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)

The pathophysiology and clinical significance of high signal lesions, visualized on magnetic resonance imaging (MRI) in patients with Alzheimer's disease (AD), remain controversial. Since they are known to correlate with vascular disease and vascular risk factors, we reviewed the clinical correlates of periventricular high signal (PVH) and subcortical white matter lesions (WML) in a sample of 106 patients with probable AD, excluding persons with treated vascular risk factors or symptomatic cerebrovascular and cardiovascular disease. Grade 2 PVH were seen in 26 (25%) and scattered WML were identified in 29 (18%). PHV were associated with advancing age and gait disturbance. WML were associated with gait disturbance and incontinence. Neither radiologic finding was related to dementia severity. The findings suggest that these lesions are common in patients with AD even when those with evidence of cerebrovascular disease are excluded; their presence, therefore, should not preclude a diagnosis of AD. Additionally, the data suggest that HSL on MRI may be one of many risk factors associated with functional disability in persons with probable AD.
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PMID:Clinical correlates of high signal lesions on magnetic resonance imaging in Alzheimer's disease. 159 84

Neutral cholesteryl ester hydrolase activity (EC 3.1.1.13) present in microsomes isolated from lactating rat mammary glands was found to be inhibited by a factor (or factors) occurring in the cytosolic fraction of male rat liver. The inhibitor was heat-labile, non-dialyzable, destroyed by proteolysis, and was stable following preparation of an acetone/diethyl ether powder of the cytosolic fraction. The protein also inhibited the activity of hormone-sensitive lipase (HSL) (from bovine adipose tissue) and esterase from Candida cylindracea, but seemed to be more active against the neutral hydrolase found in rat liver microsomes. For the mammary gland microsomal cholesteryl ester hydrolase, the extent of the inhibitory effect was dependent on the concentration of the cytosolic protein, 50% inhibition being achieved by about 100 micrograms of cytosolic protein, and on the method of initiating the enzyme assay. Kinetic analysis indicated that, under circumstances where the reaction was initiated by the addition of substrate, the inhibition was characterized as "uncompetitive." When an inhibitor/substrate complex was allowed to form in the absence of enzyme, an element of "competitive" inhibition was introduced into the reaction. Food withdrawal reduced the activity of the inhibitor in liver by 56%, but activity was fully restored by short-term re-feeding. In contrast, feeding a diet high in fat led to a 34% increase in activity. The present findings suggest that the inhibitory factor(s) may be involved in the regulation of the hydrolysis of cholesteryl esters in the liver and also in other cell types.
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PMID:Characterization of a cytosolic protein in rat liver inhibiting neutral cholesteryl ester hydrolase. 163 Feb 74

Lipase activity in homogenates of guinea-pig adrenals was studied under conditions which exclude the hormone-sensitive lipase/cholesterol ester hydrolase. Antibody inhibition and chromatography on heparin-Sepharose showed that most of the activity was due to lipoprotein lipase (LPL), and that there was only a small amount of hepatic lipase activity. Northern blot analysis of total RNA demonstrated the same three adrenal LPL mRNA species (1.8, 3.1 and 3.5 kb) as were found in adipose tissue and heart. Hence, at least part of the LPL activity in adrenals is due to enzyme synthesized within the tissue. Immunolocalization showed that LPL was associated with the endothelium of blood vessels throughout the gland. In addition, there was cytoplasmic immunoreaction, suggesting that lipase was synthesized in a subpopulation of cells in the transitional zone between the fasciculata and reticularis layer of the cortex, particularly over lipid-filled cells. There was also intense immunofluorescence over scattered cells in the adrenal medulla. Treatment with an ACTH analogue depot (20 IU, i.m.) for 11 days induced a 12-fold increase in serum cortisol and increased adrenal weight 2.2-fold. The treatment induced increases in LPL mRNA (about twofold), LPL activity and in the number of cells in the adrenal cortex which gave an immunoreaction for LPL.
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PMID:Lipoprotein lipase in guinea-pig adrenals: activity, mRNA, immunolocalization and regulation by ACTH. 164 64

cDNAs encoding rat adipose tissue hormone-sensitive lipase were expressed in COS cells, under the control of the SV40 promoter to half the level in rat adipocytes, the richest native source of the enzyme. A cDNA lacking most of the long 5'-untranslated region of the full-length rat hormone-sensitive lipase cDNA was, with regard to the lipase activity, on the average 70% more efficiently expressed that the full-length cDNA. The recombinant protein was almost identical to hormone-sensitive lipase of rat adipose tissue with respect to specific activity, susceptibility to inhibitors, molecular size, phosphorylation and activation by cyclic AMP-dependent protein kinase. The described eukaryotic expression system will allow analysis of effects of amino acid substitutions introduced into the lipase molecule by site-directed mutagenesis.
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PMID:Expression of biologically active hormone-sensitive lipase in mammalian (COS) cells. 164 10

We established a cell-free system in which epinephrine and other lipolytic agents stimulated lipolysis of endogenous lipid droplets from fat cells by hormone-sensitive lipase. The endogenous lipid droplets were prepared by hypotonic treatment of fat cells and their successive washing with buffer containing 0.025% Triton X-100. In the cell-free system, propranolol inhibited lipolysis induced by various lipolytic agents such as norepinephrine, theophylline and cyclic AMP (cAMP), whereas phenoxybenzamine did not inhibit lipolysis. The binding of these lipolytic agents to endogenous lipid droplets was inhibited by propranolol, but not by phenoxybenzamine. The "propranolol-sensitive" binding of these lipolytic agents to the droplets may be involved in lipolysis. Treatment of the droplets with phospholipase C, but not phospholipase D, inhibited the propranolol-sensitive binding of these lipolytic agents to the droplets. These results suggest that the phosphate group of phospholipid in the droplets may be the site of propranolol-sensitive of binding of theophylline, and cAMP in addition to norepinephrine.
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PMID:Propranolol-sensitive binding of lipolytic agents to lipid droplets from adipocytes. 165 19

Enzymatically active, detergent-solubilized purified hormone-sensitive lipase (HSL) was incorporated into phosphatidylcholine (PC) vesicles, using a detergent-dialysis procedure with small PC vesicles, obtained by sonication, as phospholipid source and CHAPS, a zwitterionic bile-salt derivative, as detergent. Association of enzyme protein with the PC vesicles was verified by floatation in a discontinuous dextran gradient and by gel chromatography. An average of 35% of added HSL was incorporated into the vesicles. The vesicles were shown, by quasi-elastic light scattering and electron microscopy, to have a diameter of approximately 160 nm. The vesicle-associated HSL could be phosphorylated by cyclic AMP-dependent protein kinase. The vesicles were stable, both with regard to enzyme activity and size, for at least 4 days when stored at 4 degrees C. The preparation of detergent-free, vesicle-associated and stable HSL provides new possibilities to study some of its properties, and supports and extends the previous report (Holm, C., Fredrikson, G., and Belfrage, P., J. Biol. Chem. 261, 15659-15661, 1986) which demonstrated the amphiphilic character of HSL.
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PMID:Incorporation of hormone-sensitive lipase into phosphatidylcholine vesicles. 169 43

Hybridization studies using a panel of somatic cell hybrids with subchromosomal segments of 19q have localized the genes encoding hormone-sensitive lipase (LIPE), carcinoembryonic antigen (CEA), and small nuclear ribonucleoprotein polypeptide A (SNRPA) to various regions of 19q13.1; the cellular receptor for poliovirus sensitivity (PVS) to 19q13.2; and the genes coding for prostate-specific antigen (APS), human pancreatic kallikrein (KLK1), and small nuclear ribonucleoprotein 70-kD polypeptide (SNRP70) to 19q13.3----qter. Our results exclude several of these genes from being seriously considered as a candidate for the myotonic dystrophy gene on 19q.
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PMID:Assignment of seven genes to distinct intervals on the midportion of human chromosome 19q surrounding the myotonic dystrophy gene region. 170 Nov 11

Prospective clinical studies have shown that hypotension from hemorrhage contributes to increased morbidity and mortality in patients with traumatic brain injury. It is implied that poorer outcome is the result of secondary brain injury from impaired cerebral oxygen delivery (cO2del). We studied the early and late effects of hypertonic sodium lactate (HSL: 500 mOsm/L) resuscitation on mean arterial pressure (MAP), cardiac output (CO), systemic oxygen delivery (sO2del), cerebral perfusion pressure (CPP), intracranial pressure (ICP), cO2del, cerebral blood flow (CBF), serum osmolality, and cortical water content (CWC) in a porcine model of hemorrhagic shock. Swine were randomized to receive a bolus (4 mL/kg) of either lactated Ringer's solution (LR: 274 mOsm/L) or HSL after shock, followed by either LR or HSL to return MAP to baseline levels. Shed blood was returned 1 hour after resuscitation, and all animals were studied for 24 hours. Control animals were instrumented only. The HSL resuscitation significantly increased cO2del and CBF for 24 hours postresuscitation when compared with LR. The ICP in the HSL-treated animals was significantly lower throughout the postresuscitation phase when compared with the LR-treated animals (p less than 0.05). The CWC was significantly lower in the HSL-treated animals (p less than 0.05). We attribute these effects to hypertonic dehydration of both the brain parenchyma and the cerebrovascular endothelium. These data suggest that by decreasing ICP and improving cO2del after shock, HSL could decrease secondary brain injury when brain injury and shock occur together.
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PMID:Hypertonic fluid resuscitation improves cerebral oxygen delivery and reduces intracranial pressure after hemorrhagic shock. 174 30

The adrenergic regulation of lipolysis was studied, before and after 30 min of submaximal exercise, in isolated adipocytes removed from the abdominal and gluteal regions of healthy non-obese men and women. Noradrenaline-induced lipolysis was significantly enhanced in gluteal adipocytes from men but not in women after exercise. However, the pure beta-adrenergic responsiveness was equally increased in gluteal adipocytes of both sexes after exercise, as judged by the effect of isoprenaline. Furthermore, the alpha 2-adrenergic anti-lipolytic responsiveness was more apparent after exercise in females than in males thereby counter-balancing the increase in the beta-adrenergic effect in the gluteal region in the former. The increased beta-adrenergic responsiveness induced by exercise in gluteal adipocytes of males could be mimicked by agents acting at the levels of adenylate cyclase, coupling proteins, phosphodiesterase, and protein kinase and seems to be due to an adaptive enhancement at the hormone-sensitive-lipase level. There was no change in the stoichiometric properties of beta-adrenoceptors of gluteal adipocytes after exercise. Abdominal adipocytes of both sexes were four to five times more responsive to noradrenaline than gluteal ones. However, exercise induced no further enhancement of the catecholamine-stimulated lipolysis rate in fat cells from this site. Thus, the influence of exercise on catecholamine-stimulated lipolysis is regional and sex dependent. Men, but not women, have a greater ability to adapt lipolysis to increasing energy demands during exercise that are due to an acute increase in the effectiveness of the hormone-sensitive lipase complex.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Adrenergic regulation of lipolysis in human fat cells during exercise. 175 92

The hydrolysis of triglycerides and cholesteryl esters stored within cells is mediated by the enzyme, hormone-sensitive lipase. In adipose tissue and heart, hormone-sensitive lipase primarily hydrolyzes stored triglycerides to free fatty acids, while in steroidogenic tissues, it principally converts cholesteryl esters to free cholesterol for steroid hormone production. To determine whether hormone-sensitive lipase is under tissue-specific, developmental regulation, the steady state levels of hormone-sensitive lipase mRNA were determined in normal rats from late fetal life through 2 years of age. Hormone-sensitive lipase mRNA levels did not appear to vary in adipose tissue from epididymal fat pads obtained from animals between 3 weeks and 2 years of age. In heart, hormone-sensitive lipase mRNA levels were lowest in the fetus increased rapidly within the first day postnatally, and then gradually increased to stable adult levels by 2 months that were 3-fold higher than observed in fetal rats. Steady state mRNA levels of hormone-sensitive lipase in the adrenals were lowest in fetal rats, increased 4-fold during the first day and peaked at levels that were 9-fold higher by the end of the first week. Thereafter, levels fell and remained 3- to 4-fold higher than at birth throughout adult life. Hormone-sensitive lipase mRNA was undetectable in testes before 4 weeks of age and increased 25-fold to stable adult levels between 4 and 12 weeks. Thus, hormone-sensitive lipase is differentially expressed and regulated in a tissue-specific fashion during development and aging.
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PMID:Developmental regulation of hormone-sensitive lipase mRNA in the rat: changes in steroidogenic tissues. 177 Mar 12


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