scholarly journals Initial glucose kinetics and hormonal response to a gastric glucose load in unrestrained post-absorptive and starved rats

1990 ◽  
Vol 270 (2) ◽  
pp. 505-510 ◽  
Author(s):  
C Smadja ◽  
J Morin ◽  
P Ferré ◽  
J Girard
Keyword(s):  
Glucose Utilization ◽  
Hepatic Glucose Production ◽  
Lactate Concentration ◽  
Glucose Production ◽  
Utilization Rate ◽  
Glucose Turnover ◽  
Glucose Load ◽  
Peripheral Tissues ◽  
Glucose Ingestion ◽  
Total Glucose

A gastric [U-14C]glucose load (4.8 mg/g body wt.) was delivered to unrestrained post-absorptive or 30 h-starved rats bearing peripheral and portal vein catheters and continuously perfused with [3-3H]glucose, in order to compare their metabolic and hormonal responses. In the basal state, portal and peripheral glycaemia were less in starved rats than in rats in the post-absorptive period (P less than 0.01), whereas blood lactate was similar. Portal insulinaemia (P less than 0.05) and protal glucagonaemia (P less than 0.005) were lower in starved rats, but insulin/glucagon ratio was higher in post-absorptive rats (P less than 0.005). The glucose turnover rate was decreased by starvation (P less than 0.005). After glucose ingestion, blood glucose was similar in post-absorptive and starved rats. A large portoperipheral gradient of lactate appeared in starved rats. Portal insulinaemia reached a peak at 9 min, and was respectively 454 +/- 68 and 740 +/- 65 mu-units/ml in starved and post-absorptive rats. Portal glucagonaemia remained stable, but was higher in post-absorptive rats (P less than 0.05). At 60 min after the gastric glucose load, 30% of the glucose was delivered at the periphery in both groups. The total glucose appearance rate was higher in starved rats (P less than 0.05), as was the glucose utilization rate (P less than 0.05), whereas the rate of appearance of exogenous glucose was similar. This was due to a non-suppressed hepatic glucose production in the starved rats, whereas it was totally suppressed in post-absorptive rats. At 1 h after the glucose load, the increase in both liver and muscle glycogen concentration was greater in starved rats. Thus short-term fasting induces an increased portal lactate concentration after a glucose load, and produces a state of liver insulin unresponsiveness for glucose production, whereas the sensitivity of peripheral tissues for glucose utilization is unchanged or even increased. This might allow preferential replenishment of the peripheral stores of glycogen.

Increased insulin sensitivity and responsiveness during lactation in rats

1986 ◽  
Vol 251 (5) ◽  
pp. E537-E541 ◽  
Author(s):  
A. F. Burnol ◽  
A. Leturque ◽  
P. Ferre ◽  
J. Kande ◽  
J. Girard
Keyword(s):  
Insulin Sensitivity ◽  
Plasma Insulin ◽  
Glucose Utilization ◽  
Glucose Production ◽  
Utilization Rate ◽  
Glucose Turnover ◽  
Metabolic Clearance ◽  
Maximal Effect ◽  
Euglycemic Hyperinsulinemic Clamp ◽  
Peripheral Tissues

In 12-day lactating rats blood glucose and plasma insulin were decreased by, respectively, 20 and 35% when compared with nonlactating rats, despite a 25% increase of their glucose turnover rate. Then, by using the euglycemic hyperinsulinemic clamp technique, dose-response curves for the effects of insulin on glucose production and utilization in lactating and nonlactating rats were performed. Glucose production rate was totally suppressed at 250 microU/ml of insulin in lactating rats and for plasma insulin concentrations higher than 500 microU/ml in nonlactating rats. Plasma insulin level inducing half-maximal inhibition of glucose production was decreased by 60% during lactation. The maximal effect of insulin on glucose utilization rate and glucose metabolic clearance rate was, respectively, increased 1.5- and 2.4-fold during lactation and was obtained for plasma insulin concentrations lower in lactating than in nonlactating rats (250 vs. 500 microU/ml). Insulin concentrations inducing half-maximal stimulation of glucose utilization and glucose metabolic clearance were decreased by 50% during lactation. In conclusion, this study has shown that insulin sensitivity and responsiveness of liver and peripheral tissues are improved at peak lactation in the rat.

scholarly journals Absorption and metabolism of glucose by the mesenteric-drained viscera of sheep fed on dried-grass or ground, maize-based diets

1985 ◽  
Vol 54 (2) ◽  
pp. 449-458 ◽  
Author(s):  
A. N. Janes ◽  
T. E. C. Weekes ◽  
D. G. Armstrong
Keyword(s):  
Small Intestine ◽  
Turnover Rate ◽  
Glucose Utilization ◽  
Venous Blood ◽  
Glucose Production ◽  
Glucose Absorption ◽  
Endogenous Glucose Production ◽  
Whole Body ◽  
Glucose Turnover ◽  
Total Glucose

1. Sheep fitted with re-entrant canulas in the proximal duodenum and terminal ileum were used to determine the amount of α-glucoside entering, and apparently disappearing from, the small intestine when either dried-grass or ground maize-based diets were fed. The fate of any α-glucoside entering the small intestine was studied by comparing the net disappearance of such a-glucoside from the small intestine with the absorption of glucose into the mesenteric venous blood.2. Glucose absorption from the small intestine was measured in sheep equipped with catheters in the mesenteric vein and carotid artery. A continuous infusion of [6-3H]glucose was used to determine glucose utilization by the mesenteric-drained viscera and the whole-body glucose turnover rate (GTR).3. The amounts of α-glucoside entering the small intestine when the dried-grass and maize-based diets were given were 13.9 (SE 1.5) and 95.4 (SE 16.2) g/24 h respectively; apparent digestibilities of such α-glucoside in the small intestine were 60 and 90% respectively.4. The net absorption of glucose into the mesenteric venous blood was —2.03 (SE 1.20) and 19.28 (SE 0.75) mmol/h for the dried-grass and maize-based diets respectively. Similarly, total glucose absorption amounted to 1.52 (SE 1.35) and 23.33 (SE 1.86) mmol/h (equivalent to 7 and 101 g/24 h respectively). These values represented 83 and 11 1% of the a-glucoside apparently disappearing from the small intestine, determined using the re-entrant cannulated sheep.5. Total glucose absorption represented 8 and 61% of the whole-body GTR for the dried-grass and maize-based diets respectively. Endogenous glucose production was significantly lower when the sheep were fed on the maize-based diet compared with the dried-grass diet.6. The mesenteric-drained viscera metabolized a small amount of glucose, equivalent to 234 and 17% of the total glucose absorbed for the dried-grass and maize-based diets respectively.7. It is concluded that a large proportion of the starch entering the small intestine of sheep given a maize-based diet is digested and absorbed as glucose, and thus contributes to the whole-body GTR.

Effects of norepinephrine infusion on in vivo insulin sensitivity and responsiveness

1990 ◽  
Vol 259 (2) ◽  
pp. E210-E215 ◽  
Author(s):  
J. R. Lupien ◽  
M. F. Hirshman ◽  
E. S. Horton
Keyword(s):  
Insulin Sensitivity ◽  
Hepatic Glucose Production ◽  
Glucose Production ◽  
Glucose Disposal ◽  
Glucose Turnover ◽  
Adrenergic Blockade ◽  
Sprague Dawley ◽  
Euglycemic Hyperinsulinemic Clamp ◽  
Peripheral Tissues

The effect of a continuous infusion of norepinephrine (NE) on glucose disposal in vivo was examined in conscious restrained rats using the euglycemic-hyperinsulinemic clamp technique. NE, 1,000 micrograms.kg-1.day-1 (130 nmol.kg-1.h-1) or vehicle (CO) was infused for 10 days in adult male Sprague-Dawley rats using subcutaneously implanted osmotic minipumps. Body weight and food intake were similar in both groups of animals throughout the study. Fasting basal plasma glucose and insulin concentrations were similar in both groups. However, basal hepatic glucose production (HGP) was increased by NE treatment (9.03 +/- 0.63 vs. 13.20 +/- 1.15 mg.kg-1.min-1, P less than 0.05, CO vs. NE, respectively). Insulin infusions of 2, 6, and 200 mU.kg-1.min-1 suppressed HGP to the same degree in both groups. During 2, 6, and 200 mU.kg-1.h-1 insulin infusions the glucose disposal rate was 65, 60, and 13% greater in NE-treated animals than in controls. Acute beta-adrenergic blockade with propranolol infused at 405 nmol.kg-1.h-1 during the glucose clamps did not normalize glucose disposal. These results demonstrate that chronic NE infusion is associated with increased basal glucose turnover and increased insulin sensitivity of peripheral tissues.

Insulin resistance in the GK rat: decreased receptor number but normal kinase activity in liver

1993 ◽  
Vol 265 (5) ◽  
pp. E807-E813 ◽  
Author(s):  
S. Bisbis ◽  
D. Bailbe ◽  
M. A. Tormo ◽  
F. Picarel-Blanchot ◽  
M. Derouet ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Glucose Utilization ◽  
Hepatic Glucose Production ◽  
Glucose Production ◽  
Gk Rat ◽  
Peripheral Tissues ◽  
Relative Index ◽  
Gk Rats ◽  
Euglycemic Clamp

We have previously shown that the glucose intolerance and the hyperglycemic state in the GK rat, a new spontaneous model of non-insulin-dependent (type II) diabetes without obesity, are partly accounted for by an alteration of the pancreatic B cell response. On the other hand, the hyperglycemic-hyperinsulinemic pattern in these rats suggests a decrease of response to insulin in the basal state. In the present study, in vivo insulin action was assessed in 8-wk-old GK females at basal and submaximal (euglycemic clamp) insulin levels. Overall glucose utilization (OGU), individual tissue glucose utilization (ITGU, in vivo uptake of the glucose analogue 2-deoxy-D-glucose as the relative index of glucose metabolism), as well as hepatic glucose production (GP) and liver insulin receptor properties were determined under these two conditions. The basal OGU was significantly higher in the GK females, compared with that in control Wistar females. The hyperinsulinemic-euglycemic clamp experiments indicated that peripheral insulin resistance was installed at 8 wk of age in the GK females because 1) OGU was significantly lower and 2) in some peripheral tissues (epitrochlearis muscle, periovarian, and inguinal white adipose tissues), but not all, ITGU was significantly lower compared with corresponding ITGU in control rats. In the basal state GP was significantly higher in the GK rats. At submaximal hyperinsulinemia (and euglycemia), it was less effectively suppressed than in the controls, thus demonstrating liver insulin resistance. Under both basal state and clamp condition, binding of 125I-A14-insulin to liver membranes of GK rats was significantly decreased by 20-30%.(ABSTRACT TRUNCATED AT 250 WORDS)

Glucose utilization and insulin action in adult rats submitted to prolonged food restriction

1992 ◽  
Vol 263 (1) ◽  
pp. E1-E7 ◽  
Author(s):  
F. Escriva ◽  
C. Rodriguez ◽  
J. Cacho ◽  
C. Alvarez ◽  
B. Portha ◽  
...  
Keyword(s):  
Glucose Tolerance ◽  
Insulin Action ◽  
Food Restriction ◽  
Glucose Utilization ◽  
Glucose Production ◽  
Whole Body ◽  
Glucose Turnover ◽  
Euglycemic Hyperinsulinemic Clamp ◽  
Adult Rats ◽  
Peripheral Tissues

Glucose tolerance and insulin effects on glucose production and utilization by various tissues were studied in 70-day-old anesthetized rats submitted to food restriction from the fetal stage. Basal and glucose-induced plasma insulin levels were reduced in food-restricted rats without alterations in glucose tolerance. Insulin action was quantified by using the euglycemic-hyperinsulinemic clamp technique. Glucose turnover rates were measured by using D-[6-3H]glucose. Exogenous insulin failed to decrease glucose production in food-restricted rats. Weight-related whole body glucose utilization was higher in restricted rats than in controls both in the basal (21.9 +/- 0.7 vs. 9.4 +/- 0.6 mg.min-1.kg-1) and hyperinsulinemic states (37.5 +/- 1.1 vs. 14.0 +/- 1.2 mg.min-1.kg-1). Local glucose utilization by peripheral tissues was estimated by a 2-deoxy-D-[1-3H]glucose technique. In both basal and hyperinsulinemic conditions glucose utilization was increased in various adipose and muscle tissues of the food-restricted rats as compared with the controls. Thus we conclude that food restriction leads to an increase in the insulin-mediated glucose uptake by various peripheral tissues and to insulin resistance in the liver.

Effect of charge on hepatic specific nature of vesicle encapsulated insulin in conscious dogs

1986 ◽  
Vol 251 (5) ◽  
pp. E591-E596 ◽  
Author(s):  
R. S. Spangler ◽  
K. C. Triebwasser ◽  
M. L. Wilson
Keyword(s):  
Glucose Utilization ◽  
Hepatic Glucose Production ◽  
Glucose Production ◽  
Conscious Dogs ◽  
Therapeutic Window ◽  
Specific Nature ◽  
Comparable Amount ◽  
Peripheral Tissues ◽  
Hepatic Glucose ◽  
Dose Levels

Positively [(+)-VEI] and negatively [(-)-VEI] charged formulations of vesicle encapsulated insulin (VEI) were compared with insulin on the basis of their ability to suppress hepatic glucose production (hepatic Ra) and stimulate glucose utilization (Rd) in conscious dogs. Our results indicate that (-)-VEI and insulin have an equivalent capacity to suppress hepatic glucose production at dose levels of 0.2, 1.2, and 2.4 mU X kg-1 X min-1. (+)-VEI is less effective at suppressing hepatic Ra than both insulin and (-)-VEI at dose levels of 1.2 and 2.4 mU X kg-1 X min-1. Both (+)-VEI and (-)-VEI induced significantly less glucose utilization than a comparable amount of insulin at dose levels of 1.2 and 2.4 mU X kg-1 X min-1. The amount of glucose utilization stimulated by (+)-VEI was significantly less than that induced by insulin at 0.6 mU X kg-1 X min-1. This difference was not evident with (-)-VEI. These results suggest that the insulin contained in (+)-VEI is less bioavailable than that contained in (-)-VEI. This difference in bioavailability is believed to be the result of greater serum stability of (+)-VEI vesicles when compared with that of (-)-VEI. In conclusion, both (+)-VEI and (-)-VEI have the capacity to shield encapsulated insulin from interacting with peripheral tissues and deliver insulin selectively to the liver. Both formulations afford one an opportunity to expand the therapeutic window for hepatically active compounds where their utility is limited by systemic toxicity.

scholarly journals Development of insulin-sensitivity at weaning in the rat. Role of the nutritional transition

1988 ◽  
Vol 251 (3) ◽  
pp. 685-690 ◽  
Author(s):  
T Issad ◽  
C Coupé ◽  
M Pastor-Anglada ◽  
P Ferré ◽  
J Girard
Keyword(s):  
Insulin Resistance ◽  
Insulin Sensitivity ◽  
Clearance Rate ◽  
Glucose Utilization ◽  
Hepatic Glucose Production ◽  
Glucose Production ◽  
Glucose Turnover ◽  
Turnover Rates ◽  
Suckling Rats ◽  
Glucose Clearance

This study was undertaken to determine the factors involved in the development of insulin-sensitivity at weaning. Glucose kinetics were studied in suckling rats and in rats weaned on to a high-carbohydrate (HC) or a high-fat (HF) diet, in the basal state and during euglycaemic-hyperinsulinaemic-clamp studies. These studies were coupled with the 2-deoxyglucose technique, allowing a measure of glucose utilization by individual tissues. In the basal state, the glycaemia was higher in HF-weaned rats (124 +/- 4 mg/dl) than in suckling (109 +/- 1 mg/dl) and HC-weaned rats (101 +/- 3 mg/dl). Glucose turnover rates were similar in the three groups of animals (14 mg/min per kg). Nevertheless, basal metabolic glucose clearance rate was 20% lower in HF-weaned rats than in the other groups. During the euglycaemic-hyperinsulinaemic experiments, hepatic glucose production was suppressed by 90% in HC-weaned rats, whereas it remained at 40% of basal value in suckling and HF-weaned rats, indicating an insulin resistance of liver of these animals. Glucose clearance rate during the clamp was 18.3 +/- 0.9 ml/min per kg in suckling rats, whereas it was 35.3 +/- 1.2 ml/min per kg in HC-weaned rats and 27.8 +/- 1.1 ml/min per kg in HF-weaned rats, indicating an insulin resistance of glucose utilization in suckling, and to a lower extent, in HF-weaned rats. The deoxyglucose technique showed that peripheral insulin resistance was localized in muscles and white adipose tissue of suckling and HF-weaned rats. These results indicate that the switch from milk to a HC diet is an important determinant of the development of insulin-sensitivity at weaning in the rat.

Absorption and disposition of a glucose load in the conscious dog

1982 ◽  
Vol 242 (6) ◽  
pp. E398-E406 ◽  
Author(s):  
N. N. Abumrad ◽  
A. D. Cherrington ◽  
P. E. Williams ◽  
W. W. Lacy ◽  
D. Rabin
Keyword(s):  
Hepatic Glucose Production ◽  
Control Period ◽  
Glucose Production ◽  
Glucose Disposal ◽  
Glucose Load ◽  
Insulin Levels ◽  
Glucose Ingestion ◽  
Hepatic Glucose ◽  
Glucose Output ◽  
Arterial Glucose

The quantitative disposition of an intragastrically administered glucose load was studied in eight conscious 18-h fasted dogs using isotopic and arteriovenous (A-V) techniques. During the control period, the gut utilized 25% of the basal net hepatic glucose output (2.8 +/- 0.2 mg.kg-1.min-1). After glucose ingestion, 80% of the load was absorbed as glucose, 11% was converted across the gut to lactate and alanine, and 4% was oxidized to CO2. Two percent of the load remained in the gut 4 h after glucose administration and 3% was unaccounted for. During the absorptive period, net hepatic glucose balance (NHGB) varied considerably (mean range = output of 1.8 to uptake of 9.1 mg.kg-1.min-1), while endogenous hepatic glucose production (Ra hp) showed a consistent 80% suppression. The total net hepatic glucose uptake during the absorptive period (150 +/- 10 min) accounted for the disposal of 24 +/- 10% of the ingested load, and the amount of glucose escaping the splanchnic bed was 40 +/- 3%. Overall NHGB correlated positively with basal arterial glucose and insulin levels and negatively with basal arterial glycerol and FFA and with peak absorptive arterial glucose and insulin levels. These data suggest that the hepatic response to an ingested glucose load depends in part on the degree of metabolic fast of the animal at the time of glucose ingestion; the latter may be a major determinant of the roles played by the tissues in glucose disposal.

Metabolic fate of a gastric glucose load in unrestrained rats bearing a portal vein catheter

1988 ◽  
Vol 254 (4) ◽  
pp. E407-E413 ◽  
Author(s):  
C. Smadja ◽  
J. Morin ◽  
P. Ferre ◽  
J. Girard
Keyword(s):  
Portal Vein ◽  
Body Weight Gain ◽  
Hepatic Glucose Production ◽  
Glycogen Synthesis ◽  
Glucose Production ◽  
Liver Glycogen ◽  
Glucose Turnover ◽  
Blood Flows ◽  
Vein Catheter ◽  
Glucose Ingestion

Metabolic and hormonal responses to the administration of a gastric load of glucose (2.4 mg/g body wt) were evaluated after a fast of 6-7 h in unrestrained rats bearing a portal vein catheter. For the purpose of this study, we have designed a new technique for a direct catheterization of the portal vein that allows serial blood sampling in unrestrained Wistar rats. On the 6th postoperative day, food intake, body weight gain, liver function, histology of the liver, pancreas, intestine, and splanchnic blood flows were similar to those of sham-operated control rats. In the basal state glucose turnover was 21.3 +/- 0.9 mg.kg-1.min-1. After glucose ingestion, a portoperipheral gradient of lactate was present, reflecting the production of lactate by the intestine. Insulin secretion was biphasic and peaked at 12 min (344 +/- 46 microU/ml), whereas portal glucagonemia (400-500 pg/ml) remained unchanged. Sixty minutes after gastric glucose administration, 50% of the load was delivered at the periphery, and glucose utilization was increased by 100%. Hepatic glucose production decreased after 20 min and was inhibited by 30% at 60 min. Liver glycogen concentration remained unchanged during the experiment despite a normal capacity for glycogen synthesis.

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