scholarly journals Metabolism of glucose in hyper- and hypo-thyroid rats in vivo. Minor role of endogenous insulin in thyroid-dependent changes in glucose turnover

1979 ◽  
Vol 182 (2) ◽  
pp. 577-584 ◽  
Author(s):  
F Okajima ◽  
M Ui
Keyword(s):  
Blood Glucose ◽  
Glucose Utilization ◽  
Rate Coefficient ◽  
Rate Coefficients ◽  
Glucose Turnover ◽  
Minor Role ◽  
Fed State ◽  
Endogenous Insulin ◽  
Mild Diabetes

1. Rates and rate coefficients of glucose utilization and replacement (glucose turnover) as well as its recycling were determined in rats by using [U-14C]- and [2-3H]-, [3-3H]- or [6-3H]-glucose. 2. In euthyroid rats, the blood concentration of glucose was 1.5 times and its turnover rate was 2 times as high in the fed state as in the starved state; consequently the rate coefficient, a measure of the capacity of rats to utilize blood glucose, was also higher in the former than in the latter. 3. Induction of mild diabetes by streptozotocin exerted little influence on the content and turnover of blood glucose in the starved state, whereas it caused hyperglycaemia and a decrease in the rate coefficient after feeding. 4. Induction of hyperthyroidism caused increases in rates and rate coefficients of glucose turnover to substantially the same extent whether or not the plasma concentration of insulin was lowered by treatment with streptozotocin or injection with anti-insulin serum. 5. It is concluded that thyroid hormones are capable of enhancing glucose turnover in the starved state independently of endogenous insulin, which plays a significant role in increasing glucose utilization in the fed state.

scholarly journals Glucose utilization by skeletal muscles in vivo in experimental hyperthyroidism in the rat

1990 ◽  
Vol 271 (2) ◽  
pp. 421-425 ◽  
Author(s):  
M C Sugden ◽  
Y L Liu ◽  
M J Holness
Keyword(s):  
Skeletal Muscle ◽  
Pyruvate Dehydrogenase ◽  
Skeletal Muscles ◽  
Glucose Utilization ◽  
Lower Proportion ◽  
Glucose Turnover ◽  
Fed State ◽  
Hyperthyroid State ◽  
And Storage

In the fed state, hyperthyroidism increased glucose utilization indices (GUIs) of skeletal muscles containing a lower proportion of oxidative fibres. Glycogen concentrations were unchanged, but active pyruvate dehydrogenase (PDHa) activities were decreased. Hyperthyroidism attenuated the effects of 48 h of starvation to decrease muscle GUI. Glycogen concentrations and PDHa activities after 48 h of starvation were low and similar in euthyroid and hyperthyroid rats. The increase in glucose uptake and phosphorylation relative to oxidation and storage in skeletal muscle induced by hyperthyroidism may contribute to increased glucose re-cycling in the fed hyperthyroid state and to glucose turnover in the starved hyperthyroid state.

GLUT2 and hexokinase control proximodistal gradient of intestinal glucose metabolism in the newborn pig

1997 ◽  
Vol 272 (6) ◽  
pp. G1530-G1539 ◽  
Author(s):  
C. Cherbuy ◽  
B. Darcy-Vrillon ◽  
L. Posho ◽  
P. Vaugelade ◽  
M. T. Morel ◽  
...  
Keyword(s):  
Glucose Metabolism ◽  
Glucose Transporter ◽  
Glucose Utilization ◽  
Specific Effect ◽  
Glucose Consumption ◽  
Utilization Rate ◽  
Glucose Turnover ◽  
Proximal Jejunum ◽  
A Site

We have reported previously that a high glycolytic capacity develops soon after birth in enterocytes isolated from suckling newborn pigs. In the present work, we investigated whether such metabolic changes could affect intestinal glucose utilization in vivo and examined possible variations in glucose metabolism along the small intestine. Glucose utilization by individual tissues was assessed using the 2-deoxyglucose technique. The overall glucose utilization rate was doubled in suckling vs. fasting 2-day-old pigs because of significantly higher rates in all tissues studied, except for the brain. In parallel, enterocytes were isolated from the proximal, medium, or distal jejunoileum of newborn vs. 2-day-old pigs and assessed for their capacity to utilize, transport, and phosphorylate glucose. Intestinal glucose consumption accounted for approximately 15% of glucose turnover rate in suckling vs. 8% in fasting pigs. Moreover, there was a proximal-to-distal gradient of glucose utilization in the intestinal mucosa of suckling pigs. Such a gradient was also evidenced on isolated enterocytes. The stimulation of both hexokinase activity (HK2 isoform) and basolateral glucose transporter (GLUT2), as observed in the proximal jejunum, could account for such a site-specific effect of suckling.

Fetal glucose utilization in response to maternal starvation and acute hyperketonemia

1989 ◽  
Vol 256 (6) ◽  
pp. E699-E703 ◽  
Author(s):  
A. Leturque ◽  
S. Hauguel ◽  
J. P. Revelli ◽  
A. F. Burnol ◽  
J. Kande ◽  
...  
Keyword(s):  
Blood Glucose ◽  
Ketone Body ◽  
Glucose Utilization ◽  
Fetal Liver ◽  
Rat Tissues ◽  
Pregnant Rats ◽  
Hindlimb Muscles ◽  
Decrease Blood Glucose ◽  
Beta Hydroxybutyrate

The effects of maternal hypoglycemia and/or hyperketonemia on glucose utilization by individual fetal rat tissues have been studied in vivo. To decrease blood glucose and to raise fetal blood ketone body concentrations, 19-day pregnant rats were submitted to 48 or 96 h of starvation. To differentiate between the effects of decreased blood glucose and increased ketone body concentrations, fed pregnant rats were infused for 2 h with DL-beta-hydroxybutyrate. After 96 h of maternal starvation, fetal 2-deoxy-D-glucose (2DG) uptake decreased from 13.6 +/- 0.5 to 8.6 +/- 1.15 micrograms.min-1.g-1. This was mainly due to a decrease in 2DG uptake by fetal hindlimb muscles and heart. By contrast, 2DG uptake in fetal liver and brain was not affected by maternal starvation. Acute hyperketonemia in fed pregnant rats induced a 23% decrease in 2DG uptake by the whole fetus mainly as the result of a lowered 2DG uptake in fetal hindlimb muscles. These data suggest that fetal 2DG uptake does not simply depend on lowered blood glucose level during maternal starvation but that other hormonal, cardiovascular, or metabolic adaptations are implicated. In the rat, most of the fetal tissues including brain are protected against maternal hypoglycemia.

scholarly journals Metabolism of glucose in hyper- and hypo-thyroid rats in vivo. Relation of catecholamine actions to thyroid activity in controlling glucose turnover

1979 ◽  
Vol 182 (2) ◽  
pp. 585-592 ◽  
Author(s):  
F Okajima ◽  
M Ui
Keyword(s):  
Hepatic Glucose Production ◽  
Glucose Production ◽  
Rate Coefficients ◽  
Glucose Turnover ◽  
Turnover Rates ◽  
Beta Adrenergic ◽  
Thyroid State ◽  
Adrenergic Antagonist ◽  
6 Hydroxydopamine

1. In euthyroid rats, treatment with reserpine of 6-hydroxydopamine, which deprived neuronal terminals of catecholamines, resulted in increases in rates and rate coefficients for blood glucose turnover in the starved states as determined by decay of [U-14C,6-3H]-glucose. Conversely, the injection of adrenaline or noradrenaline into starved euthyroid rats caused a marked decrease in rate coeeficients for glucose turnover. There was no change in the percentage glucose recycling under these conditions. 2. Adrenaline and noradrenaline caused more pronounced hyperglycaemia in hyperthyroid than in euthyroid rats owing to the greater activation of hepatic glucose production. 3. The increase in glucose turnover characteristics of hyperthyroidism was observed even after treatment with an alpha- or beta-adrenergic antagonist, showing the insignificant role of the balance between alpha- and beta-adrenergic receptors in the thyroid-dependent metabolic changes. 4. Rate coefficients for glucose turnover were not affected by reserpine treatment or catecholamine injections when rats had been rendered hyperthyroid. 5. Thus catecholamines are direct determinants of glucose-turnover rates in the starved state, and depend to some extent on the prevailing thyroid state.

scholarly journals Simplified Brain Slice Glucose Utilization

1996 ◽  
Vol 16 (5) ◽  
pp. 864-880 ◽  
Author(s):  
George C. Newman ◽  
Frank E. Hospod ◽  
Behzad Maghsoudlou ◽  
Clifford S. Patlak
Keyword(s):  
Kinetic Model ◽  
Rate Equation ◽  
Brain Slice ◽  
Glucose Utilization ◽  
Brain Slices ◽  
Rate Coefficients ◽  
Experimental Conditions ◽  
Simplified Method ◽  
Series Of Experiments

Brain slice glucose utilization (SGU) can be measured by methods analogous to those used for in vivo cerebral glucose utilization. In order to make this technique more accessible and applicable to a broad range of experimental conditions, we have derived a simplified operational rate equation and generated the table of apparent rate coefficients necessary to apply the equation under different experimental situations. Calculations of the apparent rate coefficients were based upon an eight-parameter kinetic model combined with Michaelis–Menten theory to account for changes in the rate constants as a function of buffer glucose concentration. The theory was tested with a series of experiments using rat brain slices, [14C]-2-deoxyglucose (2DG) and [14C]-3– O-methylglucose (3OMG). The errors involved in the simplified technique were estimated by a variety of techniques and found to be acceptable over a broad range of conditions. A detailed, practical protocol for the simplified method is presented.

Na and K transport across the cortical and outer medullary collecting tubule of the rabbit: evidence for diffusion across the outer medullary portion

1982 ◽  
Vol 242 (5) ◽  
pp. F514-F520 ◽  
Author(s):  
J. B. Stokes
Keyword(s):  
Rate Coefficient ◽  
Renal Medulla ◽  
Rate Coefficients ◽  
Efflux Rate ◽  
Chemical Gradients ◽  
Na Efflux ◽  
Collecting Tubule ◽  
K Transport ◽  
Cortical Collecting Tubule

The rabbit collecting tubule displays functional axial heterogeneity with respect to Na ion transport. The present experiments compared cortical collecting tubule (CCT) and outer medullary collecting tubule (OMCT) Na and K transport. Na efflux across the CCT was inhibited by ouabain, whereas Na efflux across the OMCT was smaller and unaffected by ouabain. Assessment of the equivalent conductivities of Na and K across the CCT by imposition of a Na-K bi-ionic gradient demonstrated a higher K/Na conductivity across the CCT than would be predicted from their respective limiting equivalent conductivities in water. In contrast, the ratio of their conductivities across OMCT were not different than would be predicted by their ratio in water. The "selective" nature of the Na and K pathways across CCT was confirmed by measuring the tracer efflux rate coefficients. In the amiloride-treated CCT the K/Na rate coefficient ratio was 9.8 +/- 1.5; this ratio across the OMCT was 1.51 +/- 0.10. The latter value is not different from the ratio of the mobilities of these ions in water. The diffusional nature of Na and K transfer across OMCT was confirmed by the demonstration of the concentration-independent Na efflux rate coefficient and the demonstration of appropriate net Na and K transepithelial flows in response to imposition of oppositely directed chemical gradients. Although the permeability of the OMCT is low, the chemical gradients found in vivo might be sufficient to effect some K absorption and Na secretion without completely dissipating the steep gradients generated by the CCT. These transport characteristics might be important in the regulation of Na excretion and K recycling into the renal medulla.

Insulin resistance, but normal basal rates of glucose production in patients with newly diagnosed mild diabetes mellitus

1991 ◽  
Vol 124 (6) ◽  
pp. 637-645 ◽  
Author(s):  
Ole Hother-Nielsen ◽  
Henning Beck-Nielsen
Keyword(s):  
Diabetes Mellitus ◽  
Plasma Glucose ◽  
Glucose Utilization ◽  
Ketone Bodies ◽  
Glucose Production ◽  
Glucose Turnover ◽  
Diabetic Patients ◽  
Newly Diagnosed ◽  
Turnover Rates ◽  
Mild Diabetes

Abstract. Fasting hyperglycemia in Type II (non-insulin-dependent) diabetes has been suggested to be due to hepatic overproduction of glucose and reduced glucose clearance. We studied 22 patients (10 lean and 12 obese) with newly diagnosed mild diabetes mellitus (fasting plasma glucose <15 mmol/l, urine ketone bodies <1 mmol/l), and two age- and weight-matched groups of non-diabetic control subjects. Glucose turnover rates and sensitivity to insulin were determined using adjusted primed-continuous [3-3H]glucose infusion and the hyperinsulinemic euglycemic clamp technique. Insulin-stimulated glucose utilization was reduced in both diabetic groups (lean patients: 313±35 vs 531±22 mg·m−2·min−1, p<0.01;obesepatients:311±28vs453±26mg·m−2·min−1, p<0.01). Basal plasma glucose concentrations decreased 0.43±0.05 mmol/l per h (p<0.01). Glucose production rates were smaller than glucose utilization rates (lean patients: 87±3 vs 94±3 mg·m−2·min−1, p<0.01; obese patients: 79±5 vs 88±5 mg·m−2 ·min−1, p<0.01), were not correlated to basal glucose or insulin concentrations, and were not different from normal (lean controls: 87±4 mg·−2·min−1; obese controls: 80±5 mg·m−2·min−1). These results suggest that the basal state in the diabetic patients is a compensated condition where glucose turnover rates are maintained near normal despite defects in insulin sensitivity.

Effects of medium-chain triglyceride feeding on glucose homeostasis in the newborn rat

1983 ◽  
Vol 244 (4) ◽  
pp. E329-E334 ◽  
Author(s):  
J. P. Pegorier ◽  
A. Leturque ◽  
P. Ferre ◽  
P. Turlan ◽  
J. Girard
Keyword(s):  
Blood Glucose ◽  
Medium Chain Triglyceride ◽  
Glucose Production ◽  
Glucose Turnover ◽  
Blood Levels ◽  
Newborn Rat ◽  
Hepatic Gluconeogenesis ◽  
Peripheral Tissues ◽  
Medium Chain

The mechanism of the profound hypoglycemia that develops in newborn rats during a fast of 16-h beginning at birth has been investigated. This fasting hypoglycemia was completely reversed by giving oral medium-chain fatty acids (MCT). The rise in blood glucose induced by MCT feeding was not secondary to a decreased uptake of glucose by peripheral tissues because [6-3H]glucose turnover rate was increased in MCT-fed neonates. Several lines of evidence strongly suggest that MCT feeding was associated with a stimulation of hepatic gluconeogenesis. 1) The rate of [6-3H]glucose turnover was enhanced after MCT feeding. 2) A fivefold increase in the conversion of labeled lactate into glucose was observed in vivo after MCT feeding. 3) The rise in blood glucose induced by MCT feeding was totally suppressed by an inhibitor of gluconeogenesis (3-mercaptopicolinate). Despite their utilization for glucose synthesis, blood levels of lactate, alanine, and pyruvate were increased two- to threefold after MCT feeding. When MCT feeding was given in association with dichloroacetate, an activator of pyruvate dehydrogenase (PDH), no increase in blood lactate, alanine, and pyruvate was observed and the rise in glycemia was prevented. This suggested that hyperketonemia due to MCT feeding could decrease the oxidation of 3-carbon glucose precursors in peripheral tissues, secondary to an inhibition of PDH, and thus enhanced their release in blood. These data indicate that MCT feeding stimulates glucose production in the newborn rat, both by increasing the availability of gluconeogenic precursors and by a direct effect on hepatic gluconeogenesis.

Pulsatile hyperglucagonemia fails to increase hepatic glucose production in normal man

1987 ◽  
Vol 252 (1) ◽  
pp. E1-E7 ◽  
Author(s):  
G. Paolisso ◽  
A. J. Scheen ◽  
A. S. Luyckx ◽  
P. J. Lefebvre
Keyword(s):  
Blood Glucose ◽  
Hepatic Glucose Production ◽  
Glucose Production ◽  
Glucose Infusion ◽  
Metabolic Effects ◽  
Glucose Turnover ◽  
Continuous Administration ◽  
Hepatic Glucose ◽  
Normal Man

To study the metabolic effects of pulsatile glucagon administration, six male volunteers were submitted to a 260-min glucose-controlled glucose intravenous infusion using the Biostator. The endogenous secretion of the pancreatic hormones was inhibited by somatostatin (100 micrograms X h-1), basal insulin secretion was replaced by a continuous insulin infusion (0.2 mU X kg-1 X min-1), and glucagon was infused intravenously in two conditions at random: either continuously (125 ng X min-1) or intermittently (812.5 ng X min-1, with a switching on/off length of 2/11 min). Blood glucose levels and glucose infusion rate were monitored continuously by the Biostator, and classical methodology using a D-[3-3H]glucose infusion allowed us to study glucose turnover. While basal plasma glucagon levels were similar in both conditions (122 +/- 31 vs. 115 +/- 18 pg X ml-1), they plateaued at 189 +/- 38 pg X ml-1 during continuous infusion and varied between 95 and 501 pg X ml-1 during pulsatile infusion. When compared with continuous administration, pulsatile glucagon infusion initially induced a similar increase in endogenous (hepatic) glucose production and blood glucose, did not prevent the so-called “evanescent” effect of glucagon on blood glucose, and after 3 h tended to reduce rather than increase hepatic glucose production. In conclusion, in vivo pulsatile hyperglucagonemia in normal man fails to increase hepatic glucose production.

scholarly journals Metabolism of glucose in hyper- and hypo-thyroid rats in vivo. Glucose-turnover values and futile-cycle activities obtained with 14C- and 3H-labelled glucose

1979 ◽  
Vol 182 (2) ◽  
pp. 565-575 ◽  
Author(s):  
F Okajima ◽  
M Ui
Keyword(s):  
Blood Glucose ◽  
Specific Radioactivity ◽  
Glucose Production ◽  
Liver Glycogen ◽  
Glucose Turnover ◽  
Futile Cycle ◽  
Futile Cycles ◽  
The Difference ◽  
Glucose Recycling

1. A trace amount of glucose labelled with 14C uniformly and with 3H at position 2, 3 or 6 was injected intravenously into starved rats to measure the turnover rate of blood glucose. 2. Reliable estimates were made based on the semilogarithmic plot of specific radioactivity of the glucose contained in whole blood samples taken from the tail vein. 3. Glucose turned over more rapidly in hyperthyroid and more slowly in hypothyroid than in euthyroid rats. The percentage contribution of glucose recycling (determined from the difference in replacement rates between [U-14C]glucose and [6-3H]glucose) to the glucose utilization increased on induction of hyperthyroidism. 4. Futile cycles between glucose and glucose 6-phosphate (determined from the difference between replacement rates of [2-3H]glucose and [6-3H]glucose) were activated and inactivated by induction of hyperthyroid and hypothyroid states respectively. 5. The hepatic content of glycogen was much lower in hyper- and hypo-thyroid than in euthyroid rats. The enhanced glucose production in hyperthyroid rats resulted from not only activationof hepatic gluconeogenesis but also diversion of the final product of gluconeogenesis from liver glycogen to blood glucose. In hypothyroidism, the inhibition of gluconeogensis led to suppression of both glucose production and glycogenesis in the liver.

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