Developmental programming: impact of prenatal testosterone excess on insulin sensitivity, adiposity, and free fatty acid profile in postpubertal female sheep.

Prenatal T excess causes reproductive and metabolic disruptions including insulin resistance, attributes of women with polycystic ovary syndrome. This study tested whether increases in visceral adiposity, adipocyte size, and total free fatty acids underlie the insulin resistance seen in prenatal T-treated female sheep. At approximately 16 months of age, insulin resistance and adipose tissue partitioning were determined via hyperinsulinemic euglycemic clamp and computed tomography, respectively, in control and prenatal T-treated females. Three months later, adipocyte size and free fatty acid composition were determined. Results revealed that at the postpubertal time points tested, insulin sensitivity was increased, visceral adiposity and adipocyte size in both the sc and the visceral compartments were reduced, and circulating palmitic acid was increased in prenatal T-treated females relative to controls. In parallel studies, 20-month-old prenatal T-treated females tended to have increased basal insulin to glucose ratio. Relative to earlier findings of reduced insulin sensitivity of prenatal T-treated females during early life and adulthood, these findings of increased insulin sensitivity and reduced adiposity postpubertally are suggestive of a period of developmental adaptation. The disruption observed in free fatty acid metabolism a few months later correspond to a time point when the insulin sensitivity indices of prenatal T-treated animals appear to shift toward insulin resistance. In summary, current findings of improved insulin sensitivity and reduced visceral adiposity in postpubertal prenatal T-treated sheep relative to our earlier findings of reduced insulin sensitivity during early postnatal life and adulthood are indicative of a period of developmental adaptation.

Computed tomographic and magnetic resonance imaging features of canine segmental caudal vena cava aplasia.

OBJECTIVE: To describe the computed tomographic and magnetic resonance imaging features of segmental caudal vena cava aplasia and associated vascular anomalies in dogs. METHODS: A retrospective study was performed reviewing computed tomographic and magnetic resonance imaging archives of eight institutions for dogs with segmental caudal vena cava aplasia. Inclusion criteria included a computed tomographic or magnetic resonance imaging study and supportive diagnostic and follow-up information. Abdominal vessels were reviewed for size, shape, location and course (including tributaries and branches) and classified as normal, abnormal or shunt vessels. RESULTS: Ten dogs with segmental caudal vena cava aplasia were identified. In all dogs, postrenal caval blood was shunted to either a right or a left azygos vein, with seven different angiographic patterns. Affected dogs were predominantly female (70 per cent) and young (mean 2.6 years). Additional portocaval and porto-azygos shunt vessels were identified in two cases each. Computed tomographic angiography and magnetic resonance angiography depicted details of abdominal vessels including thrombus formation in one dog. CLINICAL SIGNIFICANCE: Segmental caudal vena cava aplasia is a vascular congenital anomaly in the dog that can be associated with thrombosis and portosystemic shunts. Computed tomographic angiography and magnetic resonance angiography are excellent tools to demonstrate the complex vascular anatomy and to guide treatment planning for portosystemic shunts and thrombolytic therapy.

Evaluation of foot pain in the standing horse by magnetic resonance imaging.

The records of 41 horses with previously undiagnosed foot pain that had been examined by standing magnetic resonance imaging were reviewed and follow-up information was obtained from their owners two years after the examination. A range of soft tissue and osseous abnormalities were identified, with multiple lesions frequently occurring. Deep digital flexor tendonitis was recorded in 12 of the horses, and distension of the distal interphalangeal joint was identified in 15, but it was not always associated with lameness; in contrast, distension of the navicular bursa was always associated with lameness in the seven affected horses. Navicular bone lesions were identified in 13 of the horses, often in the absence of radiographic changes. Follow-up information was obtained for 35 of the horses, 27 of which were alive; of these, 16 had returned to their previous level of performance. Of the five horses with navicular bursal changes, four had been euthanased owing to lameness and the other had returned to work at a reduced level.