Effects of ovine growth hormone and other anterior pituitary hormones on lipolysis of rat and ovine adipose tissue in vitro.

Ovine growth hormone ( oGH ) was tested for its effects on lipolysis of rat and ovine adipose tissue in vitro. Ovine growth hormone at 1, 5 and 25 micrograms/ml stimulated lipolysis (P less than .05) of chopped rat adipose tissue and isolated rat adipocytes incubated in the presence of 100 mU/ml adenosine deaminase and .2 micrograms/ml dexamethasone, but had no effect on lipolysis of chopped ovine adipose tissue or isolated ovine adipocytes. Isoproterenol, a beta-adrenergic agonist, stimulated lipolysis (P less than .05) of both rat and ovine adipose tissue. Contaminants of the oGH preparation used were examined for lipolytic effects. Thyroid-stimulating hormone (TSH), luteinizing hormone (LH) and adrenocorticotropic hormone (ACTH) content in oGH were measured by radioimmunoassay. When quantities of these hormones contaminating 5 and 25 micrograms oGH were tested for lipolysis in rat adipose tissue, the TSH contamination could account for some (30%) of the lipolysis observed with oGH , while the other hormones had no effect. Also, preincubation of oGH with anti-GH, but not with anti-TSH or anti-LH, removed the principle in oGH responsible for the lipolytic effect on rat adipose tissue.(ABSTRACT TRUNCATED AT 250 WORDS)

Effects of exogenous growth hormone and diethylstilbestrol on growth and carcass composition of growing lambs.

An 8-wk growth trial was conducted to assess the effects of ovine growth hormone (oGH; 7 mg/d, sc) on growth performance and carcass composition of normal, growing wether lambs. Diethylstilbestrol (DES; .1 mg/d, sc) and control lambs were included for comparisons. Plasma oGH levels at 8 wk were 1.9, 5.5 (P less than .05) and 138.1 ng/ml (P less than .001) for controls, DES and oGH lambs, respectively. Diethylstilbestrol did not increase plasma oGH until the fourth week. The oGH improved feed conversion 7.4% (FC; P less than .05), but did not alter average daily gain (ADG) or feed intake (ADF). Diethylstilbestrol increased ADG 15.3% (P less than .05) and improved FC 16.1% (P less than .01), with no effect on ADF. The primary effect of oGH on carcass composition was to decrease the quantity of fat 8.9% (P less than .05). In addition, oGH may have increased protein 6.5% (P less than .10) and moisture 4.0% (not significant). Diethylstilbestrol increased the quantity of carcass protein 10% (P less than .01) and moisture 8.7% (P less than .05), with no effect on fat. In these studies, the primary effect of exogenous oGH on normal, growing lambs was to reduce carcass fat, which may account for the observed improvement in FC. Diethylstilbestrol, at 1/70th of the oGH dose, was superior to oGH for improving FC (P less than .05) and ADG (P less than .10). Improvements in body weight of the lambs given DES were observed 2 wk before an increase in plasma oGH. In addition, DES, unlike exogenous oGH, did not alter the quantity of carcass fat. These observations do not support the concept that the mode of action of DES is through increased GH secretion.

Thiopeptin for the prevention of ovine lactic acidosis induced by diet change.

Inclusion of thiopeptin, a sulfur-containing peptide antibiotic, at 0, 2.75, 5.5, 8.25, 11 and 22 ppm in the feed was evaluated in 8-week growth trials with 252 lambs. An abrupt diet shift to micronized milo at the start of the trials was used to provide a lactic acidosis challenge. Five of 78 control lambs died within 48 hr after the challenge. In lambs fed diets containing thiopeptin at levels of 11 ppm or more, there was no evidence of lactic acidosis. Lambs given thiopeptin at 11 ppm or more ate 11% more (P less than .05) and gained 20% more (P less than .05) than controls during the 8-week trial. Most of the improvement occurred during the first 2 weeks. Incidence of death was lower among lambs given thiopeptin at 2.75 to 8.25 ppm, but these animals showed no improvement in performance. In another study, abruptly shifting lambs to the micronized milo diet was found to provide an acute lactic acidosis challenge. After the shift, four of eight lambs developed ruminal lactic acidosis, with one dying of systemic lactic acidosis, with one dying of systemic lactic acidosis when plasma lactate exceeded 20 mumoles/ml. In affected lambs, ruminal lactate increased rapidly from an initial level of .2 mumoles/ml to over 130 mumoles/ml within 12 hr of consumption of the milo. Ruminal lactate returned to normal levels of less than 1 mumole/ml by 30 hr in lambs that recovered. High ruminal concentrations of lactate reduced total volatile fatty acids (VFA), and ruminal pH reflected total ruminal acids. Lactic acidosis did not occur in eight lambs after the switch to micronized milo when thiopeptin was included in the feed at 22 ppm. Ruminal lactate was reduced by 68% (P less than .01) and total ruminal VFA increased by 33% (P less than .05) in lambs fed thiopeptin in comparison with average levels in all controls.

Control of wheat-induced lactic acidosis in sheep by thiopeptin and related antibiotics.

Thiopeptin, thiopeptin-like antibiotics and penicillin were shown previously to be highly active in vitro against Streptococcus bovis, the microorganism believed to be responsible for the initiation of ruminal lactic acidosis. The purpose of this work was to determine the efficacy of these antibiotics in preventing lactic acidosis in lambs challenged by intraruminal administration of ground wheat. Lambs, which were fasted and then given ground wheat at 40 g/kg body weight, showed dramatic increases in rumen and plasma lactate over the 30-hr experimental period. Rumen lactate increased from .2 to peak levels of approximately 150 mumoles/ml by 8 to 10 hr after wheat administration. Plasma lactate increased after rumen lactate was elevated and lambs succumbed when plasma levels exceeded 15 mumoles/ml. Ruminal volatile fatty acids were greatly reduced as rumen lactate increased. Over half of the lambs given ground wheat died within 30 hours. Thiopeptin given as a single dose completely prevented lactic acidosis by reducing rumen lactate 80 to 90%. In addition, thiopeptin permitted "normal" rumen fermentation to continue as indicated by a significant increase in volatile fatty acids. The minimum effective dose of thiopeptin to control acute lactic acidosis was .18 mg/kg body weight. Other members of the thiopeptin class, including sulfomycin, sporangiomycin, siomycin and taitomycin, prevented lactic acidosis in a manner similar to thiopeptin. Penicillin, however, inhibited ruminal volatile fatty acid production as well as lactate synthesis. In addition, the effective period for penicillin in the rumen was only 8 to 16 hr, after which lactate fermentation was reestablished. Thus, thiopeptin and thiopeptin-like antibiotics, but not penicillin, appear to provide prophylactic treatment against lactic acidosis in sheep.