Inhibition of lipolytic processes in rat adipose tissue by antimalarial drugs

Markus, H.; Ball, Eric G.

doi:10.1016/0005-2760(69)90045-9

Cited by 61 publications

(20 citation statements)

References 9 publications

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“…If saccharin and AceK were working through bitter taste receptors, we might predict that a bitter taste receptor activator would mimic their effects on adipose biology. Consistent with this notion, quinine, which activates nine bitter taste receptors (64), robustly stimulates adipocyte differentiation (data not shown) and represses adipocyte lipolysis (67). We have not directly tested the involvement of specific members of the bitter taste receptor family as these experiments are hampered by low receptor expression and complex and overlapping pharmacology among many receptors (64).…”

Section: Discussionmentioning

confidence: 72%

Artificial Sweeteners Stimulate Adipogenesis and Suppress Lipolysis Independently of Sweet Taste Receptors

Simon¹,

Parlee

Learman

et al. 2013

Journal of Biological Chemistry

112

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Background: Sweet taste receptors are candidate nutrient sensors in adipose tissue. Results: Sweet taste receptor ligands stimulate adipogenesis and suppress lipolysis; however, these effects do not require T1R2 and T1R3 despite their expression in adipose tissue. Conclusion: Some artificial sweeteners regulate adipocyte differentiation and metabolism through a sweet taste receptorindependent mechanism. Significance: Absorbed artificial sweeteners may regulate aspects of adipose tissue biology.

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Section: Discussionmentioning

confidence: 72%

Artificial Sweeteners Stimulate Adipogenesis and Suppress Lipolysis Independently of Sweet Taste Receptors

Simon¹,

Parlee

Learman

et al. 2013

Journal of Biological Chemistry

112

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“…Earlier evidence suggested they interacted with Ca2+ (Scherphof et al, 1972;Waite & Sisson, 1972) although later evidence suggests they interact with the phospholipids (Scherphof & Estenberg, 1975). Vane and his coworkers have used mepacrine as a phospholipase A inhibitor (Vane, 1976), though this drug, like other antimalarials, is a good inhibitor of triglyceride lipases (Markus & Ball, 1969). It also inhibits prostaglandin synthetase (Flower & Blackwell, 1976) (Naylor & Poyser, 1975).…”

Section: Discussionmentioning

confidence: 99%

EFFECT OF p‐BROMOPHENACYL BROMIDE, AN INHIBITOR OF PHOSPHOLIPASE A₂, ON ARACHIDONIC ACID RELEASE AND PROSTAGLANDIN SYNTHESIS BY THE GUINEA‐PIG UTERUS in vitro

Mitchell

Poyser

Wilson

1977

British J Pharmacology

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The synthesis of prostaglandins F2α and E2 by guinea‐pig uterine homogenates was inhibited by p‐bromophenacyl bromide (PBPAB), an inhibitor of phospholipase A2. Metabolism of prostaglandin F2α by uterine homogenates was undetectable; this was not affected by PBPAB. There was no significant difference between the amounts of arachidonic acid released from uterine homogenates on days 7 and 15 of the oestrous cycle. Small amounts of dihomo‐γ‐linolenic acid were detected in the homogenates. The release of arachidonic acid from uterine homogenates was greatly inhibited by PBPAB. Addition of exogenous arachidonic acid to uterine homogenates did not overcome the inhibition of uterine prostaglandin F2α synthesis produced by PBPAB. It is concluded that PBPAB inhibits both the release of arachidonic acid from the guinea‐pig uterus and its subsequent conversion into prostaglandins.

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“…Cycloxygenase metabolites do not appear to be linked to ACTH release. The participation of arachidonic acid in the secretion of ACTH is suggested by the suppression of release of the peptide by the two phospholipase A2 inhibitors mepacrine and p-bromophenacylbromide at concentrations similar to those reported to block phospholipase A2 activity (13)(14)(15)(16)(17). It is unlikely that arachidonic acid is the agent directly concerned with ACTH release.…”

Section: Discussionmentioning

confidence: 99%

Inhibitors of the cytochrome P-450 enzymes block the secretagogue-induced release of corticotropin in mouse pituitary tumor cells.

Luini

Axelrod

1985

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

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A mouse pituitary tumor cell line (AtT-20) releases corticotropin (ACTH) in response to a number of secretagogues, iWciuding corticotropin-releasing factor (CRF), j3-adrenergic aints, N6,02'-dibutyryladenosine 3',5'-cyclic monophosphate (Bt2 cAMP), and potassium. The AtT-20 mouse pituitary cell line is a well-characterized model system to study corticotropin (ACTH) secretion. These cells release ACTH in response to a number of secretagogues, including corticotropin-releasing factor (CRF), isoproterenol, vasoactive intestinal peptide, the Ca2+ ionophore A23187, and potassium (1). It has been shown that the second messengers cAMP and Ca2+ (1), as well as phospholipid methylation (2), are involved in the mediation of these secretory responses. There has also been indirect evidence suggesting that arachidonic acid and/or its metabolites may be involved in ACTH secretion in AtT-20 cells. Phorbol esters and melittin, activators of phospholipase A2 (3-7), the enzyme that liberates arachidonic acid from lipids, are potent stimulators of ACTH secretion (8, 9). The synthetic corticosterone dexamethasone, which exerts some of its actions by inhibiting phospholipase A2 (10), blocks ACTH release (1). These findings prompted an investigation as to whether arachidonic acid or one or more of its many metabolites are involved in receptor-mediated ACTH secretion.Arachidonic acid is metabolized via three pathways: cycloxygenase, which generates prostaglandins and tromboxanes, lipoxygenase, which forms leukotrienes, and the NADPH-dependent cytochrome P-450 enzymes (epoxygenase), which forms epoxide metabolites (11). To ascertain whether metabolites of these pathways are involved in ACTH release, inhibitors of each of these enzymes as well as phospholipase A2 were used. We find that inhibitors of phospholipase A2, lipoxygenase, and epoxygenase, but not cycloxygenase, block the release of ACTH in AtT-20 cells. MATERIALS AND METHODSSynthetic CRF was obtained from Bachem Fine Chemicals (Torrance, CA), (-)-isoproterenol (+)-bitartrate, human serum albumin, 3-isobutyl-1-methylx4thine (IBMX), melittin, phorbol myristate acetate, nordihydrbguaieretic acid, butylated hydroxytoluene, p-bromophenacyl-bromide, mepacrine, A23187, N6,02'-dibutyryladenosine 3',5'-cyclic monophosphate (Bt2cAMP), 8-bromoadenosine 3',5'-cyclic monophosphate (8-Br-cAMP), and barbital were from Sigma. Forskolin was purchased from Calbiochem-Behring. Icosatetraynoic acid was kindly supplied by F. Hirata. Piperonyl butoxide and 2-diethylaminoethyl-2,2-diphenylvalerate (SKF 525A) were a generous gift from J. Gillette.Cell Culture Methods. AtT-20/D16-16 cells were grown and subcultured in Dulbecco's modified Eagle's medium (DME medium) with 10% calf serum, as described (12). Cells were plated in 30-mm (diameter) culture dishes at an initial density of 1.5 x 105 cells per well and were used 5-6 days after plating (60-80% confluency). For ACTH secretion studies, cells were equilibrated for 30 min at 37°C in 1 ml of DME medium/25 mM Hepes, pH 7.4, containing bovine s...

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Inhibition of lipolytic processes in rat adipose tissue by antimalarial drugs

Cited by 61 publications

References 9 publications

Artificial Sweeteners Stimulate Adipogenesis and Suppress Lipolysis Independently of Sweet Taste Receptors

Artificial Sweeteners Stimulate Adipogenesis and Suppress Lipolysis Independently of Sweet Taste Receptors

EFFECT OF p‐BROMOPHENACYL BROMIDE, AN INHIBITOR OF PHOSPHOLIPASE A₂, ON ARACHIDONIC ACID RELEASE AND PROSTAGLANDIN SYNTHESIS BY THE GUINEA‐PIG UTERUS in vitro

Inhibitors of the cytochrome P-450 enzymes block the secretagogue-induced release of corticotropin in mouse pituitary tumor cells.

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Inhibition of lipolytic processes in rat adipose tissue by antimalarial drugs

Cited by 61 publications

References 9 publications

Artificial Sweeteners Stimulate Adipogenesis and Suppress Lipolysis Independently of Sweet Taste Receptors

Artificial Sweeteners Stimulate Adipogenesis and Suppress Lipolysis Independently of Sweet Taste Receptors

EFFECT OF p‐BROMOPHENACYL BROMIDE, AN INHIBITOR OF PHOSPHOLIPASE A2, ON ARACHIDONIC ACID RELEASE AND PROSTAGLANDIN SYNTHESIS BY THE GUINEA‐PIG UTERUS in vitro

Inhibitors of the cytochrome P-450 enzymes block the secretagogue-induced release of corticotropin in mouse pituitary tumor cells.

Contact Info

Product

Resources

About

EFFECT OF p‐BROMOPHENACYL BROMIDE, AN INHIBITOR OF PHOSPHOLIPASE A₂, ON ARACHIDONIC ACID RELEASE AND PROSTAGLANDIN SYNTHESIS BY THE GUINEA‐PIG UTERUS in vitro