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Maternal blood glucose, foetal blood glucose and liver carbohydrate levels were estimated after foetuses were injected with glucagon through the uterine wall on days 19½, 20½ and 21½ of gestation in the rat.

Glucagon had a hyperglycaemic effect in the foetus on all the days studied but the response was greater and more rapid on day 21½ of gestation. Glucagon was shown to decrease liver glycogen on day 20½ and 21½ but again the response was more rapid and more pronounced on day 21½.

The normal levels of foetal liver glycogen were similar to those previously found but the normal foetal blood glucose values are lower than previous results. Decrease in liver glycogen observed in the control group of foetuses on day 21½ of gestation together with a loss in foeto-maternal blood glucose relationship on that day of gestation suggest that on day 21½ the foetal rat develops the ability to mobilize hepatic glycogen and thereby to alter its blood glucose level independently from the mother.

The significance of the low blood glucose levels found in the foetus is discussed.

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An inverse age-related pattern of GH secretion has been identified in immature ducks between 2 and 9 weeks of age, the plasma level of GH falling progressively from 30–40 ng/ml at 2 weeks of age to the adult level (< 10 ng/ml) by 9 weeks of age. This decrease in GH secretion was not accompanied by any age-related changes in the concentrations of plasma immunoreactive insulin or glucagon-like immunoreactivity or in plasma glucose or free fatty acid level.

In 4- to 6-week-old ducklings the intravenous infusion of insulin (2·5 or 10 mu./kg per min for 30 min) and glucagon (0·1 or 0·5 μg/kg per min for 30 min) induced some inhibition of GH secretion, independently of changes in blood glucose level. These results suggest that although insulin and especially glucagon have direct effects on GH secretion in the duck, maturational differences in pancreatic function are unlikely to be causally related to the decrease in GH secretion during growth.

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The plasma insulin response to glucose and arginine was increased in intact female rats implanted with progesterone. This change was not mediated by increased energy intake since the insulin response to glucose was similarly enhanced in progesterone-treated rats pair-fed with controls. In contrast, similar levels of pancreatic glucagon were observed in the plasma of both control and experimental rats during arginine stimulation. Thus the molar ratio of insulin to glucagon may be increased in the plasma of progesterone-treated rats following a mixed meal. This change may represent a physiological adaption to a demonstrable resistance to the peripheral actions of insulin in non-adipose soft tissue. The hyperglycaemic and lipolytic actions of exogenous glucagon were also impaired in progesterone-treated rats. It is suggested that an increase in the molar ratio of insulin to glucagon will favour hepatic lipogenesis and the peripheral deposition of fat.

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The intravenous injection of glucagon (0·4 mg/kg) 12–30 min before the administration of a diabetogenic dose of alloxan (60 mg/kg) prevents the development of alloxan diabetes in dogs.

The protection obtained with glucagon is abolished by a subcutaneous injection of insulin (2 i.u./kg) administered 2 hr previously.

The possible mechanism of this protection and of its antagonism by insulin is discussed.

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EG Siegel, A Seidenstucker, B Gallwitz, F Schmitz, A Reinecke-Luthge, G Kloppel, UR Folsch, and WE Schmidt

Liver cirrhosis is often accompanied by a disturbed carbohydrate metabolism similar to type 2 diabetes. To investigate the severity of the defect in insulin secretion in this form of diabetes, we measured insulin release from isolated pancreatic islets of rats with CCl(4)-phenobarbital-induced liver cirrhosis. Cirrhosis was confirmed by clinical signs, elevated liver enzymes and histology. Fasting venous plasma glucose concentrations were equal in rats with liver cirrhosis and in controls. Plasma insulin and glucagon concentrations were significantly greater (P<0.01) in cirrhotic rats than in control animals. Glucose (16.7 mM)-induced stimulation of insulin release from pancreatic islets revealed a twofold increase in control and cirrhotic rats. Basal and stimulated insulin secretion, however, were significantly lower in cirrhotic animals. The incretin hormone, glucagon-like peptide-1 (GLP-1), has therapeutic potential for the treatment of type 2 diabetes. Therefore, islets from control and cirrhotic animals were incubated with GLP-1 in concentrations from 10(-)(11) to 10(-)(6) M. GLP-1 stimulated insulin release in a concentration-dependent manner. In islets from cirrhotic rats, basal and stimulated insulin secretion was blunted compared with controls. These data show that the hyperinsulinemia observed in liver cirrhosis is not due to an increase of insulin secretion from islets, but could be explained by decreased hepatic clearance of insulin. GLP-1 may ameliorate diabetes in patients with liver cirrhosis.

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To determine whether volatile fatty acids (VFA) are involved in the regulation of plasma concentrations of insulin or glucagon in the goat, VFA, separately or in combination, were administered into the jugular vein, the portal vein or the rumen, and their effects on pancreatic hormones as well as on VFA measured in venous blood. Propionate, n-butyrate and n-valerate, but not acetate, injected in pharmacological doses, were potent stimuli not only of the secretion into the plasma of insulin but also of glucagon. As regards insulin, the response to VFA was probably not mediated to an appreciable extent by glucose or glucagon. β-Hydroxybutyrate did not mediate the effect of n-butyrate on insulin and glucagon. The effects of VFA appear to be peculiar to the ruminant since in the rat injection of similar doses resulted in either no changes or very small changes of plasma insulin and glucagon.

Intraportal infusions over 4 h of mixtures of VFA, resulting in less extreme, more physiological blood concentrations of VFA, elicited sudden transient increases in insulin and to a lesser extent in glucagon. After these peaks insulin and glucagon declined to preinfusion levels and remained virtually unaltered during the remainder of the infusion in spite of sustained, raised concentrations of VFA in the peripheral circulation. These results suggest that under these conditions the rate of increase of VFA is a signal for the secretion of pancreatic hormones. Intraruminal infusions, representing a more physiological route of administration, of single VFA at high rates resulted in a small increase in insulin for propionate infusion only, whereas a mixture of VFA at a physiological rate induced barely any change in insulin or glucagon. It is concluded that under physiological conditions the rate of increase of VFA may contribute to the insulin secretion in the free-feeding goat, but it is unlikely that VFA are the sole controlling agents of insulin release. It is even less probable that the release of glucagon is governed by VFA in the free-feeding goat.

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R. D. Gill and I. C. Hart

Glucagon and insulin receptors were examined in relation to plasma concentrations of hormones and metabolites in unmated and in 110- and 140-day pregnant ewes (four animals per group). The concentrations of insulin, growth hormone and non-esterified fatty acids in the circulation, together with the maintenance of body weight, suggested that the animals were in energy surplus. When compared with the unmated group the binding of insulin to isolated hepatocytes increased by 110 days of pregnancy, attaining statistical significance (P < 0·02) after 140 days. Conversely, glucagon binding was reduced by 110 days of pregnancy, also attaining statistical significance (P < 0·02) after 140 days.

The changes in both insulin and glucagon binding were primarily due to changes in the number of receptors on each hepatocyte, although some fluctuations in receptor affinity were also found.

These observations suggested that the number of hepatic insulin and glucagon receptors are altered during the metabolic demands of pregnancy in sheep, but unlike the changes reported during lactation in the ewe and restricted energy intake in the goat, they are not related either to energy deficit or to changes in the concentration of insulin, and probably of glucagon, in the circulation.

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An antibody to porcine calcitonin (CT) was selected which cross-reacted completely to bovine CT in a radioimmunoassay using a synthetic porcine CT preparation (CT-s) labelled with 125I (Lequin, Hackeng, Schopman & Care, 1970). With this radioimmunoassay it has been possible to measure CT concentrations in samples of bovine peripheral and thyroid venous plasma. All concentrations of CT reported here are expressed in terms of immunologically active CT-s/ml. The standard error of the CT measurements was ± 50 pg CT-s/ml over the range of concentration 250–2000 pg/ml.

One lobe of the thyroid gland was isolated in situ in each of three calves (33–38 kg body wt) and in one adult Jersey cow (300 kg body wt). The glands were perfused with blood which contained various concentrations of calcium. Glucagon and the kallikrein inhibitor (KI) aprotinin (Zymofren) were also added in an experiment with the cow to give perfusing concentrations of

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Third Division, Department of Medicine, University of Kobe, Kobe, Japan

(Received 21 November 1975)

It has been shown that glucagon secretion from the perfused rat pancreas is enhanced by arginine (Assan, Boillot, Attali, Soufflet & Ballerio, 1972) and suppressed by glucose (Gerich, Charles & Grodsky, 1974). However, the effect of fructose on glucagon secretion remains unclear, although fructose is known to potentiate glucose- and mannose-induced insulin secretion (Curry, Curry & Gometz, 1972; Curry, 1974). The present study investigated the effect of fructose on arginine-induced glucagon and insulin release in perfused rat pancreas.

The perfusion of isolated rat pancreas was performed by the procedure described by Grodsky, Batts, Bennett, Vcella, McWilliams & Smith (1963) with minor modifications. The splenic vessels were ligatured at the hilum, and the left gastric vessels were also ligatured. Perfusate (3·8% dextran and 0·25% bovine serum albumin in Krebs-Ringer-bicarbonate buffer) containing 2·8 mm-glucose (Expt 1),

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Ch. Foltzer, M. Th. Strosser, S. Harvey, and P. Mialhe


The effects of plasma free fatty acids (FFA) and somatostatin-14 (S-14) on concentrations of plasma GH, glucagon and insulin were investigated in juvenile ducks. Oleic acid, S-14 or both were infused into 4- to 7-week-old birds and plasma GH, glucagon-like immunoreactivity (GLI), immunoreactive insulin (IRI) and FFA were measured.

An increase in plasma GH and a decrease in GLI but no change in IRI was observed after infusion of 9 mg oleic acid/kg per min. A decrease in plasma GH, FFA and IRI and an increase in plasma GLI was seen after infusion of 800 ng S–14/kg per min. These effects of S-14 on IRI and GLI were abolished when S-14 was infused simultaneously with oleic acid.

It is concluded that FFA have a direct stimulatory effect on GH secretion and an inhibitory effect on glucagon secretion. Somatostatin-14 directly inhibits the secretion of GH and its stimulatory effect on the secretion of glucagon is mediated by a depression in concentrations of plasma FFA. Finally, S-14 has no effect on plasma insulin when basal levels of plasma FFA are maintained.

J. Endocr. (1985) 106, 21–25