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The incretin glucagon-like peptide 1 (GLP-1) enhances insulin secretion. The aim of this study was to assess GLP-1, glucose and insulin concentrations, Homeostatic Model Assessment (HOMAinsulin sensitivity and HOMAβ-cell function) in dogs with pituitary-dependent hyperadrenocorticism (PDH), and compare these values with those in normal and obese dogs. The Oral Glucose Tolerance Test was performed and the glucose, GLP-1 and insulin concentrations were evaluated at baseline, and after 15, 30, 60 and 120 minutes. Both basal concentration and those corresponding to the subsequent times, for glucose, GLP-1 and insulin, were statistically elevated in PDH dogs compared to the other groups. Insulin followed a similar behaviour together with variations of GLP-1. HOMAinsulin sensitivity was statistically decreased and HOMAβ-cell function increased in dogs with PDH. The higher concentrations of GLP-1 in PDH could play an important role in the impairment of pancreatic β-cells thus predisposing to diabetes mellitus. [ABSTRACT FROM AUTHOR]

Abstract: Diabetes is often associated with pituitary-dependent hyperadrenocorticism (PDH). Hypercortisolism causes insulin resistance and affects β-cell function. The purpose of this study was to test if daily administration of a long-acting insulin analogue during the first month of anti-PDH treatment can prevent progress to diabetes in these animals. Twenty-six PDH dogs were divided into three groups: one group with glycaemia <5.83mmol/L and two groups with glycaemia >5.83mmol/L and <9.35mmol/L, one of which received insulin detemir during 4months. Dogs with glycaemia <5.83mmol/L and those with glycaemia >5.83mmol/L which received insulin did not develop diabetes. In the non-insulin group, 6/7 dogs developed diabetes after the third month. There is a 13-fold higher risk of diabetes in dogs with glycaemia >5.83mmol/L and no insulin treatment. Administering insulin detemir to dogs with PDH and glycaemia >5.83mmol/L could prevent progression to diabetes. [Copyright &y& Elsevier]

Abstract: Pituitary-dependent hyperadrenocorticism (PDH) is frequent in dogs. Little is known about its presentation in different age groups and its characteristics. Dividing the population under study (n =107) into three age groups we observed that 11.2% were young, 51.4% adults and 37.4% aged. Using magnetic resonance, pituitary tumours were intra-sellar (IS) in 30.8% and extra-sellar (ES) in 62.6% and the pars intermedia (PI) was affected in 6.5%. ES are predominant in females and IS in males (p <0.0001). In the adult-aged population, the ES and PI are predominant, while in the young, the IS predominate (p <0.0001). ACTH concentration was greater in the ES vs. IS (p <0.05). α-MSH did not present significant differences according to tumour size, showing a negative correlation (r =−0.47; p <0.01) vs. ACTH. Differences in adenoma size according to gender and their age-related frequency of apparition could be because of different origins of the corticotrophinoma. [Copyright &y& Elsevier]

Objective– To describe a case of spontaneous pneumothorax secondary to pulmonary thromboembolism possibly associated with pituitary dependent hyperadrenocorticism. Case Summary– A 7-year-old spayed female Collie weighing 26 kg was referred for evaluation of spontaneous pneumothorax. An exploratory thoracotomy was performed and revealed 2 lung lobes to be diffusely hemorrhagic and they were resected. Histologic examination of multiple sections documented diffuse thromboembolism. A 2–3 cm thrombus was visualized distal to the bifurcation of the pulmonary artery during an echocardiographic examination postoperatively. The dog was discharged to the owner after recovery from surgery. The thrombus had resolved at the 4-week recheck examination. Diagnosis of pituitary dependent hyperadrenocorticism was confirmed based on follow-up endocrine testing. New or Unique Information Provided– This is the first report of pulmonary thromboembolism causing spontaneous pneumothorax in the dog. [ABSTRACT FROM AUTHOR]

Abstract: Pituitary-dependent hyperadrenocorticism (PDH) in dogs is caused by a pituitary corticotroph adenoma. Although PDH is a common disorder in dogs, little is known about the underlying pathogenesis. In the pituitary glands of humans and mice, the pro-opiomelanocortin (POMC)-expressing cell lineages, the corticotrophs and melanotrophs, have a specific marker in common, the T-box transcription factor Tpit (Tbx19), which is obligate for POMC expression. Tpit also regulates the late differentiation of the corticotrophs and melanotrophs, and therefore may contribute to the pathogenesis of the corticotroph adenomas. The aim of this study was to perform an expression and mutation analysis of Tpit in the normal canine pituitary and in corticotroph adenomas. The distribution of the Tpit protein in the pituitary gland was studied with immunohistochemistry and the expression of the gene with RT-PCR. The coding region of Tpit cDNA from 14 dogs with PDH was screened for mutations. Tpit was expressed in corticotroph and melanotroph cells of the normal and adenomatous canine pituitary, and remained present in non-adenomatous corticotrophs of pituitaries from PDH dogs. No tumor-specific mutation in the Tpit cDNA from the corticotroph adenomas was found. However, a missense polymorphism in the highly conserved DNA-binding domain, the T-box, was discovered in one dog. It is concluded that Tpit can be used as a reliable marker for the corticotroph and melanotroph cells in the canine pituitary tissue and that mutations in the Tpit gene are unlikely to play a major role in the pathogenesis of canine corticotroph adenomas. [Copyright &y& Elsevier]

Background Trilostane is commonly used in the treatment of dogs with naturally occurring pituitary-dependent hyperadrenocorticism ( PDH). Dose recommendations have varied from the manufacturer and the literature. Hypothesis As body weight increases, dose/kg or dosage/day of trilostane required to control the clinical signs of PDH decreases. Animals 70 dogs with naturally occurring hyperadrenocorticism. Methods Retrospective study. Each dog must have been treated for at least 6 months and should have shown a 'good response' to trilostane, as determined by owners. Statistical comparisons of dose and dosage were made after the dogs were separated into groups weighing <15 or >15 kg; groups weighing ≤10, 10.1-20, 20.1-30, and ≥30 kg; and then groups based on body surface area versus dose/kg and total amount of trilostane required to control the condition. Results There was no significant difference in trilostane dose in mg/kg of body weight or in the total amount of trilostane required daily to control clinical signs, except when the dose for dogs weighing >30 kg was compared with that for the other groups. However, despite lack of statistical significance when comparing groups, there was a significant trend using polynomial regression analysis, suggesting that as body weight increases, the amount of trilostane (mg/kg/dose as well as mg/kg/daily dosage) required to control clinical signs decreases. Conclusions and Clinical Importance Dogs weighing >30 kg, and possibly those weighing >15 kg, might require smaller amounts of trilostane per dose or per day than those weighing less, to control PDH-associated clinical signs. [ABSTRACT FROM AUTHOR]