Decreased inhibition by gravidin of arachidonate release from transformed compared to nontransformed cells

Obesity is a major risk factor for morbidity and mortality, and a series of pharmacologic approaches are available for helping to manage the problem. Obesity is caused by an imbalance between caloric intake and energy expenditure, which is influenced by both environmental and genetic factors. Pharmacologic treatments include anorexigenic agents, which fall into two broad categories: those that act via brain catecholamine pathways and those that act via serotonin pathways. The most recent oral agents approved are dexfenfluramine, which is currently being marketed, and sibutramine. Both agents inhibit the control reuptake of serotonin but in addition may have effects on thermogenesis. Under investigation are agents that increase energy expenditure: the beta 3-adrenergic receptor agonists and drugs that prevent the intestinal absorption of free fatty acids and cholesterol. In development are innovative approaches to influence leptin and its receptors, various obesity genes, and biologic substances thought to influence satiety (neuropeptide Y, enterostatin, cholecystokinin, bombesin, and amylin). Obesity has now become a major target for drug development not only for affecting obesity per se but also for managing and preventing comorbid conditions such as diabetes and cardiovascular disease.

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The Pharmacologic Approach to the Treatment of Obesity

Weiser

Frishman

Michaelson

et al. 1997

The Journal of Clinical Pharma

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β₃ and Atypical β‐Adrenoceptors

Arch

Kaumann

1993

Medicinal Research Reviews

314

220

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RU486 inhibits synthesis of an endogenous inhibitor of cell arachidonate release from choriodecidua tissue

Schuster-Woldan

Hilton²,

Wilson³

1997

Molecular Human Reproduction

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Gravidin is a potent phospholipase A2 inhibitor that may contribute to the maintenance of human pregnancy. The aims of this study were to determine firstly, the site of gravidin synthesis within placental membranes and secondly, whether the antiprogestin compound, RU486, regulates synthesis. Membrane explants were taken from placentae, dissected and cultured in the presence of RU486, progesterone or inhibitors of DNA or protein synthesis and gravidin production was measured by a specific enzyme-linked immunosorbent assay. Production of gravidin was consistently greatest from choriodecidua compared with amnion and decidua. The antibiotics, cycloheximide and actinomycin D inhibited production of gravidin. The progesterone receptor antagonist RU486 at 10(-8) and 10(-7) M reduced gravidin production to 55 and 39% of the control value in membranes cultured after and before the onset of labour respectively. Progesterone at 10(-6) M stimulated gravidin production by 47% after the onset of labour. The increase in gravidin production was correlated with progesterone concentration (r = 0.47, F = 6.38, P = 0.019) in labour tissue. We conclude that the data are consistent with the hypothesis that gravidin production may be partially regulated by progesterone.

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Decreased inhibition by gravidin of arachidonate release from transformed compared to nontransformed cells

Abstract: 1 Gravidin (a phospholipase A2 inhibitor) reduced the release of arachidonic acid from human lymphocytes by 51% at 10-8M.

Cited by 4 publications

References 15 publications

The Pharmacologic Approach to the Treatment of Obesity

The Pharmacologic Approach to the Treatment of Obesity

β₃ and Atypical β‐Adrenoceptors

RU486 inhibits synthesis of an endogenous inhibitor of cell arachidonate release from choriodecidua tissue

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Decreased inhibition by gravidin of arachidonate release from transformed compared to nontransformed cells

Abstract: 1 Gravidin (a phospholipase A2 inhibitor) reduced the release of arachidonic acid from human lymphocytes by 51% at 10-8M.

Cited by 4 publications

References 15 publications

The Pharmacologic Approach to the Treatment of Obesity

The Pharmacologic Approach to the Treatment of Obesity

β3 and Atypical β‐Adrenoceptors

RU486 inhibits synthesis of an endogenous inhibitor of cell arachidonate release from choriodecidua tissue

Contact Info

Product

Resources

About

β₃ and Atypical β‐Adrenoceptors