Feeding-unrelated factors influencing the plasma leptin level in ruminants.

The triglyceride content of lipid depots associated with the current feeding level is the primary determinant of leptin gene expression and the circulating leptin level. In laboratory rodents and primates the plasma leptin is influenced also by the age, gender and physiological status (puberty, pregnancy, lactation, postpartum period), and by the health condition such as sepsis due to Gram-negative (GN) bacteria. Some pathologic conditions with intensive cytokine release evoke an increase in plasma leptin, which is thought to depress the subsequent feed intake. However, the effect of these secondary factors may be species-dependent, with still unknown clinical relevance in ruminants. In our ovine and bovine models plasma leptin increased after castration and dexamethasone treatment, decreased after experimental administration of synthetic androgens in castrated rams, but remained unchanged throughout the ovarian cycle and after ovariectomy. The circulating leptin level increased temporarily during synthetic progestin (fluorogestone) treatment in ewes, but similar changes were not seen in progesterone-supplemented ewes and norgestomet-treated cows. In a second trial on dairy cows we wanted to study whether elevated plasma leptin levels are induced by experimental endotoxin mastitis, or by natural outbreak of GN mastitis and puerperal metritis. Experimental endotoxin mastitis resulted in some-hour elevation in cortisol and insulin, with a simultaneous decrease in IGF-I and thyroid hormones. In the first 14 days of lactation GN mastitis induced the same endocrine alterations as the experimental endotoxin challenge, but in natural cases these changes varied within a wider range, and were more protracted and robust. Cows with puerperal metritis had more obvious catabolic changes in the early weeks of lactation, than their healthy counterparts. However, both mastitis and puerperal metritis failed to increase the circulating leptin level, showing that in cows the plasma leptin is not responsible for the anorexia associated with these inflammatory diseases.

Massive goitre (struma parenchymatosa) in geese.

In a goose flock consisting of 2300 birds of 6 months of age severe goitre was diagnosed. To the best of our knowledge this is the first report of naturally occurring goitre in geese, which is not related to the feeding of rapeseed meal. The major pathological findings included retarded growth and plumage development, significantly (300%) increased relative thyroid weight, fat accumulation in the mesenteric and abdominal region, and lipid infiltration of liver and kidney cells. Subsequent hormone analysis showed undetectable thyroxine (T4) levels and a dramatic drop in triiodothyronine (T3) plasma levels of the diseased geese. Thyroidal histology displayed the typical signs of struma parenchymatosa. In order to get more information about the possible causes of the goitre, 10 geese from the affected farm were transferred into the laboratories of the Central Veterinary Institute. The geese were allotted into two groups. Group I received iodine supplementation for 55 days, while the other group served as sick control (Group S). Iodine treatment caused a dramatic improvement in the birds' clinical condition except in plumage growth in Group I, while the clinical and main pathological signs of goitre remained unchanged or worsened in the untreated Group S. Contrary to this, the serum levels of thyroid hormones and responsiveness to thyrotropin releasing hormone (TRH) improved not only in Group I but also in Group S. Almost euthyroid biochemical parameters were found after 55 days of iodine treatment in Group I and, surprisingly, a considerable improvement (especially in serum T3 levels) occurred also in Group S. These findings confirm the diagnosis of goitre but also call attention to the fact that iodine deficiency was not the only factor eliciting the disorder. The underlying possible goitrogenic substance could not be traced down.