Insulin response following intravenous glucose administration in dogs with obstructive jaundice

Yoshiya, Kenichi; Kishimoto, Takumi; Ishikawa, Yoshihiro; Utsunomiya, Joji

doi:10.1016/0022-4804(87)90081-3

Cited by 6 publications

(3 citation statements)

References 22 publications

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“…For this reason, the hyperglycaemia may have been related to glucose intolerance mediated by stress or exogenous glucocorticoids, rather than diabetes mellitus, by increasing gluconeogenesis and decreasing glucose utilisation in the peripheral tissues (Middleton & Watson 1985, Behrend & Kemppainen 1997. Another explanation for the hyperglycaemia could be the concomitant hepatopathy, accompanied by decreased glycogenesis and glucocorticoid clearance (Yoshiya et al 1987, Shaw & Ihle 1997.…”

Section: Discussionmentioning

confidence: 99%

Iatrogenic Hyperadrenocorticism in a Cat following a Short Therapeutic Course of Methylprednisolone Acetate

Ferasin

2001

Journal of Feline Medicine and Surgery

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Iatrogenic hyperadrenocorticism (or iatrogenic Cushing's syndrome) is an adrenal disorder that may result from long-term administration of glucocorticoids for therapeutic purposes, most often given to treat allergic or immune-mediated disorders. Prolonged treatment with synthetic glucocorticoids can suppress hypothalamic corticotrophin releasing hormone and plasma adrenocorticotrophic hormone (ACTH), thus causing a functional inactivity of the adrenal cortex. The result is a clinical syndrome of hyperadrenocorticism but with basal and ACTH-stimulated plasma cortisol concentrations that are consistent with spontaneous hypoadrenocorticism (Addison's disease). Whilst iatrogenic hyperadrenocorticism is relatively frequent in dogs, the diagnosis of iatrogenic hyperadrenocorticism in cats is very uncommon because this species has been found to be remarkably resistant to prolonged administration of glucocorticoids. To the author's knowledge, there are only two published clinical cases of feline iatrogenic Cushing's syndrome. This report describes a case of iatrogenic hyperadrenocorticism in a cat, and shows how normalisation of the adrenal function was achieved with supportive treatment and withdrawal of glucocorticoid administration.

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Section: Discussionmentioning

confidence: 99%

Iatrogenic Hyperadrenocorticism in a Cat following a Short Therapeutic Course of Methylprednisolone Acetate

Ferasin

2001

Journal of Feline Medicine and Surgery

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“…Although ob structive jaundice is related to a decrease in insulin response in peripheral blood, the mechanism of this decrease has not been established. Proposed mechanisms include an increase in insulin extraction in the liver [23,24] or in peripheral tissues [25],…”

Section: Discussionmentioning

confidence: 99%

Thromboxane A<sub>2</sub> Receptor Antagonist (ONO 3708) Protects from Liver Damage Induced by Cholestasis and Ischemia-Reperfusion

Haba

Kuroda²

1995

Eur Surg Res

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The effect of a thromboxane (Tx) A₂receptor antagonist, ONO 3708, on cholestasis and injury related to ischemia and subsequent reperfusion (I–R) was investigated in the dog liver by assessing changes in insulin and glucagon metabolism. The left hepatic duct was ligated for 4 weeks to create a cholestatic lobe. Sixty-minute ischemia was induced by Pringle’s procedure. ONO 3708 (200 µg/kg/min) was initiated 60 min before induction of ischemia and continued throughout the experiment. The rate of insulin metabolism was higher in the right noncholestatic lobe than in the left cholestatic lobe. There was no significant difference in the rate of glucagon metabolism between the right and left lobes. After induction of I–R, the rate of insulin metabolism, but not glucagon metabolism, decreased. The lipid peroxide level was higher and the glutathione level was lower in the cholestatic lobe than in the noncholestatic lobe. There was no significant difference in the α-tocopherol level between lobes. After induction of I–R, the lipid peroxide level increased and the α-tocopherol level decreased. There was no change in the glutathione level. I–R accelerated the release of 6-keto-prostaglandin (PG) F_1α, a stable metabolite of PGI2, and of TxB₂ a stable metabolite of TxA₂, from the liver. After I–R, cholestasis accelerated the release of TxB₂, but not 6-keto-PGFι_α. I–R also increased the TxTSyö-keto-PGF_1α ratio. ONO 3708 reduced these metabolic changes in the cholestasis and after I–R. These findings suggest that ONO 3708 protects liver function, especially in the cholestatic lobe, from I–R-related injury by reducing peroxidation of lipids and the TXA2/PGI₂ ratio, which predicts cellular damage, and by increasing levels of α-tocopherol and glutathione.

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“…Plasma insulin concentrations have been reported to be decreased in bile duct-ligated (BDL) dogs (13,17,25). Some morphological changes of pancreatic islet cells in BDL dogs have been demonstrated (17), and secretory response of the pancreatic ␤-cell to cholecystokinin showed deterioration in perfused pancreas in situ in BDL dogs (13).…”

mentioning

confidence: 99%

Lack of effect of incretin hormones on insulin release from pancreatic islets in the bile duct-ligated rats

Niwa

Nimura

Niki³

2001

American Journal of Physiology-Endocrinology and Metabolism

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Hyperglycemia associated with obstructive jaundice seriously affects the prognosis of patients with hepatobiliary diseases. We investigated secretory properties of isolated islets from bile duct-ligated (BDL) rats. Pancreatic islets from BDL rats lost their secretory responses to glucagon-like peptide-1 (GLP-1), although their responses to glucose were normal. Loss of potentiation of insulin release was also observed in glucagon and glucose-dependent insulinotropic peptide (GIP), whereas modulation of the release by forskolin, dibutyryl cAMP, or epinephrine remained unaffected. cAMP production by BDL islets was not increased by these insulinotropic hormones. Serum levels of glucagon, but not GIP, were increased in BDL rats. GLP-1 levels were also elevated, although they did not reach statistical significance. Immunoblotting of trimeric G protein subunits demonstrated that G(s)alpha L and G(s)alpha S, but not G(i)alpha 1/2 and G(i)alpha 3/o alpha, were less expressed in BDL islets. Therefore, unresponsiveness of the beta-cell to cAMP-raising hormones is involved in glucose intolerance under cholestasis. It results from diminished expression of alpha-subunits of the relevant G protein, G(s), and desensitization of receptors of these hormones.

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Insulin response following intravenous glucose administration in dogs with obstructive jaundice

Cited by 6 publications

References 22 publications

Iatrogenic Hyperadrenocorticism in a Cat following a Short Therapeutic Course of Methylprednisolone Acetate

Iatrogenic Hyperadrenocorticism in a Cat following a Short Therapeutic Course of Methylprednisolone Acetate

Thromboxane A<sub>2</sub> Receptor Antagonist (ONO 3708) Protects from Liver Damage Induced by Cholestasis and Ischemia-Reperfusion

Lack of effect of incretin hormones on insulin release from pancreatic islets in the bile duct-ligated rats

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