Disease relevance of Lipolysis

• In summary, in vivo lipolysis, which mostly reflects the mobilization of lipid stores from subcutaneous adipose tissue, shows a decreased sensitivity to epinephrine in childhood onset obesity [1].
• The effects of adenosine deaminase and of pertussis toxin on hormonal regulation of lipolysis were investigated in isolated human fat cells [2].
• When insulin is deficient, on the other hand, elevated rates of lipolysis may contribute to hyperglycemia not by competition for fuel utilization, but through an enhancement of endogenous glucose output [3].
• To test the hypothesis that FFA mediate changes in glucose metabolism that occur during counterregulation, we examined the effects of acipimox, an inhibitor of lipolysis, on glucose production and utilization ([3-3H]glucose), and incorporation of [U-14C]-alanine into glucose during insulin-induced hypoglycemia [4].
• Hyperinsulinemia for 2 or 6 wk did not alter basal or epinephrine-stimulated lipolysis in adipose cells or the antilipolytic effect of insulin [5].

Psychiatry related information on Lipolysis

• Although increased insulin sensitivity of glucose disposal and lipolysis has been reported, the exact mechanism by which the risk reduction is conferred is not clear [6].
• These results indicate that the fasting-induced rise in lipolysis results predominantly from changes in the lipolytic cascade downstream from protein kinase A. The antagonism of the adenosine A (1) receptor and the inhibition of cAMP phosphodiesterase also induced lipolysis, which was potentiated by food deprivation [7].
• Moderate alcohol consumption, glucose metabolism and lipolysis: the effect on adiponectin and tumor necrosis factor alpha [8].

High impact information on Lipolysis

• Cidea-null mice had higher metabolic rate, lipolysis in BAT and core body temperature when subjected to cold treatment [9].
• Our results demonstrate a role for perilipin in reining in basal HSL activity and regulating lipolysis and energy balance; thus, agents that inactivate perilipin may prove useful as anti-obesity medications [10].
• The beta 3-adrenergic receptor, located mainly in adipose tissue, is involved in the regulation of lipolysis and thermogenesis [11].
• We believe that glucose infusion lowers exercise tolerance by inhibiting lipolysis and thus depriving muscle of oxidative substrate (plasma free fatty acids and ketones); this impairs the capacity of working muscle to extract oxygen and lowers maximal oxygen consumption [12].
• Agents that increase cAMP content (Dibutyryl cAMP, theophylline, and isoproterenol) are known to induce lipolysis in fat cells; but the same agents are shown here to reduce the synthesis of the lipogenic enzymes during adipose differentiation [13].

Chemical compound and disease context of Lipolysis

• We conclude that the abnormal apoprotein composition of HDL in experimental nephrosis is the result of altered entry of apolipoproteins from triglyceride-rich lipoproteins, probably because of decreased lipolysis [14].
• Hyperinsulinemia suppressed systemic and forearm lipolysis to similar degrees, however, hypoinsulinemia consistently increased systemic palmitate flux without increasing forearm palmitate release [15].
• Phenylalanine release from adipose tissue like lipolysis, is relatively sensitive to hyperinsulinemia [16].
• Pertussis toxin eliminated the inhibition of lipolysis and the stimulation of adenylate cyclase by isoprenaline and lipid-mobilizing factor in the presence of EPA, but not DHA [17].
• The effects of fasting show that during periods of lipolysis beta-HCH can be released in quantities sufficient to stimulate estrogen target tissues, suggesting a novel mechanism linking obesity and the progression of estrogen-responsive tumors [18].

Biological context of Lipolysis

• Insulin resistance affects glucose-transporter activity and recruitment, counterregulation of lipolysis, and activation of glycogen synthase, all of which are cardinal responses to insulin [19].
• Corticosteroids as well as non-steroid anti-inflammatory drugs inhibit the prostaglandin-mediated vasodilatation accompanying lipolysis in subcutaneous fat [20].
• The body fat distribution and the metabolic profile in nonobese and obese individuals is discussed relative to lipolysis, antilypolysis and lipogenesis, insulin sensitivity, and glucose, lipid, and protein metabolism [21].
• The beta3 adrenergic receptor, located on chromosome 8, is a regulator of energy expenditure and lipolysis [22].
• We, therefore, conclude that lipolysis is increased in NIDDM and, although more glycerol is thus available, increased activity of the intrahepatic pathway for conversion of glycerol into glucose, due at least in part to increased plasma free fatty acids, is the predominant mechanism responsible for enhanced glycerol gluconeogenesis [23].

Anatomical context of Lipolysis

• Although catecholamines stimulate lipolysis in human fat cells, activation by epinephrine of adenylate cyclase in human fat cell membranes is not readily observed [24].
• We conclude that significant amounts of glycerol are released from skeletal muscle, which suggests that muscle lipolysis provides an important endogenous energy source in humans [25].
• Here we report, using digitonin-permeabilized rat adipocytes, that physiological concentrations of insulin inhibit cyclic AMP-activated lipolysis despite the absence of cytosolic and plasma membrane integrity [26].
• A unique defect in the regulation of visceral fat cell lipolysis in the polycystic ovary syndrome as an early link to insulin resistance [27].
• In the normal individual, the direct effect of the hormone on the hepatocyte is far more important in restraining glucose production than its indirect effect mediated via a suppression of lipolysis [28].

Associations of Lipolysis with chemical compounds

• The effects of the agents on the synthesis of lipogenic enzymes are not dependent on lipolysis, since they take place to the same degree in cells not permitted to accumulate triglyceride [13].
• The head group was reported to activate a high-affinity cyclic AMP-phosphodiesterase and pyruvate dehydrogenase, to inhibit catecholamine-stimulated lipolysis, and also to inhibit phospholipid methyltransferase and adenylate cyclase [29].
• In contrast, isoprenaline, fenoterol and salbutamol are less potent as stimulants of lipolysis than as stimulants of atrial rate or tracheal relaxation [30].
• Fifth, the contribution of adipose tissue lipolysis is reviewed with an emphasis on the various regulatory factors of the lipolytic pathways including catecholamines, insulin, adenosine, steroids, and other modulators [31].
• These antibodies have the insulin-like activities of enhancing glucose oxidation and inhibiting epinephrine-induced lipolysis in rat adipocytes [32].

Gene context of Lipolysis

• The addition of ApoC-III-2 resulted in a decreased rate of lipolysis of human very low density lipoproteins by LPL [33].
• In dog fat cells NPY and PYY inhibited adenosine deaminase-, isoproterenol- and forskolin-induced lipolysis [34].
• This study indicates that, in addition to alpha 2-adrenergic agonists, NPY and PYY are also involved in the regulation of lipolysis in human and dog adipose tissue as powerful antilipolytic agents [34].
• Chylomicron remnants, produced by lipolysis, are rapidly taken up by the liver via an apolipoprotein E (apoE)-mediated, receptor-dependent process [35].
• The Adfp-deficient mice have unaltered adipose differentiation or lipolysis in vitro or in vivo [36].

Analytical, diagnostic and therapeutic context of Lipolysis

• Glucose turnover was assessed during a euglycemic clamp at two insulin levels (low approximately 20 mU/l; high approximately 90 mU/l), and abdominal subcutaneous adipose tissue (SAT) lipolysis and blood flow were concomitantly studied with microdialysis and 133Xe clearance [37].
• During 45-min perfusions, the lipolysis of very low density lipoprotein (VLDL) triglyceride was significantly less in hearts from diabetics than in controls (41.9 +/- 7.3% of control) [38].
• Subjects were studied with indirect calorimetry and microdialysis of skeletal muscle and adipose tissue in order to analyze substrate utilization and glycerol (lipolysis index) in connection with a two-step euglycemic-hyperinsulinemic (12 and 80 mU/m(2). min) clamp [39].
• Diglyceride mixtures resulting from lipolysis were derivatized with optically active R-(+)-1-phenylethylisocyanate, to give diastereomeric carbamate mixtures, which were further separated by high performance liquid chromatography [40].
• Adipocytes isolated from AFABP-KO and WT mice fed high- or low-fat diets exhibited similar rates of basal and norepinephrine-stimulated lipolysis and insulin-stimulated rates of glucose conversion to fatty acids and glyceride-glycerol [41].

References