting on the pathways of insulin-stimulated glucose disposal were explored in three groups of seven normal subjects. Group 1 was submitted to a euglycemic hyperinsulinemic clamp (∼100 μU/ml) after both a 12-h and a 4-day fast. The combined use of [3-3H]- and [U-14C]glucose allowed us to demonstrate that fasting inhibits, by ∼50%, glucose disposal, glycolysis, glucose oxidation, and glycogen synthesis via the direct pathway. In group 2, in which the clamp glucose disposal during fasting was restored by hyperglycemia (155 ± 15 mg/dl), fasting stimulated glycogen synthesis (+29 ± 2%) and inhibited glycolysis (−32 ± 3%) but only in its oxidative component (−40 ± 3%). Results were similar in group 3 in which the clamp glucose disposal was restored by a pharmacological elevation of insulin (∼2,800 μU/ml), but in this case, both glycogen synthesis and nonoxidative glycolysis participated in the rise in nonoxidative glucose disposal. In all groups, the reduction in total carbohydrate oxidation (indirect calorimetry) induced by fasting markedly exceeded the reduction in circulating glucose oxidation, suggesting that fasting also inhibits intracellular glycogen oxidation. Thus prior fasting favors glycogen retention by three mechanisms: 1) stimulation of glycogen synthesis via the direct pathway; 2) preferential inhibition of oxidative rather than nonoxidative glycolysis, thus allowing carbon conservation for glycogen synthesis via the indirect pathway; and 3) suppression of intracellular glycogen oxidation.

scholarly journals Postprandial glucose, insulin and glucagon-like peptide 1 responses to sucrose ingested with berries in healthy subjects

2011 ◽  
Vol 107 (10) ◽  
pp. 1445-1451 ◽  
Author(s):  
Riitta Törrönen ◽  
Essi Sarkkinen ◽  
Tarja Niskanen ◽  
Niina Tapola ◽  
Kyllikki Kilpi ◽  
...  
Keyword(s):  
Healthy Subjects ◽  
Serum Insulin ◽  
Venous Blood ◽  
Postprandial Glucose ◽  
Carbohydrate Ingestion ◽  
Glucagon Like Peptide ◽  
Glucagon Like Peptide 1 ◽  
Meal Ingestion ◽  
Single Blind ◽  
Modest Effect

Berries are often consumed with sucrose. They are also rich sources of polyphenols which may modulate glycaemia after carbohydrate ingestion. The present study investigated the postprandial glucose, insulin and glucagon-like peptide 1 (GLP-1) responses to sucrose ingested with berries, in comparison with a similar sucrose load without berries. A total of twelve healthy subjects were recruited to a randomised, single-blind, placebo-controlled crossover study. They participated in two meal tests on separate days. The berry meal was a purée (150 g) made of bilberries, blackcurrants, cranberries and strawberries with 35 g sucrose. The control meal included the same amount of sucrose and available carbohydrates in water. Fingertip capillary and venous blood samples were taken at baseline and at 15, 30, 45, 60, 90 and 120 min after starting to eat the meal. Glucose, insulin and GLP-1 concentrations were determined from the venous samples, and glucose also from the capillary samples. Compared to the control meal, ingestion of the berry meal resulted in lower capillary and venous plasma glucose and serum insulin concentrations at 15 min (P = 0·021,P < 0·007 andP = 0·028, respectively), in higher concentrations at 90 min (P = 0·028,P = 0·021 andP = 0·042, respectively), and in a modest effect on the GLP-1 response (P = 0·05). It also reduced the maximum increases of capillary and venous glucose and insulin concentrations (P = 0·009,P = 0·011 andP = 0·005, respectively), and improved the glycaemic profile (P < 0·001 andP = 0·003 for capillary and venous samples, respectively). These results suggest that the glycaemic control after ingestion of sucrose can be improved by simultaneous consumption of berries.

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