Glucose turnover values in the dog obtained with various species of labeled glucose

Altszuler, N.; Barkai, Amiram I.; Bjerknes, C. A.; Gottlieb, B.; Steele, R.

doi:10.1152/ajplegacy.1975.229.6.1662

Cited by 139 publications

(62 citation statements)

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“…Endogenous glucose production was determined with an isotope dilution method [9] using D-[3JH]-glucose as a tracer because tritium in position three of the glucose molecule is lost to water in the glycolytic pathway and cannot be reincorporated into glucose [10]. D-[3-3H]-glucose is thus considered to be an irreversible tracer.…”

Section: Methodsmentioning

confidence: 99%

Evidence for an insulin resistance in the adult offspring of pregnant streptozotocin-diabetic rats

1991

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Summary.Our previous work has suggested the presence of an insulin resistance in the adult offspring of streptozotocindiabetic pregnant rats. In this study we used the euglycaemic hyperinsulinaemic clamp technique with an isotope-dilution method to define and quantify this postulated insulin resistance in adult offspring of streptozotocin-diabetic rats. Under basal conditions, these rats had a lower body weight than control rats, but their glucose and insulin concentrations were normal. During the hyperinsulinaemic clamp, the steady-state glucose infusion rate was significantly lower in the offspring of streptozotocin-diabetic rats than in both ageand weight-matched controls, indicating insulin resistance. Basal peripheral tissue glucose utilization was normal in the offspring of streptozotocin-diabetic rats, but the dose-response curve was shifted to the right: insulin concentrations causing half-maximal stimulation of glucose utilization were increased by about 60% in the offspring of diabetic rats; the maximal stimulation of glucose utilization, however, was unaltered. Basal hepatic glucose production was normal, but again, half-maximal suppression of glucose production occurred at insulin concentrations 50% higher than in controt rats; in addition, the maximal suppression of glucose production was significantly decreased, even at insulin concentrations of 5700 btU/ml. These data are evidence for an insulin resistance in the adult offspring of streptozotocin-diabetic rats, characterized by: (1) a decreased insulin sensitivity by peripheral glucose-utilizing tissues, and, (2) a decreased sensitivity and responsiveness of the liver. Key words:Insulin resistance, euglycaemic hyperinsulinaemic clamp, offspring of streptozotocin-diabetic rats.Metabolic changes in the pregnant streptozotocindiabetic rat have been shown to affect fetal development and fetal glucose homeostasis [1, 21. A severe hyperglycaemia ( > 20 mmol/1) in the maternal rat results in hyperglycaemia and hypoinsulinaemia of their fetuses. On histology and electronmicroscopy, we found evidence of islet hypertrophy, Beta-cell hyperplasia and Beta-cell degranulation in these fetuses: a 'Beta-cell exhaustion phenomenon' is probably the cause of decreased insulin levels in fetal serum [1,2]. Malnutrition of the newborn rats by their mothers, causes frequent postnatal death and subnormal glucose and insulin levels in the survivors until weaning [1,3]. Body weight in the offspring of severely hyperglycaemic rats is significantly lower than normal from day 20 of gestation and it remains significantly lower during postnatal life: during the lactation period and after weaning [1][2][3]. The adult offspring of severely hyperglycaemic pregnant rats (SDF-rats) have a normal pancreas on histology and normal serum glucose and insulin concentrations in basal conditions, but their glucose tolerance is clearly impaired [3,4]. Data from an in vivo 123I-insulin captation study would suggest an insulin resistance in SDF-rats [5]. In this study, we used the euglycaemic ...

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Section: Methodsmentioning

confidence: 99%

Evidence for an insulin resistance in the adult offspring of pregnant streptozotocin-diabetic rats

1991

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“…Informed consent was obtained from 8 normal subjects (2 men, 6 women) yr of age (mean, 27 yr) with no family history of diabetes and also from 13 juvenile onset-type diabetic subjects (3 men, 10 women) 18-55 yr of age (mean, 29 yr) with documented histories of ketoacidosis. All subjects were in apparent good health at the time of the study and within 15% of their ideal body weight (Metropolitan Life Insurance Co. Tables, 1959).…”

Section: Methodsmentioning

confidence: 99%

“…Glucose clearance (MCR) was calculated by dividing Rd by the simultaneous plasma glucose level. The validity of free insulin determinations (25), the formula for calculating Ra and Rd (26), and the use of [3-3H]-glucose as a nonrecycling tracer to estimate glucose turnover (27) have all been previously discussed in detail. Data in text and figures are given as mean+SEM.…”

Section: Methodsmentioning

confidence: 99%

Effect of Intermittent Endogenous Hyperglucagonemia on Glucose Homeostasis in Normal and Diabetic Man

Rizza¹,

Verdonk²,

Miles³

et al. 1979

J. Clin. Invest.

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A B S T R A C T Infusion of glucagon causes only a transient increase in glucose production in normial and diabetic man. To assess the effect ofintermittent endogenous hyperglucagonemia that might more closely reflect physiologic conditions, arginine (10 g over 30 min) was infused four times to 8 normal subjects and 13 insulin-dependent diabetic subjects (4 of whom were infused concomitantly with somatostatin to examine effects ofarginine during prevention ofhyperglucagonemia). Each arginine infusion was separated by 60 min. Diabetic subjects were infused throughout the experiments with insulin at rates (0.07-0.48 mU/kg per min) that had normalized base-line plasma glucose and rates of glucose appearance (Ra) and disappearance (Rd). Basal plasma glucagon and arginine-induced hyperglucagonemia were similar in both groups; basal serum insulin in the diabetics (16+1 ,U/ml, P < 0.05) exceeded those ofthe normal subjects (10+ 1 ,U/ml,P < 0.05) but did not increase with arginine. Serum insulin in normal subjects increased 15-20,U/ml with each arginine infusion. In both groups each arginine inifusion increased plasma glucose and Ra. Increments ofRa in the diabetics exceeded those of normal subjects, (P < 0.02); Rd was similar in both groups. In normal subjects, plasma glucose returned to basal levels after each arginine infusion, whereas in the diabetics hyperglycemia persisted reaching 151 + 15 mg/dl after the last arginine infusion. When glucagon responses were prevented by somatostatin, arginine infusions did not alter plasma glucose or Ra.

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“…Blood samples for determination of plasma insulin, C-peptide, and FFA concentrations were drawn at 1 5-min intervals throughout the study. (33). Plasma insulin and C-peptide concentrations were measured by specific radioimmunoassays (34,35), urinary nitrogen excretion by the method of Kjeldahl (36), and plasma FFA concentrations by the microfluorometric method of Miles et al (37).…”

Section: Experimental Protocolmentioning

confidence: 99%

Glucose and free fatty acid metabolism in non-insulin-dependent diabetes mellitus. Evidence for multiple sites of insulin resistance.

Groop¹,

Bonadonna²,

DelPrato³

et al. 1989

J. Clin. Invest.

767

548

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Glucose turnover values in the dog obtained with various species of labeled glucose

Cited by 139 publications

References 0 publications

Evidence for an insulin resistance in the adult offspring of pregnant streptozotocin-diabetic rats

Evidence for an insulin resistance in the adult offspring of pregnant streptozotocin-diabetic rats

Effect of Intermittent Endogenous Hyperglucagonemia on Glucose Homeostasis in Normal and Diabetic Man

Glucose and free fatty acid metabolism in non-insulin-dependent diabetes mellitus. Evidence for multiple sites of insulin resistance.

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