Effects of prostaglandin E1 and norepinephrine on glucose and lipid metabolism in isolated perfused rat liver

Lemberg, A; Wikinski, Regina; Izurieta, E.M.; Halperin, H; Paglione, A.M.; Neuman, Paul; Jauregui, Hugo O.

doi:10.1016/0005-2760(71)90007-5

Cited by 13 publications

(1 citation statement)

References 11 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Although several studies have demonstrated hyperglycaemic effects ofprostaglandins in vivo [32][33][34], studies in vitro have furnished apparently conflicting results. Whereas some studies have demonstrated glycogenolytic responses to prostaglandins in isolated hepatic systems [34][35][36], others have shown no effect [37][38][39][40] or inhibition [41] of hepatic glycogenolysis by E-series prostaglandins, leading to the suggestion [40] that the hyperglycaemia observed in response to prostaglandins in vivo may be secondary to changes in hormonal status [42][43][44]. It is clear from the present study that prostaglandin E2 has glycogenolytic effects in the perfused rat liver.…”

Section: (A) Menmentioning

confidence: 55%

Glycogenolytic and haemodynamic responses to heat-aggregated immunoglobulin G and prostaglandin E2 in the perfused rat liver

Buxton¹,

Fisher²,

Briseno³

et al. 1987

Biochemical Journal

View full text Add to dashboard Cite

Infusion of heat-aggregated immunoglobulin G (HAG) into perfused livers from fed rats caused transient increases in hepatic glycogenolysis and portal-vein pressure, accompanied by a transient increase in hepatic glycogen phosphorylase alpha content. The hepatic responses to HAG were inhibited by indomethacin (2 microM). In contrast, HAG was without effect on phosphorylase alpha content and glucose output in isolated hepatocytes. HAG infusion caused a transient decrease in hepatic cyclic AMP. Lowering the extracellular Ca2+ concentration to 6 or 50 microM attenuated markedly the glycogenolytic and haemodynamic responses to HAG; efflux of Ca2+ from the liver was not observed in response to HAG. Co-infusion of the specific platelet-activating-factor antagonist U-66985 (1-O-octadecyl-2-O-acetyl-sn-glycero-3-phosphoric acid 6'-trimethylammoniumhexyl ester) did not attenuate the glycogenolytic response to HAG. Infusion of prostaglandin E2 caused increases in glucose output, portal-vein pressure and the reduction state of the cytosolic NAD(H) redox couple similar to those seen with HAG. The present study suggests that the glycogenolytic activation after HAG infusion may be an indirect consequence of the haemodynamic response of the hepatic vasculature to stimulation of the reticuloendothelial cells of the liver.

show abstract