Methimazole-induced hypothyroidism is a clinical problem in the treatment of hyperthyroidism in people and animals and is an example of metabolic disease that can lead to fertility disorders and can give elastographic testicular changes. Ultrasound elastography using the Esaote MyLab Twice ultrasound system and a morphological examination of testes were performed in seven methimazole-administered (group E) and seven healthy rats (group C). The elasticity ratio of strains in the scrotal wall of the near-field test area to testicular tissue (ELX-T-RAT) and hardness percentage of strained tissues in the defined area of a testicle (ELX-T%HRD) in group E were statistically significantly lower than in group C. The degree of spermatogenesis was statistically significantly higher in group E than in group C and similarly seminiferous tubule diameters in group E were statistically significantly higher than in group C. Body weight and testicular weight in group E were statistically significantly lower than in group C. Changes in the elastographical parameters of testes may result from disorders secondary to hypothyroidism. The usefulness of elastography is noteworthy in the case of evaluation of testis function in patients with some metabolic disorders.

Introduction: The clinical symptoms of portosystemic shunts (PSSs) and hepatic microvascular dysplasia (HMD) – portal vein hypoplasia (PVH) in dogs are similar. PSSs are abnormal vascular connections between the portal vein system and systemic veins. HMD is a very rare developmental vascular anomaly, recognisable during histopathological examination. The study aim was to assess the prevalence of HMD–PVH and hepatocellular and vascular pathologies in the liver. Material and Methods: Liver biopsies from 140 dogs (of different breeds and both sexes) arousing clinical suspicion of PSS were examined histopathologically. Results: An initial PSS diagnosis was confirmed in 125 dogs (89.29%). HMD–PVH was found in 12.32% of dogs, as an isolated disease in 9.29%, especially in Yorkshire terriers, and with extrahepatic PSS in 6.67%. Histopathological analysis of muscles around sublobular veins showed that HMD cases presented hypertrophy or hypertrophy with fibrosis. In 2.17% of all dogs with liver vascular developmental disorders calcification was visible around vessels (without correlation by degenerative changes in those vessels), suggesting prior onset of deep metabolic disorders. Clinical suspicion of PSS was also formed upon quite different pathological processes in young dogs. Conclusion: Histopathological findings diagnosed the type of vascular anomalies (PSS or HMD–PVH) or other pathological changes conclusively, therefore detailed hepatic histopathology is an indispensable component of the clinical diagnostic process.

Objective: To characterize adiponectin protein complexes in lean and obese horses. Animals: 26 lean horses and 18 obese horses. Procedures: Body condition score (BCS) and serum insulin activity were measured for each horse. Denaturing and native western blot analyses were used to evaluate adiponectin complexes in serum. A human ELISA kit was validated and used to quantify high–molecular weight (HMW) complexes. Correlations between variables were made, and HMW values were compared between groups. Results: Adiponectin was present as a multimer consisting of HMW (> 720-kDa), low-molecular weight (180-kDa), and trimeric (90-kDa) complexes in serum. All complexes were qualitatively reduced in obese horses versus lean horses, but the percentage of complexes < 250 kDa was higher in obese versus lean horses. High–molecular weight adiponectin concentration measured via ELISA was negatively correlated with serum insulin activity and BCS and was lower in obese horses (mean ± SD, 3.6 ± 3.9 μg/mL), compared with lean horses (8.0 ± 4.6 μg/mL). Conclusions and Clinical Relevance: HMW adiponectin is measurable via ELISA, and concentration is negatively correlated with BCS and serum insulin activity in horses. A greater understanding of the role of adiponectin in equine metabolism will provide insight into the pathophysiology of metabolic disease conditions.

Nursing sickness, the largest single cause of mortality in adult female mink (Mustela vison), is an example of a metabolic disorder, which develops when the demands for lactation require extensive mobilization of body energy reserves. The condition is characterized by progressive weight loss, emaciation, and dehydration with high concentrations of glucose and insulin in the blood. Morbidity due to nursing sickness can be as high as 15% with mortality around 8%, but the incidence is known to vary from year to year. Stress has been shown to trigger the onset of the disease and old females and females with large litters are most often affected. Increasing demand for gluconeogenesis from amino acids due to heavy milk production may be a predisposing factor. Glucose metabolism is inextricably linked to that of protein and fats. In obesity (or lipodystrophy), the ability of adipose tissue to buffer the daily influx of nutrients is overwhelmed (or absent), interfering with insulin-mediated glucose disposal and leading to insulin resistance. Polyunsaturated fatty acids of the n-3 family play an important role in modulating insulin signalling and glucose uptake by peripheral tissue. The increasing demand on these fatty acids for milk fat synthesis towards late lactation may result in deficiency in the lactating female, thus impairing glucose disposal. It is suggested that the underlying cause of mink nursing sickness is the development of acquired insulin resistance with 3 contributing key elements: obesity (or lipodystrophy), n-3 fatty acid deficiency, and high protein oxidation rate. It is recommended that mink breeder females be kept in moderate body condition during fall and winter to avoid fattening or emaciation. A dietary n-3 fatty acid supplement during the lactation period may be beneficial for improved glycemic control. Lowering of dietary protein reduces (oxidative) stress and improves water balance in the nursing females and may, therefore, prevent the development and help in the management of nursing sickness. It is also surmised that other, thus far unexplained, metabolic disorders seen in male and female mink may be related to acquired insulin resistance.

Ethionine, an analogue of methionine, induces fatty liver in rats by inhibiting protein synthesis, including that of apolipoproteins in liver. Ethionine was administered to cows to elucidate the participation in fatty liver development of impaired triglyceride secretion from liver attributable to decreased apolipoprotein synthesis. The administration resulted in a significant increase of liver triglyceride contents. Several apolipoproteins were found to have decreased concentrations. In particular, apolipoprotein B-100 in very low-density (0.95 to 1.006 g/ml) lipoprotein and in low-density (1.006 to 1.063 g/ml) lipoprotein fractions was greatly reduced. The decreases of apolipoprotein B-100 concentrations in the 2 lipoprotein fractions were at least partly correlated to the decreased triglyceride concentrations in the respective fractions. Decreased concentrations of apolipoprotein A-I in high-density (1.063 to 1.210 g/ml) lipoprotein were also observed, although not as distinctly as with apolipoprotein B-100. Total cholesterol and phospholipid concentrations in low- and high-density lipoprotein fractions were decreased. The decrease in cholesterol was attributed to reduced concentrations of cholesteryl esters. It was suggested that the impaired lipid secretion from liver attributable to the decreased apolipoprotein concentrations has a role in ethionine-induced fatty liver of cows.

To test the acidifying ability of the distal portion of the nephrons in healthy dogs, 0.2 g of NH4Cl/kg of body weight was given PO. Samples for venous blood gas analysis and urine pH were taken hourly for 6 hours. Systemic acidemia developed, as evidenced by statistically significant (P less than 0.05) decrease in blood pH 1 hour after NH4Cl administration. Four hours after administration, mean urine pH decreased to a low of 5.16 +/- 0.1 and was less than 5.5 3 hours after administration. Changes in urine pH 2 hours after administration were statistically significant (P less than 0.05). In human beings, NH4Cl loading is used to detect patients with distal renal tubular acidosis (defective hydrogen ion secretion by the distal nephrons) and normal acid/base values. Distal renal tubular acidosis is diagnosed if urine pH fails to decrease to less than 5.5 after NH4Cl administration. On the basis of findings of this study, a similar value would be valid for dogs.

Nitrofurazone solution containing 0.2% nitrofurazone and 99.8% polyethylene glycol was given to 4 healthy horses (2 L in 2 L of lactated Ringer solution, intraperitoneally). Horses developed hypovolemia, hyperosmolality, and mixed respiratory and metabolic acidosis. These changes were largely attributable to polyethylene glycol, but a contribution of nitrofurazone cannot be excluded. Intraperitoneal infusion of nitrofurazone solution in horses is contraindicated.

Hypophosphatemia was induced in 2 cows by reducing phosphorus content in their feed after parturition. Serum inorganic phosphorus (Pi) values decreased to 1 mg/dl within 10 days after parturition; and RBC adenosine 5'-triphosphate (ATP) and reduced glutathione values decreased to 50 and 70% of baseline values, respectively. Methemoglobin concentration was moderately higher than normal. These changes preceded the onset of hemolysis, and anemia progressed with decreases in PCV, hemoglobin concentration, and RBC counts. Serum Pi resumed its normal value when anemia was most severe. This RBC disorder was confirmed to be characteristic of hemolytic anemia in cows resulting from hypophosphatemia. The RBC glycolytic intermediates, totaal trisoe phosphate (combined glyceraldehyde-3-phosphate and dihydroxyacetone phosphate content) and fructose-1, 6-diphosphate, greatly increased in vivo and in vitro with decreases in serum or plasma Pi and RBC ATP. From our results, we concluded that inadequate Pi in the plasma impairs the function and viability of RBC by hindering the production of ATP via disturbance of reactions at the glyceraldehyde-3-phosphate dehydrogenase step.