Prostacyclin and lipolysis in rat fat cells

Gaion, R.M.; Trento, Mariangela; Murari, Laura; Dorigo, P.; Ferro, C P; Fassina, G.

doi:10.1016/0006-2952(84)90042-x

Cited by 11 publications

(3 citation statements)

References 15 publications

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“…Previous studies had shown that PGI 2 is not lipolytic in 10 and 45 min incubations (10), that PGI 2 is antilipolytic in the presence of nonphysiological stimuli such as phosphodiesterase inhibitors (22), or that PGI 2 is lipolytic at a nonphysiological pH of 8.5 (23,24), used to prolong the half-life of PGI 2 , an unstable substance. However, the demonstration of a lipolytic effect of PGI 2 at alkaline pH does not necessarily indicate that PGI 2 is lipolytic at physiological pH because the nonphysiological pH may have effects on lipolysis independent of an effect on the stability of PGI 2 .…”

Section: Discussionmentioning

confidence: 98%

Coordinate Control of Lipolysis by Prostaglandin E2 and Prostacyclin in Rat Adipose Tissue

Chatzipanteli

Rudolph²,

Axelrod³

1992

Diabetes

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PGE2 is a potent antilipolytic agent produced by adipose tissue, but its role as a physiological regulator of triglyceride lipolysis is controversial because inhibitors of prostaglandin synthesis have not enhanced hormone-stimulated lipolysis in adipose tissue consistently. Adipose tissue also produces PGI2, but this eicosanoid has not had a demonstrated effect on lipolysis under physiological conditions previously. We investigated both PGE2 and PGI2 production and their effects on lipolysis in rat adipose tissue. We found that 1) EPI-stimulated PGE2 production (like PGI2 production) requires the cooperation of adipocytes and endothelial cells, 2) adipose tissue produces PGE2 and PGI2 at comparable rates, 3) indomethacin inhibits EPI-induced PGE2 and PGI2 production and has no effect on EPI-stimulated lipolysis when added to a mixture of adipocytes and endothelial cells or to intact epididymal fat pads, 4) PGI2 is a potent lipolytic agent when added to isolated adipocytes in the absence of endothelial cells under physiological conditions, 5) the magnitudes and the ED50s of the antilipolytic effect of PGE2 and the lipolytic effect of PGI2 in isolated adipocytes in the absence of endothelial cells are comparable, 6) PGI2 antagonizes the antilipolytic effect of PGE2 in isolated adipocytes in the absence of endothelial cells in a dosage-related manner, and 7) the antilipolytic effect of added PGE2 in isolated adipocytes is greater in the absence of endothelial cells than in their presence, suggesting that endogenous eicosanoid production reduces the effectiveness of added PGE2. These studies demonstrate that catecholamine-induced lipolysis is under the coordinate control of PGE2, a potent antilipolytic agent, and PGI2, a potent lipolytic agent.(ABSTRACT TRUNCATED AT 250 WORDS)

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Section: Discussionmentioning

confidence: 98%

Coordinate Control of Lipolysis by Prostaglandin E2 and Prostacyclin in Rat Adipose Tissue

Chatzipanteli

Rudolph²,

Axelrod³

1992

Diabetes

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“…PGE2 displayed the same properties on lipolysis [99], most likely through the same receptor EP3 known to inhibit cAMP mediated pathways induced by lipolytic agents [100].Thus, inhibition of lipolysis seems to be specific to Gαi-coupled receptor as PGF2α, which activates Gαq-coupled receptor, is unable to inhibit lipolysis induced by norepinephrine [101].Lipolysis is under the control of cAMPlevelsand downstream events, as well as cGMP levels in some situations [102], thus oxylipins able to bind to Gαs-coupled receptorsshall be considered as potential lipolytic agents. This observation has been validated for prostacyclin [92], whichpotentiates the effect of norepinephrine on lipolysis [103].The oxylipin-mediated restriction of lipolysis seems to be a preponderant eventin vivo, as recent data demonstrate that inhibition of COX activity by indomethacin favored lipolysis under fasting condition [8,104].…”

Section: Interaction Between Ppars Gpcrs and Oxylipins In Adipocyte mentioning

confidence: 79%

Control of adipogenesis by oxylipins, GPCRs and PPARs

et al. 2017

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Oxylipins are bioactive metabolites derived from the oxygenation of ω3 and ω6 polyunsaturated fatty acids, triggered essentially by cyclooxygenase and lipoxygenase activities. Oxylipins are involved in the development and function of adipose tissue and their productions are strictly related to diet quality and quantity. Oxylipins signal via cell surface membrane (G Protein-coupled receptors) and nuclear receptors (peroxisome proliferator-activated receptors), two pathways playing a pivotal role in adipocyte biology. In this review, we made an attempt to cover the available knowledge about synthesis and molecular function of oxylipins known to modulate adipogenesis, adipocyte function and phenotype conversion, with a focus on their interaction with peroxisome proliferator-activated nuclear receptor family.

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“…Although the most obvious action of the prostaglandins is to inhibit lipolysis, the literature contains a few suggestions that prostaglandins or related agents may stimulate rather than inhibit the adenylyl cyclase of rat adipocytes. Prostacyclin (PG12) under special conditions enchances cAMP accumulation by these cells, as do PGHz and PGDz (Fredholm et al, 19801, and can enhance the lipolytic effect of submaximally effective concentrations of norepinephrine (Gaion et al, 1984). Under certain experimental conditions even PGEl can enhance rather than inhibit levels of intracellular cAMP (Fatemi, 1985).…”

Section: Gs Gimentioning

confidence: 99%

Prostaglandin‐sensitive adenylyl cyclase of cultured preadipocytes and mature adipocytes of the rat: Probable role of G_i in determination of stimulatory or inhibitory action

Piñeyro

Kirkland

et al. 1988

Journal Cellular Physiology

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Preadipocytes of rats were obtained from the stromal-vascular fraction of collagenase-digested perirenal fat pads and grown in serum-containing medium. By day 8 of culture the cells reached confluence and by 12 days were lipid-laden. The adenylyl cyclase of the plasma membranes was compared to that of mature fat cells. Unlike the membranes from adipocytes, the preadipocytes showed adenylyl cyclase activity that was stimulated by GTP. Stimulation of preadipocyte membranes by Gpp(NH)p, NaF, and forskolin was comparable to that of membranes from adipocytes, but the response to epinephrine and isoproterenol was minimal (approximately 1.5-fold for preadipocytes vs. 4-5-fold for adipocytes). In contrast, GTP-dependent stimulation of adenylyl cyclase of preadipocytes by PGE1 was nearly 8-fold. Stimulation occurred even in the presence of both GTP and 140 mM NaCl, a condition that leads to inhibition by PGE1 of adenylyl cyclase in membranes of adipocytes. Other characteristics of the adenylyl cyclase of preadipocyte membranes that differ from those of adipocytes include lack of inhibition by GTP of forskolin-activated activity, and, following treatment with pertussis toxin, enhanced stimulation by PGE1. ADP-ribosylation of Gi and Gs with pertussis and cholera toxins, respectively, indicated that the membranes of preadipocytes contained only 5-11% of the Gi of adipocytes and a much lower ratio of Gi:Gs. These findings suggest that cultured preadipocytes have an incompletely developed Gi pathway that may account for the stimulatory effect of prostaglandins on the adenylyl cyclase of these cells as opposed to the inhibitory action of PG in mature fat cells.

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Prostacyclin and lipolysis in rat fat cells

Cited by 11 publications

References 15 publications

Coordinate Control of Lipolysis by Prostaglandin E2 and Prostacyclin in Rat Adipose Tissue

Coordinate Control of Lipolysis by Prostaglandin E2 and Prostacyclin in Rat Adipose Tissue

Control of adipogenesis by oxylipins, GPCRs and PPARs

Prostaglandin‐sensitive adenylyl cyclase of cultured preadipocytes and mature adipocytes of the rat: Probable role of G_i in determination of stimulatory or inhibitory action

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Prostacyclin and lipolysis in rat fat cells

Cited by 11 publications

References 15 publications

Coordinate Control of Lipolysis by Prostaglandin E2 and Prostacyclin in Rat Adipose Tissue

Coordinate Control of Lipolysis by Prostaglandin E2 and Prostacyclin in Rat Adipose Tissue

Control of adipogenesis by oxylipins, GPCRs and PPARs

Prostaglandin‐sensitive adenylyl cyclase of cultured preadipocytes and mature adipocytes of the rat: Probable role of Gi in determination of stimulatory or inhibitory action

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Prostaglandin‐sensitive adenylyl cyclase of cultured preadipocytes and mature adipocytes of the rat: Probable role of G_i in determination of stimulatory or inhibitory action