The enormous plasticity of adipose tissues, to rapidly adapt to altered physiological states of energy demand, is under neuronal and endocrine control. In energy balance, lipolysis of triacylglycerols and re-esterification of free fatty acids are opposing processes operating in parallel at identical rates, thus allowing a more dynamic transition from anabolism to catabolism, and vice versa. In response to alterations in the state of energy balance, one of the two processes predominates, enabling the efficient mobilization or storage of energy in a negative or positive energy balance, respectively. The release of noradrenaline from the sympathetic nervous system activates lipolysis in a depot-specific manner by initiating the canonical adrenergic receptor-G s -protein-adenylyl cyclase-cyclic adenosine monophosphate-protein kinase A pathway, targeting proteins of the lipolytic machinery associated with the interface of the lipid droplets. In brown and brite adipocytes, lipolysis stimulated by this signaling pathway is a prerequisite for the activation of non-shivering thermogenesis. Free fatty acids released by lipolysis are direct activators of uncoupling protein 1-mediated leak respiration. Thus, pro-and anti-lipolytic mediators are bona fide modulators of thermogenesis in brown and brite adipocytes. In this Review, we discuss adrenergic and non-adrenergic mechanisms controlling lipolysis and thermogenesis and provide a comprehensive overview of pro-and anti-lipolytic mediators.

Quantification of substrate fluxes in brown adipocytes clarifies contributors to extracellular acidification, identifies a futile cycle of lipolysis and re-esterification, and suggests a role for glycogen during activation.

Lipid species patterns are conserved within cells to maintain physicochemical properties of membranes and cellular functions. We present the lipidome, including sterols, glycerolipids (GLs), glycerophospholipids (GPLs), and sphingolipids (SLs), of primary ex vivo differentiated (I) white, (II) brite, and (III) brown adipocytes derived from primary preadipocytes isolated from (I) epididymal white, (II) inguinal white, and (III) intrascapular brown adipose tissue. Quantitative lipidomics revealed significantly decreased fractions of phosphatidylcholine (PC) and phosphatidylethanolamine (PE), with longer (C > 36) and more polyunsaturated species, as well as lower levels of cardiolipin (CL) in white than in brite and brown adipocytes. Together, the brite and brown lipidome was comparable and indicates differences in membrane lipid packing density compared with white adipocytes. Changes in ceramide species profile could be related to the degree of browning. Beta-adrenergic stimulation of brown adipocytes led to generation of saturated lyso-PC (LPC) increasing uncoupling protein (UCP) 1-mediated leak respiration. Application of stable isotope labeling showed that LPC formation was balanced by an increased de novo synthesis of PC.

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Summary Studying brown and brite adipose tissue requires precise and reliable quantification of cellular thermogenesis. This protocol describes the isolation of primary murine pre-adipocytes, differentiation into thermogenic brown and brite adipocytes, and subsequent oxygen consumption analysis. Commonly applied procedures only measure basal and maximal proton leak-linked oxygen consumption but not explicitly uncoupling protein 1 (UCP1)-dependent respiration. Meaningful oxygen consumption analyses require (1) the activation of UCP1, (2) control over intracellular free-fatty-acid levels, and (3) inhibition of ATP-consuming futile cycles. For complete details on the use and execution of this protocol, please refer to Li et al. (2014 , 2017 , 2018 ) and Schweizer et al. (2018) .

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This study compared the Zn response in selected tissues of weaned piglets fed L-glutamic acid, N,N-diacetic acid (GLDA), while challenged with short-term subclinical Zn deficiency (SZD). During a total experimental period of eight days, 96 piglets were fed restrictively (450 g/d) a high phytate (9 g/kg) diet containing added Zn at 0, 5, 10, 15, 20, 25, 45 and 75 mg/kg with and without 200 mg/kg of GLDA. No animals showed signs of clinical Zn deficiency and no phenotypical differences were observed. Broken line analysis of Zn status parameters such as liver Zn and apparently absorbed Zn indicated that the gross Zn requirement threshold was around 55 mg/kg diet. Supplementation of Zn above this threshold led to a saturation of the response in apparently absorbed Zn and linear increase in liver Zn. Bone and serum Zn responded to the dose in a linear fashion, likely due to the time-frame of Zn homoeostatic adaptation. Inclusion of GLDA into the diets yielded a higher intercept for bone Zn (P < 0·05). Liver Zn accumulation and MT1A gene expression was higher for piglets receiving GLDA (P < 0·05), indicating higher Zn influx. This study indicates that a strong chelator such as GLDA mitigates negative effects of phytate in plant-based diets, by sustaining Zn solubility, thereby improving nutritional Zn availability.