Beta-adrenergic stimulation of lipoprotein lipase in rat brown adipose tissue during acclimation to cold

Carneheim, C.; Nedergaard, Jan; Cannon, Barbara

doi:10.1152/ajpendo.1984.246.4.e327

Cited by 64 publications

(59 citation statements)

References 19 publications

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“…Indeed, the higher relative protein content measured in leptin-infused obaob mice suggests that leptin altered the BAT weight of obese mice by reducing its lipid content. The present ®ndings also suggest that any leptin-induced increase in the sympathetic drive to BAT, which would per se tend to stimulate LPL activity, 37 was overwhelmed by the lowering action of decreased insulinemia. Although still uncertain, insulin appears to directly or indirectly decrease LPL activity in muscle.…”

Section: Discussionsupporting

confidence: 59%

Effects of leptin on adipose tissue lipoprotein lipase in the obese ob/ob mouse

et al. 1998

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OBJECTIVE: To characterize the adaptations of lipid metabolism, with special emphasis on tissue lipoprotein lipase, to negative energy balance brought by chronic treatment of obese obaob mice with leptin. DESIGN: According to a 2 Â 2 factorial analysis, lean and obese C57BLa6J mice were subcutaneously infused with leptin (100 mg?kg 71 ?day 71 ) or vehicle (phosphate-buffered saline) during seven days. RESULTS: Cumulative food intake and ®nal body weight of vehicle-infused obese mice were twofold higher than in lean controls. Leptin decreased cumulative food intake and body weight of obese, but not lean mice. Lipoprotein lipase (LPL) activity in white inguinal and epididymal and brown interscapular adipose tissues of control obese mice was at least twofold higher than in lean mice, but comparable in the vastus lateralis muscle. Leptin treatment of obese mice signi®cantly lowered LPL activity to that of lean mice in all tissues examined. Vehicle-infused obese mice had higher liver triglyceride content and were hypertriglyceridemic compared to lean mice, and triglyceride concentrations in plasma and liver were decreased proportionally after leptin treatment. Leptin lowered glycemia and insulinemia of obese mice to lean levels and decreased plasma corticosterone. Leptin infusion had no notable effect on tissue lipoprotein lipase nor plasma variables of lean mice. CONCLUSIONS: Leptin infusion abolished hyperinsulinemia in the obaob mouse, an effect that was probably responsible for the concomitant normalization of adipose LPL activity. This study shows that decreased LPL activity, plasma triglyceride concentrations and hepatic triglyceride production constitute some of the adaptive peripheral adaptations of lipid metabolism, which accompany the reduction in fat mass accretion brought by leptin treatment of the obese obaob mouse.

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Section: Discussionsupporting

confidence: 59%

Effects of leptin on adipose tissue lipoprotein lipase in the obese ob/ob mouse

et al. 1998

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“…Lipoprotein lipase is anchored to the periphery of brown adipocytes and liberates fatty acids from circulating lipoproteins, thus allowing the import of fatty acids. The activity of this enzyme is rapidly increased during cold exposure ( 13,62,63 ). This demonstrates that ␤ -adrenergic stimulation of BAT simultaneously increases lipolysis and the oxidation of fatty acids as well as the uptake and the export of fatty acids, i.e., the turnover of lipids is exaggerated well beyond its need for fueling BAT metabolism .…”

Section: Bat Lipid Metabolism During Thermogenesismentioning

confidence: 89%

Brown adipose tissue dynamics in wild-type and UCP1-knockout mice: in vivo insights with magnetic resonance

Grimpo

Völker

Heppe

et al. 2014

Journal of Lipid Research

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This article is available online at http://www.jlr.org body temperature maintenance of small eutherian mammals and newborns during periods of cold exposure. BAT thermogenesis is activated by the release of noradrenaline (NA) from sympathetic innervation. Uncoupling protein 1 (UCP1) in the inner mitochondrial membrane of the brown adipocytes uncouples the respiratory chain from ATP synthesis and thus energy is dissipated as heat ( 1-3 ). Prolonged cold exposure or a short photoperiod induces the recruitment of BAT ( 4-6 ). Brown adipocytes of coldadapted mice, contain small and multilocular lipid vacuoles, which are rich in cytoplasm and have a high content of mitochondrial protein (7)(8)(9). This provides an enhanced thermogenic capacity during cold exposure, and BAT can be considered as the major site of adaptive nonshivering thermogenesis (NST) in rodents and other small mammals ( 4, 10-12 ).The breakdown of lipids via lipoprotein lipase plays an important role during UCP1-mediated heat production ( 13 ). Free fatty acids (FFAs) directly activate UCP1 and feed the respiratory chain, i.e., FFAs are the major substrate for NST ( 14,15 ). Therefore active BAT is considered as a main consumer of lipids and FFAs and its contribution to plasma clearance of administered triglycerides has been shown previously ( 16,17 ). On the other hand a release of fatty acids during thermogenesis from BAT has been assumed, indicating a substrate supply to other tissues ( 18,19 ). Sympathetic activation by cold exposure or injections of NA not only activate BAT but also stimulate sympathetic receptors in general, leading to an increase in heart rate, blood flow, and metabolic responses in other tissues. The contribution of these UCP1-independent processes to total NST remain unclear ( 20, 21 ).Abstract We used noninvasive magnetic resonance imaging (MRI) and magnetic resonance spectroscopy to compare interscapular brown adipose tissue (iBAT) of wild-type (WT) and uncoupling protein 1 (UCP1)-knockout mice lacking UCP1-mediated nonshivering thermogenesis (NST). Mice were sequentially acclimated to an ambient temperature of 30°C, 18°C, and 5°C. We detected a remodeling of iBAT and a decrease in its lipid content in all mice during cold exposure. Ratios of energy-rich phosphates (ATP/ADP, phosphocreatine/ATP) in iBAT were maintained stable during noradrenergic stimulation of thermogenesis in coldand warm-adapted mice and no difference between the genotypes was observed. As free fatty acids (FFAs) serve as fuel for thermogenesis and activate UCP1 for uncoupling of oxidative phosphorylation, brown adipose tissue is considered to be a main acceptor and consumer of FFAs. We measured a major loss of FFAs from iBAT during noradrenergic stimulation of thermogenesis. This mobilization of FFAs was observed in iBAT of WT mice as well as in mice lacking UCP1. The high turnover and the release of FFAs from iBAT suggests an enhancement of lipid metabolism, which in itself contributes to the sympathetically activated NST and which is independent fro...

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“…However, the lack of changes in skeletal muscle acyl groups in the cold suggests that this alone cannot explain the compositional differences in brown adipose tissue. Brown adipose tissue is under constant adrenergic stimulation in the cold, leading to increased lipoprotein lipase gene expression (17) and lipoprotein lipase activity (16). UCP1-ablated mice also exhibit strongly increased lipoprotein lipase gene expression in the cold (12).…”

Section: Discussionmentioning

confidence: 99%