Expression of leptin and its receptors in various tissues of ruminants

The energy metabolism of domestic animals is under the control of hormonal factors, which include thyroid hormones and leptin. Leptin signals from the periphery to the centre. It is mostly produced in the white adipose tissue and informs the central nervous system (CNS) about the total fat depot of the body. Low and high levels of leptin induce anabolic and catabolic processes, respectively. Besides controlling the food uptake and energy expenditure leptin is also involved in regulation of the reproduction and the immune system. Leptin is produced in several tissues other than fat. In the present paper the leptin expression of ruminant (Egyptian water buffalo, cow, and one-humped camel) tissues are examined. The mammary gland produces leptin in each species investigated. The local hormone production contributes to milk leptin and most probably helps to maintain lactation. Considerable leptin receptor expression was observed in the milk-producing epithelial cells, which is the same cell type that produces most of the udder leptin. Based on the results tissues participating in production have an autoregulative mechanism through which tissues can be relatively independent of the plasma leptin levels in order to maintain the desired function.     

Thyroid hormone metabolism in the brain of domestic animals

The action of thyroid hormones in the brain is strictly regulated, since these hormones play a crucial role in the development and in the physiological functioning of the central nervous system. It has been shown by many authors that brain tissue represents a special site of thyroid hormone handling. A relative independence of this tissue of the actual thyroid status was shown by our research group in birds and mammals. Hypothyroid animals can maintain a close to normal level of triiodothyronine in the brain tissue for extended periods. This phenomenon is due to at least three regulating mechanisms. (1) Uptake of thyroid hormones is enhanced. It was shown that the uptake by the telencephalon of labelled triiodothyronine (T3) was much higher in thyroidectomized (TX) animals than in controls or in thyroidectomized and T3 supplemented ones. (2) Conversion of thyroxine into triiodothyronine is increased. One of the most important elements of this process is the adjustment of the expression and activity of the type II deiodinase of the brain to a higher level. Enzyme kinetic studies, expression of TRalpha and beta nuclear thyroid hormone receptors and--after cloning the chicken type II deiodinase--in situ hybridization studies clearly supported the central role of the conversion process. (3) The rate of loss of triiodothyronine from the brain tissue is slowed down under hypothyroid conditions as evidenced by our hormone kinetic studies.     

Increased sensitivity to triiodothyronine (T3) of broiler lines with a high susceptibility for ascites

1. In the studies reported here, broiler lines divergently selected for susceptibility to ascites under low temperature conditions were tested for their sensitivity to 3,3’,5‐triiodothyronine (T3) with respect to growth rate, rate of mortality, plasma concentrations of T3, right ventricular hypertrophy (RVH) and incidence of ascites.

2. Mean body weight of the ascites‐susceptible line (BC‐line) was higher than that of the ascites‐resistant line (A‐line). Adding 0.5 mg T₃/kg of the diet depressed growth rate to the same extent in both lines. The effect of T3 on growth was more pronounced for males than for females.

3. T3‐supplementation increased the relative weight of the heart and the incidence of RVH to the same extent in both lines. More of the T3‐treated BC‐line chickens had fluid accumulation in the abdominal cavity than the T3‐treated A‐line chickens.

4. Dietary T3‐treatment depressed the plasma concentration of growth hormone (GH) profoundly and insulin‐like growth factor (IGF‐I) slightly but to the same extent in both lines. The coefficient of variation of GH concentrations indicate that T3 treatment mainly decreased GH‐pulsatility in young growing broilers.

5. Higher doses of dietary T3 (1 and 2 mg/kg) increased mortality in a dose‐dependent manner. With 2 mg T₃/kg, mortality in the BC‐line was almost double that in the A‐line.

6. These studies indicate that the development of ascites could be linked with thyroid function. Moreover, dietary T3 supplementation could be used to help identify ascites‐inducing factors or genetic lines with differential sensitivity for ascites.