Adrenergic regulation of adipocyte metabolism

Lafontan, Max; Barbe, P; Galitzky, Jean; Tavernier, Geneviève; Langin, Dominique; Carpéné, Christian; Bousquet‐mélou, Alain; Berlan, Michel

doi:10.1093/humrep/12.suppl_1.6

Cited by 117 publications

(95 citation statements)

References 69 publications

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“…After isoproterenol stimulation of the ␤2AR, the G␣-subunit G␣ s , through exchange of GTP for GDP, activates adenylyl cyclase, generating cyclic adenosine monophosphate (cAMP). In the adipocyte, cAMP activates protein kinase A, which, in turn, phosphorylates and activates hormone-sensitive lipase, the rate-limiting enzyme for triglyceride hydrolysis (3).…”

Section: Medical Sciencesmentioning

confidence: 99%

β-Arrestin 1 down-regulation after insulin treatment is associated with supersensitization of β2 adrenergic receptor Gαs signaling in 3T3-L1 adipocytes

Hupfeld

Dalle

Olefsky

2002

Proc. Natl. Acad. Sci. U.S.A.

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3T3-L1 adipocytes were incubated in serum-free media at 37°C with (dashed line) or without (solid line) 100 ng͞ml insulin for 8 h. Isoproterenol (10 M) was then added for the indicated time course at 37°C, and intracellular cAMP was determined by enzyme immunoassay, as described in Materials and Methods. Data are from a typical experiment done in triplicate wells Ϯ SEM and are representative of three separate experiments. (B) 3T3-L1 adipocytes were incubated in serum-free media for 8 h. Where indicated, 100 ng͞ml insulin was added for 15 min before isoproterenol treatment. Cells were then treated with 10 M isoproterenol for 5 min at 37°C, and intracellular cAMP was determined by enzyme immunoassay, as described in Materials and Methods. Data are from a typical experiment done in triplicate wells Ϯ SEM and are representative of three separate experiments.www.pnas.org͞cgi͞doi͞10.1073͞pnas.0630528100 After this, cells were treated with 10 M isoproterenol for 5 min at 37°C. Cells were then washed with PBS at 37°C and restimulated with a second 10 M dose of isoproterenol for an additional 5 min at 37°C; intracellular cAMP was determined by enzyme immunoassay. (B) 3T3-L1 adipocytes were incubated at 37°C in serum-free media for 8 h in the presence (dashed lines) or absence (solid lines) of 100 ng͞ml insulin. Forskolin was added for the final 5 min, and intracellular cAMP levels were determined by enzyme-linked immunoassay. Data are from typical experiments done in triplicate wells and are representative of three separate experiments.

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Section: Medical Sciencesmentioning

confidence: 99%

β-Arrestin 1 down-regulation after insulin treatment is associated with supersensitization of β2 adrenergic receptor Gαs signaling in 3T3-L1 adipocytes

Hupfeld

Dalle

Olefsky

2002

Proc. Natl. Acad. Sci. U.S.A.

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“…The effects on cAMP production and cAMP-related cellular responses are mediated through the control of adenylyl cyclase activity by the stimulatory b 1 -, b 2 -and b 3 -adrenoceptors (AR) and the inhibitory a 2 -ARs. 1,2 The b 3 -AR is highly expressed in rodent adipose tissues 3,4 and several studies have suggested that it plays a signi®cant role in adipocyte metabolism and might be involved in the development of obesity, 4 ± 6 thus making b 3 -AR a possible target for anti-obesity drugs. In this way, numerous selective b 3 -AR agonists have been synthesized and have been found to possess, with various degrees of speci®city, anti-obesity and also anti-diabetic properties.…”

Section: Introductionmentioning

confidence: 99%

Effects of cafeteria diet feeding on β3-adrenoceptor expression and lipolytic activity in white adipose tissue of male and female rats

et al. 2000

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OBJECTIVE: To investigate the effects of short term (15 days) cafeteria diet feeding on the expression of b b 3 -AR in vivo and its association with lipolytic stimulation induced by b b 3 -AR agonist CGP12177A in isolated white adipocytes. ANIMALS: Six female and 6 male Wistar rats (at 4 weeks of age) were fed on a cafeteria diet plus standard diet for 15 days. The remaining 12 age-and sex-matched rats always received standard diet only. MEASUREMENTS: White gonadal adipose tissue was isolated and used for the determination of b b 3 -AR and leptin expression, and for in vitro studies of lipolytic activity. RESULTS: Control male rats had higher levels of both b b 3 -AR and leptin mRNA in white adipose tissue than their female counterparts. Both male and female rats up-regulated the levels of both b b 3 -AR and leptin mRNA in response to 15 day cafeteria diet feeding. Noradrenaline-and isoprenaline-induced lipolysis were signi®cantly increased in fat cells from control females compared to their male counterparts. CGP12177A stimulation resulted in signi®cantly higher glycerol release in fat cells from cafeteria diet-fed female rats, whereas there were no differences due to dietary treatment in male rats. The maximal lipolytic response of forskolin (stimulating adenylyl cyclase) and dibutyryl cyclic AMP (cyclic AMP analogous) was not affected by sex or cafeteria diet feeding. CONCLUSION: Cafeteria diet feeding brings about higher excess body weight and impaired adipose tissue lipolytic activity in female rats compared to male rats. Thus, the higher levels of b b 3 -AR mRNA induced by cafeteria feeding are not indicative per se of an increase of the lipolytic response of the adipocytes. The changes seen in other adrenoceptor subtypes (b b 1 and b b 2 ) may be more determinant of the overall lipolytic response of adipocytes.

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“…On the other hand, DAG is hydrophobic and remains in the membrane, acting as a signal messenger for activation of protein kinase C (PKC), and facilitates its translocation to the cellular membrane. DAG-mediated PKC activation in adipocytes through b-adrenergic receptors, in turn, increases glycogenolysis and gluconeogenesis (Lafontan et al, 1997).…”

Section: Dagmentioning

confidence: 99%

Role of bioactive lipid mediators in obese adipose tissue inflammation and endocrine dysfunction

Lopategi

López‐Vicario

Alcaraz‐Quiles

et al. 2016

Molecular and Cellular Endocrinology

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a b s t r a c tWhite adipose tissue is recognized as an active endocrine organ implicated in the maintenance of metabolic homeostasis. However, adipose tissue function, which has a crucial role in the development of obesity-related comorbidities including insulin resistance and non-alcoholic fatty liver disease, is dysregulated in obese individuals. This review explores the physiological functions and molecular actions of bioactive lipids biosynthesized in adipose tissue including sphingolipids and phospholipids, and in particular fatty acids derived from phospholipids of the cell membrane. Special emphasis is given to polyunsaturated fatty acids of the omega-6 and omega-3 families and their conversion to bioactive lipid mediators through the cyclooxygenase and lipoxygenase pathways. The participation of omega-3-derived lipid autacoids in the resolution of adipose tissue inflammation and in the prevention of obesity-associated hepatic complications is also thoroughly discussed.

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Adrenergic regulation of adipocyte metabolism

Cited by 117 publications

References 69 publications

β-Arrestin 1 down-regulation after insulin treatment is associated with supersensitization of β2 adrenergic receptor Gαs signaling in 3T3-L1 adipocytes

β-Arrestin 1 down-regulation after insulin treatment is associated with supersensitization of β2 adrenergic receptor Gαs signaling in 3T3-L1 adipocytes

Effects of cafeteria diet feeding on β3-adrenoceptor expression and lipolytic activity in white adipose tissue of male and female rats

Role of bioactive lipid mediators in obese adipose tissue inflammation and endocrine dysfunction

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