Effects of somatotropin and substrates on patterns of liver metabolism in lactating dairy cattle

• Published in: Journal of dairy science Vol. 75; no. 4; p. 1025
• Main Authors: Knapp, J R, Freetly, H C, Reis, B L, Calvert, C C, Baldwin, R L
• Format: Journal Article
• Language: English
• Published: United States 01-04-1992
• Subjects: Acetates - metabolism; Animals; Cattle - metabolism; Cattle - physiology; Culture Techniques; Female; Gluconeogenesis; Growth Hormone - pharmacology; Lactation - drug effects; Lactation - metabolism; Liver - drug effects; Liver - metabolism; Liver Glycogen - metabolism; Oxidation-Reduction; Propionates - metabolism; Pyruvates - metabolism; Random Allocation; Recombinant Proteins - pharmacology
• ISSN: 0022-0302
• DOI: 10.3168/jds.S0022-0302(92)77846-1

Objectives of this study were to quantitate metabolite fluxes in ruminant liver and to delineate effects of recombinant bST on patterns of nutrient metabolism by liver. Nineteen multiparous cows ranging in previous lactational performance from 6400 to 13,500 kg per 305-d lactation were treated with either placebo or bST (40 mg/d) from wk 11 to 18 of lactation. Liver tissue was collected at slaughter. Tissue slices were incubated with various 14C-labeled substrates, and rates of conversion of label to CO2 and metabolites were measured. In vivo recombinant bST treatment increased in vitro conversion of [1-14C]propionate and [2-14C]acetate to glucose more than twofold. At 2.5 mM propionate, bST-treated cows converted propionate to glucose at 90% efficiency. Recombinant bST increased [14C]bicarbonate incorporation into glucose five-fold. Overall, bST treatment resulted in greater C flow from propionate and acetate through the TCA cycle. Acetate had only small effects on propionate metabolism and no effects on lactate plus pyruvate metabolism. Unexpectedly, propionate decreased acetate conversion to ketone bodies. Suggested mechanisms for this observation include depletion of coenzyme A and allosteric regulation of carnitine palmitoyltransferase I by methylmalonyl-coenzyme A formed from propionate. In summary, bST treatment resulted in increased rates of gluconeogenesis and oxidation in liver in support of lactation.