Natural estrous cycle in normal and diabetic bitches. II). Serum nonesterified fatty acids and serum free glycerol levels during glucose and insulin tests.

Actions and interactions of spontaneous diabetes mellitus (DM) and natural estrous cycles (sex seasons) on the regulation of serum nonesterified fatty acids (NEFAs) and free glycerol (FG) levels in bitches in the fasting condition and during i.v. glucose (IVGTT) and insulin (ITT) tolerance tests, were studied. DM increased serum NEFAs concentration both in the basal condition and during IVGTT; it provoked a fall response to glucose load which is absent in normal controls. Estrous cycles did not modify these observations. Serum NEFAs levels during ITT were unresponsive in normal and diabetic bitches at every sex stage; flat, overlapped serum NEFAs profiles were then observed except for the diabetic group at A, which showed an early abrupt fall response of this variable from its high base line. DM increased also serum FG concentration in the fasting condition and during IVGTT. In the normal controls, serum FG base line was not affected by sex status; similarly shaped, increasing, overlapped curves during the test were observed. In the diabetic bitches "in season" (either phase), serum FG basal value was hardly above in respect to anestrous, but during IVGTT their flat profiles coincided. DM increased serum FG concentration in the basal condition and during ITT, and modified the profiles of this variable. In normal dogs in the basal condition, serum FG concentration remained unaffected by sex status; this variable hard, transiently increased during ITT, which was not influenced by "sex seasons"; therefore, similarly shaped, overlapped serum FG profiles were then observed. In the normal and diabetic bitches, serum-FG base line was not changed by "sex seasons". During ITT, serum FG mean profile in the diabetic bitches at EP was modestly above that observed in those at LP; differences for any other comparisons in normals or diabetic bitches were nonsignificant. As reported by us elsewhere, impaired glucose metabolism and absolute insulin deficiency induced ketose-prone, acidotic, insulin-dependent diabetic chryses in certain normal and diabetic beaches "in season" studied here. The unability of these animals for hydrolizing glyceride-glycerol via lipoproteinlipase (IVGTT) or via hormone sensitive fractions of lipase (ITT) and the abolished serum NEFAs suppressibility during modest hiperinsulinemia (ITT) appear to contribute to the production of such chryses. Results are discussed on the basis of interactions of serum NEFAs and FG with respective blood sugar and serum immunoreactive insulin levels as influenced by DM and estrous cycle.

Natural estrous cycle in normal and diabetic bitches. II) serum nonesterified fatty acids and serum free glycerol levels during glucose and insulin tests

Actions and interactions of spontaneous diabetes mellitus (DM) and natural estrous cycles (sex seasons) on the regulation of serum monesterified fatty acids (NEFAs) and free glycerol (FG) levels in bitches in the fasting condition and during i.v. glucose (IVGTT) and insulin (ITT) tolerance tests, were studied. DM increased serum NEFAs concentration both in the basal condition and during IVGTT; it provoked a fall response to glucose load which is absent in normal controls. Estrous cycles did not modify these observations. Serum NEFAs levels during ITT were unresponsive in normal and diabetic bitches at every sex stage; flat, overlapped serum NEFAs profiles were then observed except for the diabetic group at A, which showed an early abrupt fall response of this variable from its high base line. DM increased also serum FG concentration in the fasting condition and during IVGTT. In the normal controls, serum FG base line was not affected by sex status; similary shaped, increasing, overlapped curves during the test were observed. In the diabetic bitches "in season" (either phase), serum FG basal value was hardly above in respect to anestrous, but during IVGTT their flat profiles coincided. DM increased serum FG concentration in the basal condition and during ITT, and modified the profiles of this variable. In normal dogs in the basal condition, serum FG concentration remained unaffected by sex status; this variable hard, transiently increased during ITT, which was not influenced by "sex seasons"; therefore, similarly shaped, overlapped serum FG profiles were then observed. In the normal and diabetic bitches, serum FG base line was not changed by "sex seasons". During ITT, serum FG mean profile in the diabetic bitches at EP was modestly above that observed in those at LP; differences for any other comparisions in normals or diabetic bitches were nonsignificant. As reported by us elsewhere, impaired glucose metabolism and absolute insulin dificiency induced ketose-prone, acidotic, insulin-dependent diabetic chryses in certain normal and diabetic beaches "in season" studied here. The unability of these animals for hydrolizingglyceride-glycerol via lipoproteinlipase (IVGTT) or via hormone sensitive fractions of lipase (ITT) and the abolished serum NEFAs suppressibility during modest hiperinsulinemia (ITT) appear to contribute to the production of such chryses...(AU)

Natural estrous cycle in normal and diabetic bitches. II) serum nonesterified fatty acids and serum free glycerol levels during glucose and insulin tests

Actions and interactions of spontaneous diabetes mellitus (DM) and natural estrous cycles (sex seasons) on the regulation of serum monesterified fatty acids (NEFAs) and free glycerol (FG) levels in bitches in the fasting condition and during i.v. glucose (IVGTT) and insulin (ITT) tolerance tests, were studied. DM increased serum NEFAs concentration both in the basal condition and during IVGTT; it provoked a fall response to glucose load which is absent in normal controls. Estrous cycles did not modify these observations. Serum NEFAs levels during ITT were unresponsive in normal and diabetic bitches at every sex stage; flat, overlapped serum NEFAs profiles were then observed except for the diabetic group at A, which showed an early abrupt fall response of this variable from its high base line. DM increased also serum FG concentration in the fasting condition and during IVGTT. In the normal controls, serum FG base line was not affected by sex status; similary shaped, increasing, overlapped curves during the test were observed. In the diabetic bitches "in season" (either phase), serum FG basal value was hardly above in respect to anestrous, but during IVGTT their flat profiles coincided. DM increased serum FG concentration in the basal condition and during ITT, and modified the profiles of this variable. In normal dogs in the basal condition, serum FG concentration remained unaffected by sex status; this variable hard, transiently increased during ITT, which was not influenced by "sex seasons"; therefore, similarly shaped, overlapped serum FG profiles were then observed. In the normal and diabetic bitches, serum FG base line was not changed by "sex seasons". During ITT, serum FG mean profile in the diabetic bitches at EP was modestly above that observed in those at LP; differences for any other comparisions in normals or diabetic bitches were nonsignificant. As reported by us elsewhere, impaired glucose metabolism and absolute insulin dificiency induced ketose-prone, acidotic, insulin-dependent diabetic chryses in certain normal and diabetic beaches "in season" studied here. The unability of these animals for hydrolizingglyceride-glycerol via lipoproteinlipase (IVGTT) or via hormone sensitive fractions of lipase (ITT) and the abolished serum NEFAs suppressibility during modest hiperinsulinemia (ITT) appear to contribute to the production of such chryses...

Natural estrous cycle in normal and diabetic bitches. II). Serum nonesterified fatty acids and serum free glycerol levels during glucose and insulin tests.

Actions and interactions of spontaneous diabetes mellitus (DM) and natural estrous cycles (sex seasons) on the regulation of serum nonesterified fatty acids (NEFAs) and free glycerol (FG) levels in bitches in the fasting condition and during i.v. glucose (IVGTT) and insulin (ITT) tolerance tests, were studied. DM increased serum NEFAs concentration both in the basal condition and during IVGTT; it provoked a fall response to glucose load which is absent in normal controls. Estrous cycles did not modify these observations. Serum NEFAs levels during ITT were unresponsive in normal and diabetic bitches at every sex stage; flat, overlapped serum NEFAs profiles were then observed except for the diabetic group at A, which showed an early abrupt fall response of this variable from its high base line. DM increased also serum FG concentration in the fasting condition and during IVGTT. In the normal controls, serum FG base line was not affected by sex status; similarly shaped, increasing, overlapped curves during the test were observed. In the diabetic bitches [quot ]in season[quot ] (either phase), serum FG basal value was hardly above in respect to anestrous, but during IVGTT their flat profiles coincided. DM increased serum FG concentration in the basal condition and during ITT, and modified the profiles of this variable. In normal dogs in the basal condition, serum FG concentration remained unaffected by sex status; this variable hard, transiently increased during ITT, which was not influenced by [quot ]sex seasons[quot ]; therefore, similarly shaped, overlapped serum FG profiles were then observed. In the normal and diabetic bitches, serum-FG base line was not changed by [quot ]sex seasons[quot ]. During ITT, serum FG mean profile in the diabetic bitches at EP was modestly above that observed in those at LP; differences for any other comparisons in normals or diabetic bitches were nonsignificant. As reported by us elsewhere, impaired glucose metabolism and absolute insulin deficiency induced ketose-prone, acidotic, insulin-dependent diabetic chryses in certain normal and diabetic beaches [quot ]in season[quot ] studied here. The unability of these animals for hydrolizing glyceride-glycerol via lipoproteinlipase (IVGTT) or via hormone sensitive fractions of lipase (ITT) and the abolished serum NEFAs suppressibility during modest hiperinsulinemia (ITT) appear to contribute to the production of such chryses. Results are discussed on the basis of interactions of serum NEFAs and FG with respective blood sugar and serum immunoreactive insulin levels as influenced by DM and estrous cycle.

Natural estrous cycle in normal and diabetic bitches in relation to glucose and insulin tests.

The influence of spontaneous "sex seasons" on blood sugar (BS) and serum insulin levels was studied in bitches with natural diabetes mellitus (DM) and normal controls, in the basal condition and during glucose and insulin tests, was studied. DM increased basal BS, reduced glucose tolerance, distribution space (DS) and clearance from blood, and induced resistance to insulin hypoglycemic action. In normals occurrence of "seasons", inconsistently modified basal BS, increased glucose tolerance and DS; during estrogenic phase (EP), these variables were above those during luteal phase (LP). In diabetics at LP, BS found in lasting condition and during glucose test were higher than in diabetic bitches at EP (respective values at anestrous (A) in between) and glucose DS was smaller. Rate of glucose clearance from blood remained unaffected by "seasons" in both dog groups. Basal serum IRI was not modified by DM or "seasons". In normals, serum IRI response to glucose load was nonsignificant during A and increased during the "seasons"; either insulin DS or the rate of insulin clearance from blood stream remained unchanged under the circumstances, the increase being mediated by insulin secretion. During EP, the increase was particularly intense and mean insulinogenic index (MII) rose. During LP, MII returned to A value, whereby diabetic states might be manifest. Serum IRI profiles during insulin test were not modified by "seasons" in normal bitches; such response in diabetic bitches was intense during A, then decreased (EP) or was later abolished (LP). Either in normal or diabetic bitches, the sensitivity to exogenous insulin hypoglycemic action remained unchanged in spite of "seasons". In diabetic bitches at A, serum IRI after glucose challenge peaked higher than in respective normal controls (insulin clearance and insulin DS were similar): they exhibited relative insulin shortage and resistance to insulin hypoglycemic action partly compensated by promoted insulin secretion. Along with "season", abolished serum IRI response to glucose load in diabetics was observed. During EP, extrapancreatic factors regulating serum IRI concentration and MII did not change in respect to A, whereby abolishment appears mediated by depressed insulin secretion. During LP, insulin antagonism in conjunction with 1) absolute insulin deficiency and 2) intense decrease in MII appears as a powerful factor exposing diabetic bitches to a severe or fatal derangement in diabetic disease.

Adrenocorticotrophic hormone, cortisol and catecholamine concentrations during insulin hypoglycaemia in dogs anaesthetized with thiopentone.

Glucose homeostasis is maintained by complex neuroendocrine control mechanisms. Increases in plasma concentrations of various glucose-raising hormones such as glucagon, catecholamines, adrenocorticotrophic hormone (ACTH), and cortisol are observed under certain conditions associated with stress (haemorrhage and hypoglycaemia). The purpose of this study was to determine the effect of thiopentone anaesthesia on the catecholamine, ACTH and cortisol response to insulin hypoglycaemia in dogs. Blood sugar (BS), plasma catecholamine, and ACTH, and serum cortisol concentrations were measured during the course of (1) an intravenous insulin test (ITT) and (2) an ACTH test in conscious and in anaesthetized fasted dogs. During the ITT, the anaesthetized dogs showed a moderate resistance, compared with conscious dogs, to the hypoglycaemic action induced by insulin (blood sugar concentration 30 min after insulin injection: 2.91 +/- 0.25 vs 1.93 +/- 0.12 mM.L-1; P < 0.01). In addition, decreased epinephrine (220 +/- 27 vs 332 +/- 32 pg.ml-1), ACTH (65 +/- 6 vs 90 +/- 5 pg.ml-1) and cortisol (4.48 +/- 0.3 vs 6.25 +/- 0.5 micrograms.ml-1) concentrations were detected 60 min after insulin injection (P < 0.01). The norepinephrine response to hypoglycaemia was not altered by anaesthesia (273 +/- 33 vs 325 +/- 25 pg.ml-1). Anaesthetized dogs showed a decreased cortisol response to ACTH at 45 min (5.68 +/- 0.54 vs 8.87 +/- 0.47 micrograms.ml-1) when compared with control dogs (P < 0.001). Haemodynamic variables during anaesthesia showed little changes (P < NS); while respiratory rate was altered (P < 0.01 between 60 and 105 min).(ABSTRACT TRUNCATED AT 250 WORDS)

[Effects of beta-adrenergic blocking with propranolol on the mechanisms of glucose regulation in the dog]. / Efectos del bloqueo beta-adrenérgico con propranolol sobre los mecanismos de regulación de la glucemia en el perro.

Propranolol (P) administration is known to cause hypoglycemia in insulin-dependent diabetic patients. The mechanisms whereby this response is produced remain controversial. Some authors postulate an inhibition in the beta-adrenergic action of catecholamines, responsible for hepatic glycogenolysis, while others indicate that these hormones are not so important in the regulation of blood sugar (BS) level. The present studies were undertaken to assess the mechanism whereby hypoglycemia is developed in the dog, with or without beta-adrenergic blockade. Unanesthetized male mongrel dogs were used, weighing 10-20 kg body wt., fed on dog chow pellets and water ad libitum up to 18-22 hours before the test performances. The dogs were randomly grouped into two groups, A and B in which the effect of P on several hormonal and metabolic responses basally and during insulin (I) test, were respectively studied. Group A was constituted by two subgroups of 6 animals each; the animals of one subgroup were beta-blocked, receiving P p.o. for 10 days (80 mg every 8 hours); the dogs of the remaining subgroup received only P excipient in the same way as the treated ones, for the same period. As P treatment was completed, blood samples were taken by venipuncture, in a peripheral vein, at 0 and 60 min. Some biological controls of beta-blockade, assessed at 0, 30 and 60 min, indicated that mean pulse rate (+/- SE) in the control dogs was 123 +/- 2, 128 +/- 2 and 128 +/- 3 beats/min while in the P treated ones was 106 +/- 2, 103 +/- 1 and 103 +/- 3 respectively.(ABSTRACT TRUNCATED AT 250 WORDS)

Efectos del bloqueo ß-adrenergico con propranolol sobre los mecanismos de regulación de la glucemia en el perro / Effects of ßeta-adrenergic blocking with propranolol about mechanisms of glucose regulation in the dog

Conociendo que el bloqueo ß-adrenérgico con propranolol (P) puede provocar cuadros hipoglucémicos en pacientes diabéticos insulino-dependientes, hemos analizado la respuesta de algunas variables hormonales (insulina (I) y cortisol (C) séricos, adrenalina (A) y noradrenalina (NA) plasmáticas) y metabólicas (glucemia y ácidos grasos libres (AGL) séricos) a la administración de esta droga a perros machos por la vía oral (dosis: 80 mg, 3 veces por día, durante 10 días) (grupo A) o endovenosa (dosis: 1 mg/Kg a -30 min) (grupo B), estudiándose en estos últimos, el comportamiento de dichas variables durante la hipoglucemia insulinica (HI). Se controló la frecuencia cardíaca como índice del bloqueo. Se obtuvieron muestras de sangre en condiciones basales en los perros del grupo A, a 0 y 30 min., y en los del grupo B a -30 y o min., continuandose durante la HI cada 30 min. por 2 horas. En los animales con bloqueo crónico, el P no afectó los niveles de glucemia, I sérica y catecolaminas plasmáticas, pero redujo los de AGL y C séricos cuando se los comparó con los respectivos controles. Durante la HI (grupo B), el tratamiento con P no afectó el comportamiento de la glucemia o de la insulinemia, observándose descensos en los niveles de AGL (p < 0,001) y C (p < 0,05) séricos junto con un aumento de la repsuesta adrenalínica a la hipoglucemia, al compararlos con los de los perros no bloqueados. Los resultados expuestos indican que el mecanismo ß-adrenérgico no desempeña un papel importante en la recuperación de la HI (AU)

Efectos del bloqueo ß-adrenergico con propranolol sobre los mecanismos de regulación de la glucemia en el perro / Effects of ßeta-adrenergic blocking with propranolol about mechanisms of glucose regulation in the dog

Conociendo que el bloqueo ß-adrenérgico con propranolol (P) puede provocar cuadros hipoglucémicos en pacientes diabéticos insulino-dependientes, hemos analizado la respuesta de algunas variables hormonales (insulina (I) y cortisol (C) séricos, adrenalina (A) y noradrenalina (NA) plasmáticas) y metabólicas (glucemia y ácidos grasos libres (AGL) séricos) a la administración de esta droga a perros machos por la vía oral (dosis: 80 mg, 3 veces por día, durante 10 días) (grupo A) o endovenosa (dosis: 1 mg/Kg a -30 min) (grupo B), estudiándose en estos últimos, el comportamiento de dichas variables durante la hipoglucemia insulinica (HI). Se controló la frecuencia cardíaca como índice del bloqueo. Se obtuvieron muestras de sangre en condiciones basales en los perros del grupo A, a 0 y 30 min., y en los del grupo B a -30 y o min., continuandose durante la HI cada 30 min. por 2 horas. En los animales con bloqueo crónico, el P no afectó los niveles de glucemia, I sérica y catecolaminas plasmáticas, pero redujo los de AGL y C séricos cuando se los comparó con los respectivos controles. Durante la HI (grupo B), el tratamiento con P no afectó el comportamiento de la glucemia o de la insulinemia, observándose descensos en los niveles de AGL (p < 0,001) y C (p < 0,05) séricos junto con un aumento de la repsuesta adrenalínica a la hipoglucemia, al compararlos con los de los perros no bloqueados. Los resultados expuestos indican que el mecanismo ß-adrenérgico no desempeña un papel importante en la recuperación de la HI

Efectos del bloqueo beta-adrenérgico con propranolol sobre los mecanismos de regulación de la glucemia en el perro. / [Effects of beta-adrenergic blocking with propranolol on the mechanisms of glucose regulation in the dog]

Propranolol (P) administration is known to cause hypoglycemia in insulin-dependent diabetic patients. The mechanisms whereby this response is produced remain controversial. Some authors postulate an inhibition in the beta-adrenergic action of catecholamines, responsible for hepatic glycogenolysis, while others indicate that these hormones are not so important in the regulation of blood sugar (BS) level. The present studies were undertaken to assess the mechanism whereby hypoglycemia is developed in the dog, with or without beta-adrenergic blockade. Unanesthetized male mongrel dogs were used, weighing 10-20 kg body wt., fed on dog chow pellets and water ad libitum up to 18-22 hours before the test performances. The dogs were randomly grouped into two groups, A and B in which the effect of P on several hormonal and metabolic responses basally and during insulin (I) test, were respectively studied. Group A was constituted by two subgroups of 6 animals each; the animals of one subgroup were beta-blocked, receiving P p.o. for 10 days (80 mg every 8 hours); the dogs of the remaining subgroup received only P excipient in the same way as the treated ones, for the same period. As P treatment was completed, blood samples were taken by venipuncture, in a peripheral vein, at 0 and 60 min. Some biological controls of beta-blockade, assessed at 0, 30 and 60 min, indicated that mean pulse rate (+/- SE) in the control dogs was 123 +/- 2, 128 +/- 2 and 128 +/- 3 beats/min while in the P treated ones was 106 +/- 2, 103 +/- 1 and 103 +/- 3 respectively.(ABSTRACT TRUNCATED AT 250 WORDS)