Insulin and glucagon responses to intravenous injections of glucose, arginine and propionate in lactating cows and growing calves

1999 ◽  
Vol 79 (3) ◽  
pp. 309-314 ◽  
Author(s):  
H. Sano ◽  
H. Arai ◽  
A. Takahashi ◽  
H. Takahashi ◽  
Y. Terashima
Keyword(s):  
Plasma Insulin ◽  
Glucagon Secretion ◽  
Molar Ratio ◽  
Plasma Glucagon ◽  
Intravenous Injections ◽  
Lactating Cows ◽  
Key Words Insulin ◽  
Endocrine Status ◽  
Basal Plasma ◽  
Time Courses

Plasma insulin and glucagon responses to glucose, arginine and propionate injections were measured to establish indicators of the endocrine status in lactating cows and growing calves. The metabolites were intravenously injected at a dose of 0.625 mmol kg−1 and the time courses of changes in plasma insulin and glucagon concentrations were determined. Basal plasma glucagon concentrations were higher (P < 0.05) for lactating cows than for growing calves, while basal plasma insulin concentrations did not differ between animal groups. Concentrations of plasma insulin increased (P < 0.01) after glucose injection, whereas plasma glucagon concentrations decreased in both lactating cows (P < 0.05) and growing calves (P < 0.01). Plasma insulin and glucagon concentrations increased in response to arginine (P < 0.01) and propionate (P < 0.01 except insulin for lactating cows at P < 0.05) injections. Plasma insulin and glucagon responses were greater (P < 0.05) to arginine than to glucose or propionate. Plasma glucagon responses to arginine were greater (P < 0.05) for lactating cows than for growing calves. The insulin:glucagon molar ratio increased in response to the metabolite injections except following injections of arginine and propionate into lactating cows, when the ratio did not increase significantly. It is possible that in cows the enhanced responsiveness of glucagon secretion plays a role in the maintenance of lactation. Key words: Insulin, glucagon, arginine, propionate, lactating cow, growing calf

Endogenous glucagon regulation in genetically hyperlipemic obese rats

1976 ◽  
Vol 230 (5) ◽  
pp. 1336-1341 ◽  
Author(s):  
RP Eaton ◽  
M Conway ◽  
DS Schade
Keyword(s):  
Plasma Insulin ◽  
Autosomal Recessive ◽  
Recessive Gene ◽  
Zucker Rat ◽  
Plasma Glucagon ◽  
Exogenous Glucose ◽  
Obese Rats ◽  
Basal Plasma ◽  
Glucagon Concentration

Glucagon concentration and regulation were examined in the Zucker rat, in which obesity and hyperlipemia are phenotypic expressions of an autosomal recessive gene. Using littermate animals which are phenotypically thin and normolipemic as controls, we observed reduced basal plasma glucagon levels in the obese lipemic rats. In response to fasting, obese lipemic animals inappropriately demonstrated a further reduction in plasma glucagon concentration. In response to pharmacologic glucagon stimulation (arginine), a subnormal rise in plasma glucagon concentration was observed in the obese, lipemic animals. Glucagon suppressibility with exogenous glucose remained intact. The reduced secretion of glucagon may be a consequence of the abnormal elevation in concentration of plasma insulin, free fatty acids, and glucose, which are characteristic of the obese, lipemic animal. A possible role of glucagon deficiency in the evolution or maintenance of the lipemic state is suggested.

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

Effects of corticotropin-releasing hormone on insulin and glucagon secretion in mice

1988 ◽  
Vol 117 (1) ◽  
pp. 87-92 ◽  
Author(s):  
Sven Karlsson ◽  
Bo Ahrén
Keyword(s):  
Plasma Levels ◽  
Plasma Insulin ◽  
Glucagon Secretion ◽  
Corticotropin Releasing Hormone ◽  
Releasing Hormone ◽  
Insulin And Glucagon Secretion ◽  
Basal Plasma ◽  
Plasma Insulin Levels ◽  
Dose Levels

Abstract. Besides in the brain, corticotropin-releasing hormone occurs in the pancreas. Therefore, its effects on plasma levels of insulin and glucagon were investigated in vivo in the mouse. At 2 min after CRH injection (0.5–8.0 nmol/kg), plasma insulin was lowered: by 4.0 nmol/kg from 38 ± 4 to 28 ± 2 mU/l (P < 0.05). Plasma insulin was lowered also at 6 min, whereas at 10 min, plasma insulin levels were elevated (P < 0.05). Plasma glucagon levels were slightly lowered (P < 0.05) at 10 min after CRH injection, whereas plasma glucose was slightly elevated (P < 0.05) at 6 min after injection but not at 2 or 10 min. The effects of CRH on the plasma insulin and glucagon response to iv injections of half-maximal dose levels of glucose (2.8 mmol/kg) or the cholinergic agonist carbachol (0.16 μmol/kg) were also investigated. CRH, 4.0 nmol/kg, however, could not influence the plasma insulin or glucagon levels after the iv injection of either glucose or carbachol. Thus, CRH slightly affects basal plasma levels of insulin and glucagon in mice. In contrast, stimulated insulin and glucagon secretions are not affected by CRH. Peripheral CRH may therefore be of slight importance for the regulation of basal plasma levels of insulin and glucagon in the mouse.

THERAPIE EINES METASTASIERENDEN INSELZELLTUMORS MIT STREPTOZOTOCIN

1971 ◽  
Vol 67 (2) ◽  
pp. 405-416 ◽  
Author(s):  
E. Nieschlag ◽  
H. Wombacher ◽  
F. J. Kroeger ◽  
L.V. Habighorst
Keyword(s):  
Liver Metastases ◽  
Blood Sugar ◽  
Mechanism Of Action ◽  
Islet Cell ◽  
Plasma Insulin ◽  
Severe Hypoglycaemia ◽  
Islet Cells ◽  
Intravenous Injections ◽  
High Affinity ◽  
Methyl Nitrosourea

A patient with a metastazing functional islet cell tumour suffering from severe hypoglycaemia was treated with streptozotocin. Four intravenous injections of 1.5 g streptozotocin each were administered in 4 to 6 days intervals. After the 4th injection there were no further episodes of hypoglycaemia, parenteral glucose administration could be stopped and blood sugar and plasma insulin, showing concentrations of up to 405 μU/ml before treatment, reached normal levels. The tumours in the pancreas disappeared and the liver metastases decreased in size and number as judged by arteriography. A hypothesis for the mechanism of action of streptozotocin is proposed. The glucose moiety is considered to facilitate a high affinity to the islet cells whereas the N-methyl-nitrosourea residue serves the active antitumour part of the molecule.

scholarly journals Impacts of pre- and postnatal nutrition on glucagon regulation and hepatic signalling in sheep

2018 ◽  
Vol 238 (1) ◽  
pp. 1-12
Author(s):  
Bishnu Adhikari ◽  
Prabhat Khanal ◽  
Mette Olaf Nielsen
Keyword(s):  
Phosphoenolpyruvate Carboxykinase ◽  
Glucagon Secretion ◽  
Late Gestation ◽  
Plasma Glucagon ◽  
Glucagon Receptor ◽  
Protein Requirements ◽  
Daily Energy ◽  
Obesogenic Diet ◽  
Prenatal Undernutrition

To evaluate the long-term impacts of early-life nutritional manipulations on glucagon secretion and hepatic signalling, thirty-six twin-pregnant ewes during their last trimester were exposed to NORM (fulfilling 100% of daily energy/protein requirements), HIGH (fulfilling 150/110% of daily energy/protein requirements) or LOW (50% of NORM) diets. Twin lambs were assigned after birth to a moderate (CONV) or high-carbohydrate high-fat (HCHF) diet until 6 months. Then, responses in plasma glucagon concentrations and glucagon ratios relative to previously reported values for insulin, glucose and lactate were determined after intravenous bolus injections of glucose or propionate (fed and 2-day fasting state). Hepatic mRNA expressions of glucagon receptor (GCGR), glucose-6-phosphatase (G6PC), phosphoenolpyruvate carboxykinase (PEPCK) and fructose 1,6-biphosphatase (FBP) were also determined in a sub group of autopsied lambs. Expression of GCGR and all three enzymes were supressed by prenatal LOW compared to NORM (except PEPCK) and HIGH (except FBP) nutrition. The postnatal HCHF diet reduced plasma glucagon responses to propionate and hepatic mRNA expression of all genes. In response to propionate, insulin/glucagon ratio was decreased (fasted state), but lactate/glucagon and glucose/glucagon increased in HCHF compared to CONV lambs. In conclusion, prenatal undernutrition and postnatal overnutrition had similar long-term implications and reduced hepatic glucagon signalling. Glucagon secretory responses to propionate were, however, not related to the prenatal nutrition history, but negatively affected by the postnatal obesogenic diet. The pancreatic α-cell compared to β-cells may thus be less sensitive towards late gestation malnutrition, whereas hepatic glucagon signalling appears to be a target of prenatal programming.

ANF inhibits glucose-stimulated insulin secretion in mouse and rat

1988 ◽  
Vol 255 (5) ◽  
pp. E579-E582 ◽  
Author(s):  
B. Ahren
Keyword(s):  
Insulin Secretion ◽  
Atrial Natriuretic Factor ◽  
Plasma Insulin ◽  
Glucagon Secretion ◽  
Insulin Levels ◽  
Atrial Cells ◽  
Insulin And Glucagon Secretion ◽  
Plasma Insulin Levels ◽  
Glucose Stimulated Insulin Secretion ◽  
Dose Levels

Atrial natriuretic factor (ANF) is synthesized in atrial cells and was recently demonstrated to also occur within islet glucagon cells. Therefore, we investigated the possible effects of synthetic rat ANF-(1-28) on basal and stimulated insulin and glucagon secretion in the mouse and on glucose-induced insulin secretion in the rat. We found that ANF did not affect basal levels of insulin, glucagon, or glucose when injected intravenously at dose levels between 0.25 and 4.0 nmol/kg in mice. However, when injected together with glucose (2.8 mmol/kg), ANF (4.0 nmol/kg) inhibited the increase in plasma insulin levels by 40%, from 114 +/- 8 microU/ml in controls to 81 +/- 8 microU/ml (P less than 0.01). Likewise, the increase in plasma insulin levels during an intravenous infusion of glucose in rats (10 mg/min) was significantly reduced by ANF (100 pmol.kg-1.min-1; P less than 0.001). In contrast, the increase in plasma levels of insulin and glucagon after the intravenous injection of the cholinergic agonist carbachol in mice (0.16 mumol/kg) was not significantly affected by ANF. We conclude that ANF inhibits glucose-stimulated insulin secretion in the mouse and the rat. The peptide may therefore be a modulator of insulin secretion.

Plasma Glucagon and Free Fatty Acid Responses to a Glucose Load in the Obese Spontaneous Hypertensive Rat (SHROB) Model of Metabolic Syndrome X

2002 ◽  
Vol 227 (3) ◽  
pp. 164-170 ◽  
Author(s):  
Rodney A. Velliquette ◽  
Richard J. Koletsky ◽  
Paul Ernsberger
Keyword(s):  
Insulin Resistance ◽  
Metabolic Syndrome ◽  
Metabolic Syndrome X ◽  
Molar Ratio ◽  
Syndrome X ◽  
Oral Glucose ◽  
Plasma Glucagon ◽  
Glucose Load ◽  
Spontaneous Hypertensive Rat ◽  
Hypertensive Rat

Metabolic Syndrome X is a cluster of abnormalities including insulin resistance, hyperlipidemia, hypertension, and obesity. We sought to determine if excess plasma glucagon and free fatty acids (FFA) might contribute to the insulin resistance in the obese spontaneous hypertensive rat (SHROB), a unique animal model of leptin resistance and metabolic Syndrome X. SHROB were extremely hyperinsulinemic and mildly glucose intolerant compared with lean SHR. SHROB had elevated fasting plasma glucagon and FFA, and showed paradoxical responses to an oral glucose challenge, with increased glucagon at 30 and 60 min postchallenge (200% ± 45% and 91% ± 13%, respectively; n = 9). In lean SHR, glucagon was nearly unchanged by glucose loading (<30% increase, P > 0.05; n = 5). Plasma FFA were not affected by a glucose load in SHROB, whereas SHR showed a decrease of 40% ± 6% (n = 5–9). The I/G molar ratio changed in opposite directions in the two genotypes, with a decrease in SHROB at 30 and 60 min, in contrast to the appropriate increase at 30 and 60 min postchallenge in the lean SHR (P < 0.01; n = 5–9). Administration of 500 ng/kg exogenous glucagon to SHR raised glucagon 56% ± 5% to a level that was similar to fasting SHROB. This level of circulating glucagon was sufficient to elevate glucose and insulin during the 7 hr of observation (n = 9). Based on these results, we suggest that fasting hyperglucagonemia and impaired suppression of glucagon secretion and FFA in response to an oral glucose load may contribute to insulin resistance and glucose intolerance in the SHROB model of metabolic Syndrome X.

Thermogenic effect of thyroid hormones: interactions with epinephrine and insulin.

1990 ◽  
Vol 259 (3) ◽  
pp. E305
Author(s):  
V Piolino ◽  
K J Acheson ◽  
M J Müller ◽  
N Jeanprêtre ◽  
A G Burger ◽  
...  
Keyword(s):  
Energy Expenditure ◽  
Thyroid Hormones ◽  
Basal Insulin ◽  
Plasma Insulin ◽  
Resting Energy Expenditure ◽  
Fat Free Mass ◽  
Short Term ◽  
Epinephrine Infusion ◽  
Before And After ◽  
Basal Plasma

The interactions between thyroid hormones, epinephrine, and insulin in the regulation of energy expenditure were investigated in a group of healthy young men before and after thyroxine (T4) treatment (300 micrograms/day for 14 days) at basal plasma insulin concentrations and during hypoinsulinemia with and without epinephrine infusion (0.05 micrograms.kg fat-free mass-1.min-1). T4 treatment induced moderate hyperthyroidism and increased resting energy expenditure (RMR). The effect was more pronounced during short-term hypoinsulinemia, but hypoinsulinemia by itself did not influence RMR. Epinephrine infusion caused a significant increase in energy expenditure. The effect was most pronounced at hypoinsulinemia and with T4 treatment. Hypoinsulinemia and T4 treatment were not additive in their effects. We conclude that basal insulin concentrations mask some of the thermogenic effects of thyroid hormones and epinephrine. Thus insulin antagonism may suppress some of the thermogenic actions of thyroid hormones and epinephrine.

scholarly journals Effect of early dietary restriction on insulin action and secretion in the GK rat, a spontaneous model of NIDDM

2000 ◽  
Vol 278 (6) ◽  
pp. E1097-E1103 ◽  
Author(s):  
Carmen Alvarez ◽  
Danielle Bailbe ◽  
Françoise Picarel-Blanchot ◽  
Eric Bertin ◽  
Ana-Maria Pascual-Leone ◽  
...  
Keyword(s):  
Insulin Secretion ◽  
Weight Gain ◽  
Glucose Tolerance ◽  
Glucose Uptake ◽  
Insulin Action ◽  
Food Restriction ◽  
Plasma Insulin ◽  
Insulin Level ◽  
Gk Rat ◽  
Basal Plasma

The availability of the Goto-Kakisaki (GK) rat model of non-insulin-dependent diabetes mellitus prompted us to test the effect of a limited period of undernutrition in previously diabetic young rats on their insulin secretion and insulin action during adult age. Four-week-old female GK rats were either food restricted (35% restriction, 15% protein diet) or protein and energy restricted (35% restriction, 5% protein diet) for 4 wk. Food restriction in the young GK rat lowered weight gain but did not aggravate basal hyperglycemia or glucose intolerance, despite a decrease in basal plasma insulin level. Furthermore, the insulin-mediated glucose uptake by peripheral tissues in the GK rat was clearly improved. We also found that food restriction, when it is coupled to overt protein deficiency in the young GK rat, altered weight gain more severely and slightly decreased basal hyperglycemia but conversely aggravated glucose tolerance. Improvement of basal hyperglycemia was related to repression of basal hepatic glucose hyperproduction, despite profound attenuation of basal plasma insulin level. Deterioration of tolerance to glucose was related to severe blunting of the residual glucose-induced insulin secretion. It is, however, likely that the important enhancement of the insulin-mediated glucose uptake helped to limit the deterioration of glucose tolerance.

The influence of vanadate on insulin counter-regulatory hormones in obese fa/fa rats

1991 ◽  
Vol 131 (2) ◽  
pp. 185-191 ◽  
Author(s):  
S. M. Brichard ◽  
L. N. Ongemba ◽  
J. Kolanowski ◽  
J. C. Henquin
Keyword(s):  
Body Weight ◽  
Food Restriction ◽  
Body Weight Gain ◽  
Plasma Corticosterone ◽  
Plasma Glucagon ◽  
Lower Plasma ◽  
Peripheral Tissues ◽  
Insulin Resistant ◽  
Glucose Homoeostasis ◽  
Basal Plasma

ABSTRACT Vanadate has been shown to improve glucose homoeostasis in mildly glucose-intolerant and severely insulin-resistant fa/fa rats. The present study examined whether changes in insulin counter-regulatory hormones contribute to this beneficial effect of vanadate. Since oral administration of Na3VO4 caused a decrease in food intake and stopped the increase in body weight, vanadate-treated fa/fa rats were compared with both controls with food available ad libitum and pair-fed rats. Slightly lower plasma glucose levels were maintained in conjunction with markedly lower plasma insulin levels in vanadatetreated rats, and this effect was not simply due to the smaller body weight of the animals. Compared with control rats, treatment with vanadate affected neither basal plasma glucagon levels nor the increase in glucagon levels observed after insulin-induced hypoglycaemia or after i.v. injection of arginine. Compared with pair-fed rats, treatment with vanadate prevented the fall in basal plasma glucagon and its exaggerated rise in response to insulin that mere food restriction produced. Plasma corticosterone levels were high in fa/fa rats. Vanadate and pair-feeding similarly decreased basal plasma levels of corticosterone as well as nocturnal corticosteronuria. Thus the attenuation of the hypercorticism of fa/fa rats results from the reduction in body weight gain rather than from a specific action of vanadate. Vanadate did not influence urinary excretion of noradrenaline, an index of neural sympathetic activity, but prevented the increase in adrenaline excretion, an index of adrenal medulla activity, that was produced by food restriction in pair-fed rats. In conclusion, vanadate administration has no or little specific effects on three major insulin counter-regulatory hormones. This reinforces the suggestion that the beneficial effects of vanadate on glucose homoeostasis in fa/fa rats are mainly due to a correction of insulin resistance in peripheral tissues. Journal of Endocrinology (1991) 131, 185–191

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