Effect of reducing milk production using a prolactin-release inhibitor or a glucocorticoid on metabolism and immune functions in cows subjected to acute nutritional stress

Abstract

When cows are unable to consume enough feed to support milk production, they often fall into severe negative energy balance. This leads to a weakened immune system and increases their susceptibility to infectious diseases. Reducing the milk production of cows subjected to acute nutritional stress decreases their energy deficit. The aim of this study was to compare the effects on metabolism and immune function of reducing milk production using quinagolide (a prolactin-release inhibitor) or dexamethasone in feed-restricted cows. A total of 23 cows in early/mid-lactation were fed for 5 d at 55.9% of their previous dry matter intake to subject them to acute nutritional stress. After 1 d of feed restriction and for 4 d afterward (d 2 to 5), cows received twice-daily i.m. injections of water (control group; n=8), 2mg of quinagolide (QN group; n=7), or water after a first injection of 20mg of dexamethasone (DEX group; n=8). Feed restriction decreased milk production, but the decrease was greater in the QN and DEX cows than in the control cows on d 2 and 3. As expected, feed restriction reduced the energy balance, but the reduction was lower in the QN cows than in the control cows. Feed restriction decreased plasma glucose concentration and increased plasma nonesterified fatty acid (NEFA) and β-hydroxybutyrate (BHB) concentrations. The QN cows had higher glucose concentration and lower BHB concentration than the control cows. The NEFA concentration was also lower in the QN cows than in the control cows on d 2. Dexamethasone injection induced transient hyperglycemia concomitant with a reduction in milk lactose concentration; it also decreased BHB concentration and decreased NEFA initially but increased it later. Feed restriction and quinagolide injections did not affect the blood concentration or activity of polymorphonuclear leukocytes (PMN), whereas dexamethasone injection increased PMN blood concentration but decreased the proportion of PMN capable of inducing oxidative burst. Incubation of peripheral blood mononuclear cells in serum harvested on d 2 of the restriction period reduced their ability to react to mitogen-induced proliferation, and injection of quinagolide or dexamethasone could not alleviate this effect. This experiment shows that prolactin-release inhibition could be an alternative to dexamethasone for reducing milk production and energy deficit in cows under acute nutritional stress, without disturbing immune function.

Effect of inhibiting the lactogenic signal at calving on milk production and metabolic and immune perturbations in dairy cows

“…In cows, a prepartum injection of bromocriptine also suppressed the PRL surge normally observed at calving, and PRL was depressed for several days after the end of the treatment (Johke and Hodate, 1978;Akers et al, 1981). In the present experiment, as in Ollier et al (2016), the PRL concentration in the QUIN cows caught up rapidly to concentrations in the CTL cows after the end of the treatment, suggesting that shortterm treatment with a dopamine agonist after calving has no negative carryover effect on PRL secretion in lactating cows.…”

“…Similarly, Akers et al (1981) reported that prepartum injections of bromocriptine reduced milk production to about 50% of that of control cows, and that the inhibition persisted until the euthanasia of the cows at 10 DIM. Conversely, the inhibition of milk production with quinagolide during an established lactation does not have a carryover effect on milk production (Ollier et al, 2016), indicating that the effects of short-term PRL inhibition on milk secretion are easier to reverse when inhibition occurs during galactopoiesis than when it occurs during lactogenesis. Lactogenesis is triggered by the peripartum surge of PRL and glucocorticoids.…”

Effects of chronic dexamethasone administration on hyperglycemia and insulin release in goats

“…It has been reported that Dex reduces insulin secretion by pancreatic β cells due to the oxidative stress on these cells, and β cells have been found to be particularly vulnerable and susceptible to reactive oxygen species (ROS) toxicity [ 16 ]. In cows, a single Dex injection induced a sharp increase in blood glucose concentration and then quickly returned to normal level [ 17 ]. The milk-reducing effect of Dex in cows is well known [ 18 ] and is related to its ability to decrease glucose uptake by skeletal muscle, adipose tissue as well as the mammary gland, which leads to an insulin resistance state [ 11 , 18 ].…”

Involução da glândula mamária durante o final da lactação e período seco de cabras Saanen: respostas de sobrevivência celular ao estresse agudo e relações com a temperatura por infravermelho

“…Com o aumento da capacidade leiteira dos animais nos últimos anos, têm sido estudadas técnicas mais eficazes de secagem. Manejos adotados como a restrição alimentar gradual, utilização de alimentos de baixa qualidade e restrição ou diminuição de água antes e durante a secagem, são considerados importantes para diminuir a produção leiteira (ODENSTEN; CHILLIARD;HOLTENIUS, 2005;OLLIER;. Em cabras, ovelhas e vacas lactantes, alguns animais tendem a diminuir gradativamente a produção leiteira, conhecida como secagem espontânea, a qual é normal em animais que possuem maior tempo de lactação e/ou estejam prenhes (ANNEN et al, 2004;CAJA;SALAMA; COLLIER; ANNEN-DAWSON; PEZESHKI, 2012).…”

“…No entanto, as altas concentrações de glicocorticoides plasmático podem ser prejudiciais para o desenvolvimento e atividades da glândula mamária, respondendo principalmente à diminuição na produção de leite em vacas OLLIER et al, 2016;PONCHON et al, 2017) Palavras-chave: células epiteliais mamárias, cortisol, secagem, sobrevivência celular.…”