INSULIN AND GLUCOSE METABOLISM IN SHEEP FED DRIED GRASS OR GROUND MAIZE-BASED DIETS

1984 ◽  
Vol 64 (5) ◽  
pp. 298-299 ◽  
Author(s):  
A. N. JANES ◽  
T. E. C. WEEKES ◽  
D. G. ARMSTRONG
Keyword(s):  
Glucose Metabolism ◽  
Key Words ◽  
Plasma Insulin ◽  
Glucose Utilization ◽  
Insulin Concentration ◽  
Plasma Insulin Concentration ◽  
Key Words Insulin ◽  
Basal Plasma ◽  
Dietary Starch

Feeding a maize-based compared with a dried grass diet increased rates of glucose utilization in sheep, with no effect on the basal plasma insulin concentration or on the sensitivity or responsiveness to insulin. The increased utilization of glucose appeared to be non-insulin-mediated. Key words: Insulin, glucose, sheep, dietary starch

Dose-response characteristics for effects of insulin on production and utilization of glucose in man

1981 ◽  
Vol 240 (6) ◽  
pp. E630-E639 ◽  
Author(s):  
R. A. Rizza ◽  
L. J. Mandarino ◽  
J. E. Gerich
Keyword(s):  
Glucose Metabolism ◽  
Insulin Receptor ◽  
Dose Response ◽  
Plasma Insulin ◽  
Glucose Utilization ◽  
Glucose Production ◽  
Receptor Occupancy ◽  
Insulin Concentration ◽  
Plasma Insulin Concentration ◽  
Response Characteristics

To determine the dose-response characteristics for the effects of insulin on glucose production, glucose utilization, and overall glucose metabolism in normal man, 15 healthy subjects were infused with insulin for 8 h at sequential rates ranging from 0.2 to 5.0 mU.kg-1.min-1; each rate was used for 2 h. Glucose production and utilization were measured isotopically ([3-3H]glucose). Tissue insulin receptor occupancy was estimated from erythrocyte insulin binding. Glucose production was completely suppressed at plasma insulin concentrations of approximately 60 microunits/ml. Maximal glucose utilization (10–11 mg.kg-1.min-1) occurred at insulin concentrations of 200–700 microunits/ml. The concentration of insulin causing half-maximal glucose utilization (55 + 7 microunits/ml) was significantly greater than that required for half-maximal suppression of glucose production (29 +/- 2 microunits/ml, P less than 0.01). Maximal effects of insulin on glucose production and utilization occurred at plasma insulin concentrations causing 11 and 49% insulin receptor occupancy, respectively. The above dose-response relationships indicate that in man 1) glucose production is more sensitive to changes in plasma insulin concentration than is glucose utilization; 2) both hepatic and peripheral tissues may contain “spare” insulin receptors; and 3) relatively minor changes in plasma insulin concentration or insulin receptor function can cause appreciable alterations in glucose metabolism.

Glucose intolerance following chronic metabolic acidosis in man.

1979 ◽  
Vol 236 (4) ◽  
pp. E328 ◽  
Author(s):  
R A DeFronzo ◽  
A D Beckles
Keyword(s):  
Metabolic Acidosis ◽  
Glucose Metabolism ◽  
Plasma Glucose ◽  
Glucose Concentration ◽  
Plasma Insulin ◽  
Glucose Infusion ◽  
Insulin Concentration ◽  
Plasma Insulin Concentration ◽  
Chronic Metabolic Acidosis ◽  
Tissue Sensitivity

The effect of chronic metabolic acidosis (0.1 g/(kg . day) X 3 days) on carbohydrate metabolism was examined with the glucose-clamp technique in 16 healthy volunteers. Hyperglycemic clamp. Plasma glucose concentration is acutely raised and maintained 125 mg/dl above the basal level. Because the glucose concentration is held constant, the glucose infusion rate is an index of glucose metabolism (M). Following NH4Cl, M decreased from 8.95 +/- 1.12 to 7.35 +/- 0.76 (P less than 0.05) despite an increased plasma insulin concentration (I) 23 +/- 9%, P less than 0.05). Consequently the M/I ratio, an index of tissue sensitivity to insulin, decreased by 32 +/- 5% (P less than 0.005). Euglycemic clamp. Plasma insulin concentration is acutely raised and maintained 101 +/- 3 microU/ml above basal and plasma glucose is held constant at the fasting level by a variable glucose infusion (M). Following NH4Cl both M and M/I decreased by 15 +/- 4% (P = 0.005) and 15 +/- 5% (P = 0.01), respectively. Metabolic acidosis had no effect on basal [3-3H]glucose production or the percent of decline (91 +/- 4%) following hyperinsulinemia. Both hyperglycemic and euglycemic clamp studies indicate that impaired glucose metabolism following metabolic acidosis results from impaired tissue sensitivity to insulin.

Sodium-lithium countertransport and platelet cytosolic free calcium concentration in relation to peripheral insulin sensitivity in postmenopausal women

1992 ◽  
Vol 83 (3) ◽  
pp. 319-324 ◽  
Author(s):  
Ingrid Mattiasson ◽  
Kerstin Berntorp ◽  
Folke Lindgärde
Keyword(s):  
Blood Pressure ◽  
Body Mass Index ◽  
Glucose Tolerance ◽  
Plasma Insulin ◽  
Normal Glucose Tolerance ◽  
Insulin Concentration ◽  
Glucose Disposal ◽  
Plasma Insulin Concentration ◽  
Normal Glucose ◽  
Basal Plasma

1. Peripheral glucose disposal (assessed by the euglycaemic-hyperinsulinaemic clamp technique), Na+-Li+ countertransport in erythrocytes and the cytosolic free Ca2+ concentration in platelets were determined in 41 women with impaired glucose tolerance and in 38 women with normal glucose tolerance. The groups were matched for body mass index (range 18–44 kg/m2) and diastolic blood pressure (range 58–109 mmHg). 2. Na+-Li+ countertransport was correlated significantly with body mass index, basal plasma insulin concentration and basal plasma glucose concentration, and was inversely correlated with peripheral glucose disposal rate. Stepwise regression analysis showed that Na+-Li+ countertransport was positively correlated with basal plasma insulin concentration (r2 = 8.7%). 3. Systolic blood pressure was correlated with fasting plasma insulin concentration (model r2 = 25%) and with Na+-Li+ countertransport (model r2 = 34%) in the group with impaired glucose tolerance. In the group with normal glucose tolerance there were no correlations between blood pressure and Na+-Li+ countertransport. 4. No correlation was found between platelet cytosolic free Ca2+ concentration and any of the variables measured. 5. It is concluded that Na+-Li+ countertransport is correlated with the degree of peripheral insulin sensitivity and with the plasma insulin concentration. Platelet cytosolic free Ca2+ concentration was not correlated with any of these variables, and there was no relationship between Na+-Li+ countertransport and the platelet cytosolic free Ca2+ concentration.

INHIBITORY EFFECT OF SOMATOSTATIN ON INSULIN SECRETION DURING α-ADRENERGIC BLOCKADE IN THREE DIFFERENT SPECIES

1979 ◽  
Vol 92 (1) ◽  
pp. 166-173 ◽  
Author(s):  
Johannes Järhult ◽  
Bo Ahrén ◽  
Ingmar Lundquist
Keyword(s):  
Insulin Secretion ◽  
B Cell ◽  
Insulin Release ◽  
Plasma Insulin ◽  
Inhibitory Effect ◽  
Insulin Concentration ◽  
Adrenergic Blockade ◽  
Plasma Insulin Concentration ◽  
Basal Plasma ◽  
Stimulation Of

ABSTRACT It has recently been suggested from experiments in dogs that somatostatin suppresses insulin release via a stimulation of the inhibitory α-adrenoceptors of the pancreatic B-cell. The effect of somatostatin on insulin secretion during α-adrenergic blockade with phentolamine was therefore studied in three different species; the rat, the cat and the mouse. It was found that somatostatin significantly depressed insulin release during α-adrenoceptor blockade in all three species. In the rat, infusion of somatostatin at a dose of 0.3 μg/kg/min decreased basal plasma insulin concentration by 92 %. In the presence of phentolamine, the same dose of somatostatin lowered plasma insulin by 85 %. In the cat, a similar infusion of somatostatin lowered basal plasma insulin concentration by 87 %, but its depressive effect during α-adrenergic blockade was comparatively less pronounced (68 %) than in the rat. In the mouse, a single iv injection of somatostatin induced a short-lasting depression of plasma insulin concentration during α-adrenergic blockade. From these results it seems unlikely that somatostatin should inhibit insulin release simply by stimulation of α-adrenoceptors on the B-cell. It cannot be ruled out, however, that a more complex interaction exists between somatostatin and the sympatho-adrenal system with regard to the control of insulin secretion.

The parasympathetic nervous system and glucocorticoid-mediated hyperinsulinaemia in the genetically obese (fa/fa) Zucker rat

1988 ◽  
Vol 118 (1) ◽  
pp. 87-92 ◽  
Author(s):  
J. M. Fletcher ◽  
N. McKenzie
Keyword(s):  
Nervous System ◽  
Plasma Glucose ◽  
Plasma Insulin ◽  
Parasympathetic Nervous System ◽  
Insulin Concentration ◽  
Zucker Rats ◽  
Glucose Load ◽  
Plasma Insulin Concentration ◽  
Obese Rats ◽  
Basal Plasma

ABSTRACT Lean (Fa/-) and genetically obese (fa/fa) Zucker rats were adrenalectomized at 18 days of age (3 days before weaning) before the onset of hyperinsulinaemia. At 40–41 days of age, basal and glucose-stimulated insulin concentrations did not differ significantly between lean and obese rats. Plasma insulin and glucose concentrations were higher in both phenotypes 24 h after administration of corticosterone (2·0 mg at 12-h intervals). Corticosterone-treated obese rats had higher basal and glucose-stimulated insulin levels than similarly treated lean animals, although plasma glucose concentrations did not differ between phenotypes. The basal plasma insulin concentration of obese rats treated with corticosterone for 24 h was reduced 15, 30 and 45 min after injection of atropine (0·3 mg) without any significant change in the plasma glucose level. Injection of atropine (0·3 mg) 20 min before a glucose load prevented the greater increment in plasma insulin concentration of corticosterone-treated obese rats compared with similarly treated lean animals. Atropine administration (0·3 mg) to intact obese rats at 40 days of age reduced, but did not abolish, their hyperinsulinaemia compared with intact lean animals. It is concluded that (1) pre-weaning adrenalectomy prevents the development of hyperinsulinaemia in genetically obese rats, (2) corticosterone replacement for only 24 h restores the hyperinsulinaemia of obese rats, (3) the differential effects of corticosterone on insulin secretion by lean and obese rats are mediated by the parasympathetic nervous system and (4) the parasympathetic nervous system contributes to, but is not the only cause of, hyperinsulinaemia in intact obese rats. J. Endocr. (1988) 118, 87–92

Effect of insulin on in vivo glucose utilization in individual tissues of anesthetized lactating rats

1987 ◽  
Vol 252 (2) ◽  
pp. E183-E188 ◽  
Author(s):  
A. F. Burnol ◽  
P. Ferre ◽  
A. Leturque ◽  
J. Girard
Keyword(s):  
Adipose Tissue ◽  
Mammary Gland ◽  
White Adipose Tissue ◽  
Skeletal Muscles ◽  
Plasma Insulin ◽  
Glucose Utilization ◽  
Insulin Concentration ◽  
Utilization Rate ◽  
Plasma Insulin Concentration ◽  
Euglycemic Hyperinsulinemic Clamp

Glucose utilization rate has been measured in skeletal muscles, white adipose tissue, and mammary gland of anesthetized nonlactating and lactating rats. During lactation, basal glucose utilization is decreased by 40% in periovarian white adipose tissue and by 65% in epitrochlearis and extensor digitorum longus but not in soleus muscle. This may be related to the lower blood glucose and plasma insulin concentrations observed during lactation. Basal glucose utilization rate in the mammary gland was, respectively, 18 +/- 2 and 350 +/- 50 micrograms/min in nonlactating and lactating rats. During the euglycemic hyperinsulinemic clamp, a physiological increment in plasma insulin concentration (231 +/- 18 in lactating vs. 306 +/- 24 microU/ml in nonlactating rats) induces a similar increase in glucose utilization rate in skeletal muscles (except soleus) and white adipose tissue in the two groups of rats. Furthermore this low increase in plasma insulin concentration does not alter mammary glucose utilization rate in nonlactating rats but induces the same increase (sevenfold over basal) as a maximal insulin concentration in lactating rats. These data show that the active mammary gland is the most insulin-sensitive tissue of the lactating rat that has been tested. The overall increase in insulin sensitivity and responsiveness that has been described in lactating rats can then mainly be attributed to the presence of the active mammary gland.

scholarly journals 146 Nutritional Advances in Fetal and neonatal development: effect of fatty acid supplementation

2020 ◽  
Vol 98 (Supplement_3) ◽  
pp. 121-122
Author(s):  
Alejandro E Relling
Keyword(s):  
Small Intestine ◽  
Fatty Acid ◽  
Plasma Insulin ◽  
Linear Increase ◽  
Late Gestation ◽  
Insulin Concentration ◽  
Plasma Insulin Concentration ◽  
Pufa Supplementation ◽  
Epa And Dha ◽  
Offspring Growth

Abstract Data from a series of experiments demonstrates that maternal supply of polyunsaturated fatty acids, particularly eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA), during late gestation affects offspring growth. The increase in growth is independent on the fatty acid supplemented during the growing or finishing phase of the offspring; but it is sex dependent. Dam PUFA supplementation increases wether growth. Supplementation with EPA and DHA to pregnant ewes and to their offspring after weaning showed a treatment interaction in mRNA concentration of hypothalamic neuropeptides associated with dry matter intake (DMI) regulation. A dose increased in EPA and DHA in pregnant ewe diets shows a linear increase in growth, but a quadratic change in DMI or feed efficiency; growth was associated with a linear increase in plasma glucose concentration and a linear decrease in plasma ghrelin concentration. In lambs born from ewes supplemented with different sources of FA during a glucose tolerance test; males’ plasma insulin concentration increased as FA unsaturation degree increased in the dam diet, the opposite happened with females’ plasma insulin concentration. Recent data from our lab showed that the supplementation with EPA and DHA during the last third of gestation to pregnant ewes increased liver and small intestine global DNA methylation and small intestine transporters for amino acids in the fetus. Despite EPA and DHA during late gestation increase growth in the offspring; when EPA and DHA were supplemented in early gestation, offspring growth was lesser that lambs born from ewes supplemented a saturated and monounsaturated lipid. The reason for the difference in results it is not clear. However, more studies focusing in some aspect of the biology will help to understand what specific fatty acid needs to be supplemented at different stages of gestation to improve offspring growth.

scholarly journals Fetal growth, glucose tolerance and plasma insulin concentration in rats given a marginal-zinc diet in the latter stages of pregnancy

1988 ◽  
Vol 59 (2) ◽  
pp. 315-322 ◽  
Author(s):  
Susan Southon ◽  
Susan J. Fairweather-Tait ◽  
Christine M. Williams
Keyword(s):  
Blood Glucose ◽  
Glucose Concentration ◽  
Plasma Insulin ◽  
Insulin Concentration ◽  
Oral Glucose ◽  
Fetal Blood ◽  
Plasma Insulin Concentration ◽  
Pregnant Rats ◽  
Zn Content ◽  
Tail Blood

1. Wistar rats were fed on a control semi-synthetic diet throughout pregnancy, or a control diet in the first 2 weeks and a marginal-zinc diet in the 3rd week of pregnancy. On day 20, after an overnight fast, half the animals in each group were given glucose by gavage and the 0–30 min rise in blood glucose measured in tail blood. After 60 min blood was taken by cardiac puncture for glucose and insulin assay. Maternal pancreases were removed and the Zn contents measured. Fetuses from each litter were combined for wet/dry weights, protein and DNA determinations.2. Plasma insulin concentration was higher, and glucose concentration and pancreatic Zn content lower, in pregnantv. non-pregnant animals of similar age, fed on the same diet. Pancreatic Zn content was lowest in the marginal-Zn group of pregnant rats. Fetuses from mothers fed on the marginal-Zn diet during the last week of pregnancy were slightly heavier than controls and had a significantly higher protein: DNA ratio. The 0–30 min rise in blood glucose was significantly greater in the marginal-Zn animals.3. In a second experiment, pregnant rats were given similar diets to those used in the first study, but the marginal-Zn diet was given for a shorter period (days 15–19 of pregnancy). On day 19 the rats were meal-fed and on day 20, after an overnight fast, an oral glucose dose was administered. Tail-blood was taken at timed intervals up to 60 min post-dosing for glucose assay. Both maternal and fetal blood glucose and insulin concentration was measured 70 min post-dosing.4. Values for maternal and fetal blood glucose and plasma insulin, measured 70 min after the administration of a glucose dose, were similar in the two groups, but the initial rise in blood glucose concentration was again significantly higher in pregnant rats given the marginal-Zn diet towards term.5. It is suggested that the change in growth and composition, observed in fetuses from rats given a marginal-Zn diet in later pregnancy, is associated with altered maternal carbohydrate metabolism.

scholarly journals The effect of acetoacetate on plasma insulin concentration

1971 ◽  
Vol 125 (2) ◽  
pp. 541-544 ◽  
Author(s):  
R. A. Hawkins ◽  
K. G. M. M. Alberti ◽  
C. R. S. Houghton ◽  
D. H. Williamson ◽  
H. A. Krebs
Keyword(s):  
Fatty Acids ◽  
Blood Glucose ◽  
Free Fatty Acids ◽  
Glucose Concentration ◽  
Plasma Insulin ◽  
Blood Glucose Concentration ◽  
Diabetic Rats ◽  
Insulin Concentration ◽  
Plasma Insulin Concentration ◽  
Arterial Blood

1. Sodium acetoacetate was infused into the inferior vena cava of fed rats, 48h-starved rats, and fed streptozotocin-diabetic rats treated with insulin. Arterial blood was obtained from a femoral artery catheter. 2. Acetoacetate infusion caused a fall in blood glucose concentration in fed rats from 6.16 to 5.11mm in 1h, whereas no change occurred in starved or fed–diabetic rats. 3. Plasma free fatty acids decreased within 10min, from 0.82 to 0.64mequiv./l in fed rats, 1.16 to 0.79mequiv./l in starved rats and 0.83 to 0.65mequiv./l in fed–diabetic rats. 4. At 10min the plasma concentration rose from 20 to 49.9μunits/ml in fed unanaesthetized rats and from 6.4 to 18.5μunits/ml in starved rats. There was no change in insulin concentration in the diabetic rats. 5. Nembutal-anaesthetized fed rats had a more marked increase in plasma insulin concentration, from 30 to 101μunits/ml within 10min. 6. A fall in blood glucose concentration in fed rats and a decrease in free fatty acids in both fed and starved rats is to be expected as a consequence of the increase in plasma insulin. 7. The fall in the concentration of free fatty acids in diabetic rats may be due to a direct effect of ketone bodies on adipose tissue. A similar effect on free fatty acids could also be operative in normal fed or starved rats.

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