The realiability of rates of glucose appearance <i>in vivo</i> calculated from constant tracer infusions

Allsop, John R.; Wolfe, Robert R.; Burke, John F.

doi:10.1042/bj1720407

Cited by 76 publications

(20 citation statements)

References 21 publications

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“…The volume of distribution in which rapid changes in glucose concentration and specific activity of (3 -3 H)glucose occur was set to 188 ml/kg body wt. Smoothing of glucose and specific activity values to reduce rapid changing of these variables with respect to time was conducted by an independent researcher using curve fitting by hand [1].…”

Section: Glucose Turnovermentioning

confidence: 99%

Evidence of Hepatic Glucagon Resistance Associated with Hepatic Steatosis: Reversal Effect of Training

Charbonneau

Couturier²,

Gauthier³

et al. 2005

Int J Sports Med

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The present study was undertaken to test the hypothesis that a high-fat diet-induced hepatic steatosis is associated with a reduction in hepatic glucose output (HGO) in response to a hyperglucagonemic infusion, and that this postulated state of hepatic glucagon resistance in high-fat fed rats is attenuated by concurrent exercise training. In four groups of anesthetized rats, glucagon (2 ug/kg/min iv) was infused over a period of 60 min to measure HGO. Two groups of rats were either fed a standard (SD) or a high-fat (HF; 42 % kcal) diet for eight weeks and were assigned either to a Sedentary (Sed) or a treadmill-trained (TR) group. Training was initiated two weeks after the beginning of the diet protocol and was progressively increased over a period of 6 weeks reaching 60 min at 26 m/min, 10 % grade, for the last 3 weeks. The HF compared to the SD diet resulted in approximately 28 % higher (p < 0.01) liver triglyceride levels in Sed rats. This increase was completely prevented by the exercise training program in the HF-TR group. Plasma glucagon ( approximately 90,000 pg/ml) and insulin ( approximately 500 pmol/l) levels were increased to a similar extent in all four groups, with the exception of higher (p<0.05) insulin levels in SD-Sed group. Glucagon induced-hyperglycemia ( approximately 300 mg/dl) was higher (p<0.05) in the SD-Sed than in HF-Sed and SD-TR groups. Glucagon infusion resulted in a significantly (p<0.05) lower increase ( approximately 35 %) in HGO in HF-Sed compared to SD-Sed group. The lower level of HGO in HF-Sed compared to SD-Sed rats was observed whether HGO was measured after 25, 40, or 60 min of glucagon infusion. Exercise training in HF fed rats resulted in a significant (p<0.05) attenuation (50 %) of the state of HF-induced glucagon resistance. Comparisons of all individual liver triglyceride and 60-min HGO values revealed that liver triglyceride values were highly (p<0.001) predictive of the decreased glucagon action on HGO (R= -0.849). The present results indicate that the feeding of a high-fat diet induces a state of hepatic glucagon resistance, which is partially attenuated by concurrent exercise training. It is suggested that liver lipid infiltration may interfere with the action of glucagon, thus inducing glucagon resistance in liver.

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Section: Glucose Turnovermentioning

confidence: 99%

Evidence of Hepatic Glucagon Resistance Associated with Hepatic Steatosis: Reversal Effect of Training

Charbonneau

Couturier²,

Gauthier³

et al. 2005

Int J Sports Med

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“…With this in mind, we questioned whether the diabetic rat, subjected to endotoxin-induced shock would demonstrate the early alterations of glucose metabolism similar to those seen in the non-diabetic rat. We chose to study the kinetics of glucose turnover using radio-tracer techniques (Allsop, Wolfe and Burke 1978), prior to and following administration of a sub-lethal dose of E. coli endotoxin. A significant route of glucose disappearance in the diabetic rat is urinary loss.…”

Section: Introductionmentioning

confidence: 99%

Glucose Metabolism Following Endotoxin Administration in Diabetic Rats

Kelleher¹,

Bagby²,

Spitzer³

1980

Horm Metab Res

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The altered glucose metabolism characteristic of endotoxin-induced shock was studied in diabetic and non-diabetic rats. Endotoxin administration led to an exaggerated hyperglycemia in the diabetic rats. The exaggerated hyperglycemia appeared to be a consequence of an increased hepatic output of glucose, presumably via gluconeogenesis, as evidenced by an exaggerated glucose turnover following endotoxin. Diabetic and non-diabetic rats responded to endotoxin similarly with respect to blood pressure, heart rate, hematocrit, blood pH and plasma lactate. Endotoxin administration did not affect urine flow rate or urinary glucose excretion in either diabetic or non-diabetic rats.

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“…Diabetic Medicine ª 2013 Diabetes UK the total rate of glucose appearance [29]. As extensively discussed in a number of reports [29][30][31][32], the marked nonsteady-state condition of the tracer:tracee ratio that occurs with the dual-tracer method introduces errors and renders the calculation of rate of appearance of ingested glucose, endogenous glucose production and glucose disposal dependent on both the model used in the calculation (e.g. one or two compartments) and its parameters (e.g.…”

Section: Dual Tracer Mixed Meal Testmentioning

confidence: 99%

Assessment of insulin action on carbohydrate metabolism: physiological and non‐physiological methods

et al. 2013

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Carbohydrate metabolism in humans is regulated by insulin secretion from pancreatic β-cells and glucose disposal by insulin-sensitive tissues. Insulin facilitates glucose utilization in peripheral tissues and suppresses hepatic glucose production. Any defects in insulin action predispose an individual to glucose intolerance and Type 2 diabetes mellitus. Early detection of defects in insulin action could provide opportunities to prevent or delay progression of the disease state. There are different approaches to assess insulin action. Initial methods, such as peripheral insulin concentration and simple indices, have several limitations. Subsequently, researchers developed methodologies using intravenous glucose infusion to determine glucose fluxes. However, these methodologies are limited by being non-physiological. Newer, innovative techniques that have been developed are more sophisticated and physiological. By modelling glucose kinetics using isotope dilution techniques, several robust parameters can be obtained that are physiologically relevant and sound. This brief review summarizes most of the non-physiological and physiological methodologies used to measure the variables of insulin action.

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The realiability of rates of glucose appearance in vivo calculated from constant tracer infusions

Cited by 76 publications

References 21 publications

Evidence of Hepatic Glucagon Resistance Associated with Hepatic Steatosis: Reversal Effect of Training

Evidence of Hepatic Glucagon Resistance Associated with Hepatic Steatosis: Reversal Effect of Training

Glucose Metabolism Following Endotoxin Administration in Diabetic Rats

Assessment of insulin action on carbohydrate metabolism: physiological and non‐physiological methods

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