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Biomedical subjects

J A Spitzer

Publications and source records attributed to J A Spitzer.

107 records · Page 6Linked to original sources
PubMed1974

Metabolism of isolated fat cells from various tissue sites in the rat: influence of hemorrhagic hypotension.

The in vitro lipolytic response to norepinephrine by rat adipocytes from epididymal, subcutaneous, perirenal, mesenteric, and omental tissue sites was studied in control and hypotensive animals. Lipolysis per millimole of triglyceride was found to be three to four times higher in mesenteric and omental fat cells than in adipocytes of the other sites sampled. The high lipolytic activity of mesenteric and omental adipocytes was partly attributable to their smaller cell size; however, lipolysis per cell was also higher. Hemorrhagic hypotension caused a 50-60% decrease in lipolytic activity at four of the five sites studied. Adipocytes of omental origin maintained their lipolytic activity at the prehypotensive level, however, indicating that the metabolic adjustments brought about by hemorrhagic hypotension are not uniform at all adipose tissue sites.

Adipose Tissue↗
PubMedDate not supplied

Alterations in binding of inositol 1,4,5-trisphosphate to subcellular structures of rat liver during chronic endotoxemia.

Inositol 1,4,5-trisphosphate (IP3) binding to, and Ca2+ uptake and release by plasma membrane- and endoplasmic reticulum-enriched fractions of rat liver were measured after continuous Escherichia coli endotoxin (ET) administration in vivo. IP3 binding to both fractions was significantly reduced by ET treatment. This was associated with decreased Ca2+ uptake and impaired IP3-dependent Ca2+ release. A decrease of 5'-nucleotidase specific activity of plasma membrane-enriched fraction was also observed in ET treated rats. The results suggest that previously observed impairments in the ability of hepatocytes to mobilize Ca2+, to activate glycogen phosphorylase and to respond--when saponin permeabilized--by Ca2+ release upon IP3 addition during chronic endotoxemia are due to alterations in both IP3 binding to the subcellular fractions that are imputed to be targets of IP3, and a decrease in the size of IP3-sensitive pool of releasable Ca2+.

5'-Nucleotidase↗
PubMedDate not supplied

Endotoxicosis modulates cytosolic free calcium and basal and ACTH-stimulated lipolysis in rat adipocytes.

Lipolytic rates and intracellular Ca2+ concentration ([Ca2+]i) were determined under basal conditions and upon stimulation with adrenocorticotropic hormone (ACTH), norepinephrine (NE) and insulin (I), in adipocytes isolated from control and acutely endotoxin (ET)-treated rats (1 mg/100 g body weight, LD50 at 6 h). [Ca2+]i measurements were done using the fluorescent Ca2(+)-indicator Fura-2. NE and ACTH, but not I, produced a marked increase of [Ca2+]i in cells of both control and ET-treated rats. ET treatment elicited a significant increase in [Ca2+]i of resting cells, and enhanced the ACTH effect on this parameter. The changes in lipolytic activity correlated well with changes of [Ca2+]i induced by ACTH. The results indicate that ET-induced alterations in intracellular calcium homeostasis of adipocytes may contribute to the mediation of effects on fat mobilization during endotoxemia.

Adipose Tissue↗