Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:3.1.1.79 (hormone-sensitive lipase)
 2,163 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

These studies examined the cellular mechanisms for lower adiposity seen with nicotine ingestion. Rats were infused with nicotine or saline for 1 wk and adipocytes isolated from epididymal fat pads. Nicotine-infused rats gained 37% less weight and had 21% smaller fat pads. Basal lipolysis was 78% higher, whereas the maximal lipolytic response to isoproterenol was blunted in adipocytes from nicotine-infused rats. The antilipolytic actions of adenosine and the levels of serum catecholamines were unaffected by nicotine. The nicotine-induced alteration in lipolysis was not associated with any changes in hormone-sensitive lipase. Nicotine caused a 30% decrease in lipoprotein lipase (LPL) activity, without any changes in LPL mass or mRNA levels, in epididymal fat in the fed state. In contrast, LPL activity, mass, and mRNA levels in heart were increased by nicotine whether animals were fed or fasted. These studies provide evidence for multiple mechanistic events underlying nicotine-induced alterations in weight and suggest that nicotine diverts fat storage away from adipose tissue and toward utilization by muscle.
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PMID:Alterations of lipolysis and lipoprotein lipase in chronically nicotine-treated rats. 877 41

We studied changes in lipid metabolism in adipose tissue in 24 healthy adults during early starvation (14-20 h) by cannulating the venous drainage of the subcutaneous adipose tissue of the anterior abdominal wall. Net nonesterified fatty acid (NEFA) efflux from adipose tissue increased steadily from 1,790 +/- 300 to 2,360 +/- 290 nmol.100 g-1.min-1 (P = 0.03), due to increasing transcapillary efflux of NEFA (release from adipocytes; P < 0.01). The reesterification rate after an overnight fast was close to zero; thus, reduction in the rate of reesterification played no part in the increased transcapillary efflux of NEFA. One-quarter of the net efflux of NEFA after an overnight fast arose from the action of lipoprotein lipase (LPL), although this relative contribution decreased during the study (P < 0.02). The increased transcapillary efflux of NEFA reflected a significant increase in the rate of action of hormone-sensitive lipase (HSL; P = 0.03). There was a strong relationship between mean arterial NEFA concentration and net NEFA release from adipose tissue (P < 0.001), implying that the particular depot studied reflects the behavior of adipose tissue as a whole. Thus the increasing efflux of NEFA from adipose tissue observed during early starvation is due to an increased rate of action of HSL, which may in turn be regulated by a fall in the plasma insulin concentration.
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PMID:Regulation of lipid metabolism in adipose tissue during early starvation. 884 49

Female rats receiving alcohol (20%) in drinking water during lactation (AL) were compared to pair-fed animals (PF) and normal controls (C) fed ad lib. All animals were killed on the 12th day of lactation. When compared to C rats, food intake decreased in both AL and PF groups, and this effect was followed by a lower body weight and mammary gland (MG), liver, and parametrial adipose tissue weights. Mammary glands triacylglyceride concentration (TG) was much lower in PF than in AL, although in the latter, values did not reach those of C, and had higher liver TG concentration than any of the other groups. Both PF and AL rats had lower plasma TG, glycerol, and free fatty acid concentrations and higher beta-hydroxybutyrate concentration than C rats. When compared to C rats, the rate of lipogenesis in MG was higher in both PF and AL rats, whereas in liver it was higher in PF and lower in AL rats, and in adipose tissue it was higher in PF and unchanged in AL rats. The appearance of 14C lipids 4 h after oral [14]triolein in both MG and liver was lower in AL and PF rats and only lower in adipose tissue of AL rats as compared to the c rats. Lipoprotein lipase and hormone-sensitive lipase activities were lower in MG in both PF and AL rats than in C, whereas in adipose tissue the activity of lipoprotein lipase did not differ between AL and C rats and the activity of HSL was lower in the former. These findings therefore show that in spite of reduced uptake of orally administered triglycerides due to decreased LPL activity, maternal alcohol feeding during lactation in the rat preserves the mammary gland triglyceride content thanks to enhanced lipogenetic activity. On the other hand, it causes liver triglycerides accumulation, probably as a result of the decreased rate of triglycerides released into circulation, and these changes are not caused by the reduced food intake of the animals.
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PMID:Effects of ethanol intake on lipid metabolism in the lactating rat. 888 39

The effects of in vivo lipopolysaccharide administration on serum lipid metabolism were studied in normal and hepatoma-bearing rats. Changes in serum lipid levels and adipose tissue lipase (lipoprotein lipase and hormone-sensitive lipase) activities following injection of lipopolysaccharide into normal rats resembled those in hepatoma-bearing rats. These results suggest the presence of some common factor(s) involved in the incidence of abnormal lipid metabolism upon lipopolysaccharide injection and hepatoma transplantation.
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PMID:Responses of serum lipids and adipose tissue lipases to lipopolysaccharide administration in normal and hepatoma-bearing rats. 890 Nov 18

Epinephrine has effects on both blood flow and metabolism in adipose tissue. To investigate how these effects might interact in vivo, epinephrine was infused into six healthy volunteers at a rate of 25 ng.kg-1.min-1. The rates of action of lipoprotein lipase and hormone-sensitive lipase in adipose tissue were calculated by measurement of arteriovenous differences across subcutaneous abdominal adipose tissue, and adipose tissue blood flow was measured. Epinephrine caused a significant rise in adipose tissue blood flow (P < 0.001), and the net efflux of nonesterified fatty acids (NEFA) from adipose tissue increased significantly (P < 0.05). Most of this efflux could be accounted for by hormone-sensitive lipase-derived NEFA efflux from cells (P < 0.05), but there was also a significant rise in the contribution of lipoprotein lipase-derived NEFA (P < 0.05). We conclude that adipose tissue blood flow plays an important role in the regulation of lipid metabolism, controlling substrate presentation for lipoprotein lipase and also preventing the local accumulation of fatty acids derived from both hormone-sensitive lipase and lipoprotein lipase.
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PMID:Effects of epinephrine infusion on adipose tissue: interactions between blood flow and lipid metabolism. 894 69

To better characterize the increase in lipoprotein lipase (LPL) translation by hypothyroidism, adipocytes were prepared from control and hypothyroid rats. Whereas LPL synthesis was higher in hypothyroid adipocytes, with no change in mRNA levels, there was no increase in hormone-sensitive lipase (HSL) synthesis. To determine whether a transacting translation regulatory factor was present, a cytoplasmic fraction was prepared from control and hypothyroid adipocytes, and added to an in vitro translation system containing the hLPL mRNA. The hypothyroid cell fraction from adipose and heart yielded an increase in LPL translation, when compared to control extracts. Further experiments determined that the control adipocyte extract contained a translation-inhibitory factor that was 8-fold lower in activity in the hypothyroid extract. Using different LPL mRNA constructs in the in vitro translation reaction, the region that controlled translation was localized to nucleotides 1599 to 1638 (proximal 3' untranslated region (UTR)). To confirm the presence of a transacting factor, a sense RNA strand corresponding to this region was added to the in vitro translation reaction. This sense strand competed for the transacting factor in the control cell extract, yet had no effect on the hypothyroid cell extract. Thus, there is a translation repressor factor in the cytoplasm of rat adipocytes, and this factor is greatly reduced in activity in hypothyroid rat adipocytes. Because a similar mechanism of LPL regulation occurs in response to epinephrine, the absence of the translation repressor may be a mechanism for the loss of sensitivity of hypothyroid cells for catecholamines.
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PMID:Translational regulation of lipoprotein lipase by thyroid hormone is via a cytoplasmic repressor that interacts with the 3' untranslated region. 897 85

Cortisol has a well-defined circadian rhythm. The aim of the study was to examine the effect of the morning rise in cortisol concentration on lipolysis in adipose tissue. Ten healthy subjects were studied on two occasions, and six of these were studied on three occasions. During the first two occasions, either a control or cortisol suppression study was performed by using metyrapone, and on the third occasion exogenous cortisol replacement was given in addition to metyrapone. Lipolysis in the subcutaneous adipose tissue of the anterior abdominal wall was studied by measurement of arteriovenous differences. Reduction in the early morning rise in cortisol led to significantly decreased venoarterialized differences for nonesterified fatty acids (P < 0.05) and glycerol (P < 0.01), attributable in part to decreased hormone-sensitive lipase (EC 3.1.1.3) action (P < 0.05) in adipose tissue. At the same time the arterialized plasma triacylglycerol concentration increased (P < 0.005) with a significant reduction in the adipose lipoprotein lipase (EC 3.1.1.34) rate of action (P < 0.05). In the replacement study, values were identical to those of the control study, showing that metyrapone had no nonspecific effects on lipolysis. We conclude that the morning rise in plasma cortisol concentration plays an important role in the regulation of lipolysis in adipose tissue in normal healthy adults.
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PMID:Effects of morning rise in cortisol concentration on regulation of lipolysis in subcutaneous adipose tissue. 899 17

1. The effects of two chronic ethanol treatment schedules, which produce different plasma ethanol concentrations, on the specific activities of adipose tissue lipoprotein lipase (LPL) and hormone-sensitive lipase (HSL) have been investigated in brown and white fat. 2. Mice provided with 20% ethanol solution as sole drinking fluid for 28 days consumed between 13 and 15 g ethanol kg-1 body weight day-1 over days 22-28. The mean plasma ethanol concentration was 4.94 +/- 1.4 mM (n = 8) at 09 h 00 min on day 28 when the lipase assays were performed. Mice given ethanol in a liquid diet for 7 days consumed between 15 and 18 g ethanol day-1 over days 3-7. The mean plasma ethanol concentration was 15.9 +/- 4.7 mM (n = 8) at 09 h 00 min on day 7. These concentrations of ethanol had no effect on the activity of either LPL or HSL in vitro. 3. LPL activity in white and brown fat (expressed as nmol fatty acids released h-1 mg-1 acetone powder) was unaltered 60 min following an acute injection of ethanol (2.5 g kg-1, i.p.) which produced a mean blood ethanol level of 37.5 +/- 6.7 mM. HSL activity in white fat (expressed as nmol fatty acid released h-1 mg-1 protein) was also unaffected by this acute dose of ethanol, but the activity in brown fat was significantly reduced: 3.07 +/- 0.30 (n = 8) after ethanol compared to 4.36 +/- 0.25 (n = 12) in controls (P < 0.01). 4. LPL activity in white fat was little altered by either of the chronic ethanol treatment schedules whilst LPL activity in the brown fat from the same animals was significantly increased compared to the respective control values: 0.27 +/- 0.03 (ethanol drinking), control: 0.16 +/- 0.01; 0.79 +/- 0.14 (ethanol liquid diet), control: 0.39 +/- 0.05. 5. HSL activity in white fat was significantly increased by the chronic drinking treatment (7.7 +/- 0.5; control: 3.78 +/- 0.17, n = 8) at the same time that the activity in brown fat was reduced (3.76 +/- 0.2; control: 4.74 +/- 0.16). The ethanol liquid diet also reduced HSL activity in brown fat but had negligible effect in white fat. 6. The effects of the two chronic ethanol treatments on adenosine 3':5'-cyclic monophosphate (cyclic AMP) accumulation in brown and white fat were very similar, both qualitatively and quantitatively, to the effects on HSL. 7. It has been shown that brown and white adipose tissues respond differently to the presence of chronic ethanol and that the response is dependent both upon the concentration of ethanol and the nature of the diet with which the ethanol is administered. The effects of ethanol on adipose tissue HSL activity appear to be mediated via changes in the tissue cyclic AMP level and, in this respect, brown fat is more sensitive to ethanol than white fat.
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PMID:Dose-dependent effects of chronic ethanol on mouse adipose tissue lipase activity and cyclic AMP accumulation. 905 14

Human brown pre-adipocytes were immortalized by microinjection of the genes encoding simian virus 40 T and t antigens under the control of the human vimentin promotor. The transfected pre-adipocytes were cultured for several months with no loss of their morphological characteristics. These cells accumulate lipids and differentiate into adipocytes when treated with insulin, triiodothyronine and dexamethazone. The mRNA of various adipocyte markers was detected by reverse transcriptase-polymerase chain reaction analysis, including hormone-sensitive lipase, lipoprotein lipase, adipsin, glucose transporters 1 and 4, the uncoupling protein (specific of brown adipocytes), and leptin, the product of the ob gene. Pharmacological analyses indicated that the beta3-adrenoceptor is the predominant beta-adrenoceptor subtype in PAZ6 cells and that this receptor subtype is functionally coupled to adenylate cyclase and lipolysis. The immortalization of human adipocytes will permit pharmacological analysis of the human beta3-adrenoceptor function in adipose cells and will allow detailed studies of human adipocyte differentiation.
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PMID:Human immortalized brown adipocytes express functional beta3-adrenoceptor coupled to lipolysis. 913 67

Familial combined hyperlipidemia (FCHL) is characterized by different lipid phenotypes (IIa, IIb, IV) and elevated apolipoprotein B (apo B) levels in affected family members. Despite intensive research, the genes involved in the expression of this complex disorder have not been identified, probably because of problems associated with phenotype definition, unknown mode of inheritance, and most probably genetic heterogeneity. To explore the genetics of FCHL in the genetically homogeneous Finnish population, we collected 14 well-documented Finnish pedigrees with premature coronary heart disease and FCHL-like dyslipidemia. The lipolytic enzymes lipoprotein lipase (LPL), hepatic lipase (HL), and hormone-sensitive lipase (HSL) were selected as initial candidate genes because of their central roles in apo B and triglyceride metabolism. On the basis of the pedigree structures, a dominant mode of inheritance was adopted for linkage analyses, and serum total cholesterol and/or triglyceride levels exceeding the 90th percentile level were set as diagnostic criteria (criterion 1). In pairwise linkage analyses with intragenic markers, no evidence for linkage was found. Instead, the significantly negative LOD scores suggested exclusion of all three loci for single major gene effect. LOD scores were -14.63, -5.03, and -5.70 for the three LPL polymorphisms (theta=0.00); -9.40, -6.30, and -4.74 for the three HL polymorphisms (theta=0.00); and -15.29 for the HSL polymorphism (theta=0.00). The results were very similar when apo B levels over the 90th percentile were used as criteria for affected status (criterion 2). Also, when linkage calculations were carried out using an intermediate or recessive mode of inheritance, the results of pairwise linkage analysis remained negative. Furthermore, when haplotypes were constructed from multiple polymorphisms of the LPL and HL genes, no segregation with the FCHL phenotype could be observed in the 14 Finnish families. Data obtained by the affected sib-pair method supported these findings, suggesting that the LPL, HL, or HSL genes do not represent major loci influencing the expression of the FCHL phenotype.
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PMID:No evidence of linkage between familial combined hyperlipidemia and genes encoding lipolytic enzymes in Finnish families. 915 46


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