Effects of insulin, glucocorticoids and adrenaline on the activity of rat adipose-tissue lipoprotein lipase

Ashby, P.; Robinson, Dean W.

doi:10.1042/bj1880185

Cited by 101 publications

(34 citation statements)

References 25 publications

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“…The concentration of most of the hormones reported to either stimulate (4)(5)(6)(7)(8)(9) or inhibit (5, 10-12) rat adipose tissue LPL activity, are the same in both sexes. Sex steroids on the other hand account for many differences between the sexes, making it likely that these hormones also account for sex differences in LPL regulation.…”

Section: Introductionmentioning

confidence: 73%

Relationship between lipoprotein lipase activity and plasma sex steroid level in obese women.

Iverius

Brunzell

1988

J. Clin. Invest.

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In obese women (a = 16) at their usual weight, fasting adipose tissue lipoprotein lipase (LPL) activity, obtained by elution with serum and heparin at 40 and 370C, was inversely correlated to plasma estradiol levels (r = -0.724; P = 0.002) and (r = -0.641; P = 0.010), respectively. Furthermore, fasting postheparin plasma LPL activity during a heparin infusion, showed an even stronger inverse correlation to plasma estradiol when measured at 60 min (r = -0.815; P < 0.001). None of the above parameters was correlated to the body mass index.Postprandial LPL activity in postheparin plasma, measured 10 min after a heparin injection, showed a strong positive correlation with plasma free testosterone (r = 0.780; P = 0.001). Neither of these parameters was correlated with the body mass index. The origin of this LPL activity is presently unknown but could conceivably represent a pool of LPL from skeletal muscle.Since it has been shown convincingly that estrogen decreases adipose tissue LPL activity in the rat, the present studies strongly suggest that estradiol is a major negative regulator of fasting adipose tissue LPL activity in women.

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Section: Introductionmentioning

confidence: 73%

Relationship between lipoprotein lipase activity and plasma sex steroid level in obese women.

Iverius

Brunzell

1988

J. Clin. Invest.

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“…Because GC cumulate stimulatory actions on both lipogenic and lipolytic processes, 23 the net effect of GC on adipose tissue lipid metabolism is highly dependent upon many factors, including levels of GC themselves, interactions with other hormonal systems such as insulin, 34 and regional specificity. 29,35,36 Knowledge of the detailed mechanisms by which GC impact adipose tissue lipid metabolism remains fragmentary; however, a permissive action on the insulin-mediated stimulation of LPL, 37,38 an inhibitory effect on the anti-lipolytic action of insulin, 39 direct transcriptional activation of the fatty acid-synthesizing gene FAS, 40 and inhibition of the expression of the fatty acid re-esterification gene PEPCK 41 have been established. In the case of PPARg, effects on adipose tissue lipid metabolism are manifold and include stimulation of lipid uptake, esterification, recycling, lipolysis, and oxidation, 11,[42][43][44] with an overall preponderance of lipid retention over fatty acid release pathways explaining fat accretion.…”

Section: Pparc In Rats With Hypercorticosteronemia M Berthiaume Et Almentioning

confidence: 99%

Metabolic action of peroxisome proliferator-activated receptor γ agonism in rats with exogenous hypercorticosteronemia

et al. 2007

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Objective: The beneficial metabolic actions of peroxisome proliferator-activated receptor g (PPARg) agonism are associated with modifications in adipose tissue metabolism that include a reduction in local glucocorticoid (GC) production by 11b-hydroxysteroid dehydrogenase type 1 (11b-HSD1). This study aimed to assess the contribution of GC attenuation to PPARg agonism action on gene expression in visceral adipose tissue and global metabolic profile. Design: Rats were treated (2 weeks) with the PPARg agonist rosiglitazone (RSG, 10 mg/kg/day) with concomitant infusion of vehicle (cholesterol implant) or corticosterone (HiCORT, 75 mg/implant/week) to defeat PPARg-mediated GC attenuation. Measurements: mRNA levels of enzymes involved in lipid uptake (and lipoprotein lipase activity), storage, lipolysis, recycling, and oxidation in retroperitoneal white adipose tissue (RWAT). Serum glucose, insulin and lipids, and lipid content of oxidative tissues. Results: Whereas HiCORT did not alter RWAT mass, RSG increased the latter ( þ 33%) independently of the corticosterone status. Both HiCORT and RSG increased lipoprotein lipase activity, the mRNA levels of the de novo lipogenesis enzyme fatty acid synthase, and that of the fatty acid retention-promoting enzyme acyl-CoA synthase 1, albeit in a nonadditive fashion. Expression level of the lipolysis enzyme adipose triglyceride lipase was increased additively by HiCORT and RSG. PPARg agonism increased mRNA of the fatty acid recycling enzymes glycerol kinase and cytosolic phosphoenolpyruvate carboxykinase and those of the fatty acid oxidation enzymes muscle-type carnitine palmitoyltransferase 1 and acyl-CoA oxidase, whereas HiCORT remained without effect. HiCORT resulted in liver steatosis and hyperinsulinemia, which were abrogated by RSG, whereas the HiCORTinduced elevation in serum nonesterified fatty acid levels was only partially prevented. The hypotriglyceridemic action of RSG was maintained in HiCORT rats. Conclusion: The GC and PPARg pathways exert both congruent and opposite actions on specific aspects of adipose tissue metabolism. Both the modulation of adipose gene expression and the beneficial global metabolic actions of PPARg agonism are retained under imposed high ambient GC, and are therefore independent from PPARg effects on 11b-HSD1-mediated GC production.

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“…Experiments were also carried out in the presence of dexamethasone, aneffector thought to stimulate adipocyte lipoprotein lipase gene expression specifically (Ashby & Robinson, 1980;Robinson et al, 1983). Fig.…”

Section: Resultsmentioning

confidence: 99%

The lipoprotein lipase of white adipose tissue. Changes in the adipocyte cell-surface content of enzyme in response to extracellular effectors in vitro

Al‐Jafari¹,

Cryer²

1986

Biochemical Journal

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1. An indirect labelled-second-antibody cellular immunoassay for adipocyte surface lipoprotein lipase was used to assess the changes that occurred during -the incubation of cells in the presence and absence of effectors. 2. In the absence of any specific effectors, the amount of immunodetectable lipoprotein lipase present at the surface of adipocytes remained constant throughout the 4 h incubation period at 37 'C. Under such conditions total cellular enzyme activity also remained constant, with no activity appearing in the medium. 3. In the presence of heparin, cell-surface immunodetectable lipoprotein lipase increased by up to 20%, whereas in the presence of cycloheximide they decreased by up to 60%. Thus the obvious turnover of enzyme from this cell-surface site was found to be relatively rapid and dependent for its replenishment, at least in part, on protein synthesis. 4. In the presence of insulin alone, a substantial increase in cell-surface lipoprotein lipase protein occurred, only part of which was dependent on protein synthesis. The total cellular activity of lipoprotein lipase was unaffected by the presence of insulin. The insulin-dependent increase in cell-surface enzyme was potentiated somewhat in the presence of dexamethasone, which was not shown to exert any independent effect. 5. Glucagon, adrenaline and theophylline all produced a significant decline in the cell-surface immunodetectable lipoprotein lipase, which in the case examined (adrenaline) was partially additive with regard to the independent effect of cycloheximide. 6. Cell-surface immunodetectable lipoprotein lipase amounts were decreased significantly when cells were incubated in the presence of either colchicine or tunicamycin. 7. The concerted way in which cell-surface lipoprotein lipase altered during the incubations of adipocytes in the presence of effectors suggested that the translocation of enzyme to and from this cellular site was dependent on hormonal action and the integrity of intracellular protein-transport mechanisms.

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Effects of insulin, glucocorticoids and adrenaline on the activity of rat adipose-tissue lipoprotein lipase

Cited by 101 publications

References 25 publications

Relationship between lipoprotein lipase activity and plasma sex steroid level in obese women.

Relationship between lipoprotein lipase activity and plasma sex steroid level in obese women.

Metabolic action of peroxisome proliferator-activated receptor γ agonism in rats with exogenous hypercorticosteronemia

The lipoprotein lipase of white adipose tissue. Changes in the adipocyte cell-surface content of enzyme in response to extracellular effectors in vitro

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