Tracer methods and the metabolic disposal of a carbohydrate load in man

Radziuk, J.

doi:10.1002/dmr.5610030111

Cited by 37 publications

(28 citation statements)

References 83 publications

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“…The (27). However, concurrent glycogenesis and glycogenolysis and/or glucose/glucose-6-phosphate cycling may lead to an over-or underestimation of SGU, depending on the isotopes used (6).…”

Section: Discussionmentioning

confidence: 99%

A noninvasive method to measure splanchnic glucose uptake after oral glucose administration.

Ludvik¹,

Nolan²,

Roberts³

et al. 1995

J. Clin. Invest.

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We have developed a noninvasive method to estimate splanchnic glucose uptake (SGU) in humans (oral glucose clamp technique [OG-CLAMP]), which combines a hyperinsulinemic clamp with an oral glucose load (oral glucose tolerance test). We validated this method in 12 nondiabetic subjects using hepatic vein catheterization (HVC) during an oral glucose tolerance test. During HVC, splanchnic blood flow increased from 1,395±64 to 1,935±109 ml/min, returning to basal after 180 min and accounted for 45±7% of SGU in lean and 19±5% in obese subjects (P < 0.05). SGU estimated during the OG-CLAMP was 22±2% of the glucose load, and this was significantly correlated (r = 0.90, P < 0.0001) with SGU (35±4%) and with first pass SGU (24±3%; r = 0.83, P < 0.001) measured during HVC. SGU was higher in obese than in lean subjects during OG-CLAMP (27±1% vs 18±3%, P < 0.01) and HVC (44±4% vs 26±5%, P < 0.05). In conclusion, SGU during the OG-CLAMP is well correlated to SGU measured during HVC. An increase in splanchnic blood flow is a major contributor to SGU in lean subjects. SGU is increased in obese subjects as measured by both methods.

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“…The (27). However, concurrent glycogenesis and glycogenolysis and/or glucose/glucose-6-phosphate cycling may lead to an over-or underestimation of SGU, depending on the isotopes used (6).…”

Section: Discussionmentioning

confidence: 99%

A noninvasive method to measure splanchnic glucose uptake after oral glucose administration.

Ludvik¹,

Nolan²,

Roberts³

et al. 1995

J. Clin. Invest.

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“…In the dog, arterial plasma glucose levels of 160-290 mg/dl and insulin levels of 35-384 U/ml resulted in rates of NHGU of 1.0-2.9 mg/kg/min (1). These results demonstrate that the combination of hyperinsulinemia and hyperglycemia cannot account for the peak rates of NHGU (up to 7.5 mg/kg/min) present after the ingestion of glucose in either humans or the dog (1,(4)(5)(6)(7)(8)(9). In addition to the rise in insulin and glucose, meal ingestion also produces a rise in the portal vein glucose level that is greater than the glucose level in the arterial circulation.…”

Section: Introductionmentioning

confidence: 86%

Comparison of the time courses of insulin and the portal signal on hepatic glucose and glycogen metabolism in the conscious dog.

Pagliassotti¹,

Holste²,

Moore³

et al. 1996

J. Clin. Invest.

123

181

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To investigate the temporal response of the liver to insulin and portal glucose delivery, somatostatin was infused into four groups of 42-h-fasted, conscious dogs ( n ϭ 6/group), basal insulin and glucagon were replaced intraportally, and hyperglycemia was created via a peripheral glucose infusion for 90 min (period 1). This was followed by a 240-min experimental period (period 2) in which hyperglycemia was matched to period 1 and either no changes were made (CON), a fourfold rise in insulin was created (

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“…A large part of this disposal takes place in peripheral tissues, primarily muscle [40,54,55]. Insulin controls glucose transport into cells, as well as its oxidative and non-oxidative metabolism [40,[54][55][56]. The latter consists primarily of storage as glycogen and a great deal of attention has been focused on finding, for example, mutations of glycogen synthase [57] whose expression could explain the defective storage of glucose seen in type 2 diabetes.…”

Section: Determinants Of Glucose Tolerancementioning

confidence: 99%

Section: Determinants Of Glucose Tolerancementioning

confidence: 99%

Hepatic glucose uptake, gluconeogenesis and the regulation of glycogen synthesis

Radziuk

Pye

2001

Diabetes Metabolism Res

Self Cite

227

162

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Hepatic glycogen is replenished during the absorptive period postprandially. This repletion is prompted partly by an increased hepatic uptake of glucose by the liver, partly by metabolite and hormonal signals in the portal vein, and partly by an increased gluconeogenic flux to glycogen (glyconeogenesis). There is some evidence that the direct formation of glycogen from glucose and that formed by gluconeogenic pathways is linked. This includes: (i) the inhibition of all glycogen synthesis, in vivo, when gluconeogenic flux is blocked by inhibitors; (ii) a dual relationship between glucose concentrations, lactate uptake by the liver and glycogen synthesis (by both pathways) which indicates that glucose sets the maximal rates of glycogen synthesis while lactate uptake determines the actual flux rate to glycogen; (iii) the decrease of both gluconeogenesis and glycogen synthesis by the biguanide, metformin; and (iv) correlations between increased gluconeogenesis and liver glycogen in obese patients and animal models. The degree to which the liver extracts portal glucose is not entirely agreed upon although a preponderance of evidence points to about a 5% extraction rate, following meals, which is dependent on a stimulation of glucokinase. This enzyme may be linked to the expression of other enzymes in the gluconeogenic pathway. Perivenous cells in the liver may induce additional gluconeogenesis in the periportal cells by increasing glycolytically produced lactate. A number of potential mechanisms therefore exist which could link glycogen synthesis from glucose and gluconeogenic substrate.

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Tracer methods and the metabolic disposal of a carbohydrate load in man

Cited by 37 publications

References 83 publications

A noninvasive method to measure splanchnic glucose uptake after oral glucose administration.

A noninvasive method to measure splanchnic glucose uptake after oral glucose administration.

Comparison of the time courses of insulin and the portal signal on hepatic glucose and glycogen metabolism in the conscious dog.

Hepatic glucose uptake, gluconeogenesis and the regulation of glycogen synthesis

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