Abstract
Hormone sensitive lipase (HSL) activation is part of the metabolic adaptations to the negative energy balance common to the mammalian periparturient period. This study determined HSL contribution to adipose tissue (AT) lipolysis and how insulin regulates its activity in periparturient dairy cows. Subcutaneous AT (SCAT) samples were collected at 11 d prepartum (dry) and 11 (fresh) and 24 d (lactation) postpartum. Basal and stimulated lipolysis (ISO) responses were determined using explant cultures. HSL contribution to lipolysis was assessed using an HSL inhibitor (CAY). Basal lipolysis was higher in SCAT at dry compared with fresh. CAY inhibited basal lipolysis negligibly at dry, but at fresh and lactation it reduced basal lipolysis by 36.1 ± 4.51% and 43.1 ± 4.83%, respectively. Insulin inhibited lipolysis more pronouncedly in dry compared to fresh. Results demonstrate that HSL contribution to basal lipolysis is negligible prepartum. However, HSL is a major driver of SCAT lipolytic responses postpartum. Lower basal lipolysis postpartum suggests that reduced lipogenesis is an important contributor to fatty acid release from SCAT. Loss of adipocyte sensitivity to the antilipolytic action of insulin develops in the early lactation period and supports a state of insulin resistance in AT of cows during the first month postpartum.
Highlights
Excessive release of fatty acids (FA) from adipose tissue (AT) is linked with metabolic diseases of gestation and early lactation in mammals[1,2]
Reflecting the intense FA mobilization from AT during the periparturient period, serum free fatty acids (FFA) and BHB concentrations increased and body weight and body condition score were reduced in fresh and lactation compared with dry (Fig. 1 and Supplementary Table C)
Our results demonstrate that the level of basal lipolytic activity in Subcutaneous AT (SCAT) is dynamic throughout the periparturient period and decreases in the fresh compared with the dry period
Summary
Excessive release of fatty acids (FA) from adipose tissue (AT) is linked with metabolic diseases of gestation and early lactation in mammals[1,2]. Catecholamines and growth hormone are the most important hormones increasing FA release while insulin is the most important hormone decreasing FA release[7,16] These hormones act by stimulating or inhibiting the activity of hormone sensitive lipase (HSL) and adipose triglyceride lipase (ATGL) through phosphorylation by protein kinase A (PKA) or by changing the sensitivity of adipocytes to catecholamines[7,17]. The exact contribution of lipolytic enzymes, lipogenic activity, and adipocyte insulin resistance to the net release of FA during the immediate periparturient period is not well established. A complete characterization of the lipolytic activity is important in species with a high incidence of gestational and periparturient diseases including humans, dairy cows, and other small ruminants. Changes in the mRNA expression of important lipogenic, lipolytic, and glucose metabolism gene networks were determined
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