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)

Fourteen adult patients (mean age, 35 yrs) with 20-60% total body surface area (TBSA) burns (mean, 35%) were resuscitated using hypertonic sodium lactate (HSL: sodium = 250 mEq/L). Plasma concentrations of atrial natriuretic peptide (ANP), arginine vasopressin (AVP), angiotensin II (A-II), epinephrine (E) and norepinephrine (NE) were measured on admission and for 7 days following burn injury. Serum sodium concentrations and osmolalities were lowest on admission, and were persistently elevated following HSL resuscitation. Plasma AVP levels were highest on admission and correlated with the size of the burn injury. Between days 4 and 5 plasma ANP levels rose while plasma AVP levels returned to normal. Plasma concentrations of AVP and ANP did not correlate with serum osmolality or serum sodium concentrations on admission or after HSL resuscitation. Plasma levels of A-II, NE and E were elevated throughout the 7-day period and were unrelated to the size of the burn.
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PMID:The neurohumoral response to burn injury in patients resuscitated with hypertonic saline. 297 May 56

Fat cell lipolysis, the cleavage of triglycerides and release of fatty acids and glycerol, evolved to enable survival during prolonged food deprivation but is paradoxically increased in obesity, in which a surfeit of all energy metabolites is found. Essential, previously-unsuspected components have been discovered in the lipolytic machinery, at the protective interface of the lipid droplet surface and in the signaling pathways that control lipolysis. At least two adipocyte lipases are important for controlling lipolysis, hormone-sensitive lipase (HSL) and adipocyte triglyceride lipase (ATGL). Perilipin (PLIN) and possibly other proteins of the lipid droplet surface are master regulators of lipolysis, protecting or exposing the triglyceride core of the droplet to lipases. The prototypes for hormonal lipolytic control are beta adrenergic stimulation and suppression by insulin, both of which affect cyclic AMP levels and hence the protein kinase A-mediated phosphorylation of HSL and PLIN. Newly-recognized mediators of lipolysis include atrial natriuretic peptide, cyclic GMP, the ketone body 3-hydroxybutyrate, AMP kinase and mitogen-activated kinases. Lipolysis must be interpreted in its physiological context since similar rates of basal or stimulated lipolysis occur under different conditions and by different mechanisms. Age, sex, anatomical site, genotype and species differences are each important variables. Manipulation of lipolysis has therapeutic potential in several inborn errors and in the metabolic syndrome that frequently complicates obesity.
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PMID:Lipolysis and the integrated physiology of lipid energy metabolism. 1876 40

Increased myocardial autophagy has been established as an important stress-induced cardioprotective response. Three weeks after generating cardiomyocyte-specific autophagy deficiency, via inducible deletion of autophagy related protein 7 (Atg7), we found these mice (AKO) increased body weight and fat mass without altered food intake. Glucose and insulin tolerance tests indicated reduced insulin sensitivity in AKO mice. Metabolic cage analysis showed reduced ambulatory activity and oxygen consumption with a trend of elevated respiratory exchange ratio in AKO mice. Direct analysis of metabolism in subcutaneous and visceral adipocytes showed increased glucose oxidation and reduced ATGL expression and HSL phosphorylation with no change in lipid synthesis or fatty acid oxidation. Importantly, we found AKO mice had reduced myocardial and circulating levels of atrial natriuretic peptide (ANP), an established mediator of myocardial-adipose crosstalk. When normal ANP levels were restored to AKO mice using osmotic pump, the metabolic dysfunction evident in AKO mice was corrected. We conclude that cardiac autophagy deficiency alters myocardial-adipose crosstalk via decreased ANP levels with adverse metabolic consequences.
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PMID:Cardiac Autophagy Deficiency Attenuates ANP Production and Disrupts Myocardial-Adipose Crosstalk Leading to Increased Fat Accumulation and Metabolic Dysfunction. 3304 83