lipid-a and Hypoglycemia

lipid-a has been researched along with Hypoglycemia* in 2 studies

Other Studies

2 other study(ies) available for lipid-a and Hypoglycemia

Article	Year
Systemic hypoglycemia following central injection of endotoxin in mice. Brain research, 1985, Jul-29, Volume: 339, Issue:2 Intracerebroventricular microinjection of endotoxin in mice resulted in powerful hypoglycemia. The effect was reproduced by the biologically active moiety of endotoxin, lipid A, and prevented by coadministration of the polycationic peptide antibiotic polymyxin B (PMB) or by detoxification of endotoxin by means of mild alkaline hydrolysis. Central treatment with PMB also attenuated the hypoglycemic response to systemic administration of endotoxin or lipid A. These results suggest a direct role of the CNS in the mechanism of endotoxin hypoglycemia. Topics: Animals; Endotoxins; Escherichia coli; Hypoglycemia; Injections, Intraventricular; Lipid A; Male; Mice; Mice, Inbred ICR; Polymyxin B	1985
Relation of endotoxin structure to hypoglycemic and insulinlike actions. Circulatory shock, 1983, Volume: 11, Issue:1 Various endotoxin preparations were used to determine which portion of endotoxin, lipid A, polysaccharide, or lipid-associated protein (LAP), mediates the hypoglycemic and insulinlike action in rats. Salmonella enteriditis Boivin (SEB), complete endotoxin, and S enteriditis Westphal (SEW), lacking LAP, were equally lethal to endotoxin-sensitized rats; however, S minnesota (SM) glycolipid (lipid A plus 16% polysaccharide) was comparatively more toxic. Toxic effects were prevented by alteration of lipid A through alkaline hydrolysis or polymixin B treatment. SM-lipid A (0.02% polysaccharide) was less toxic than SM-glycolipid. Similar hypoglycemic effects were produced by SEB and SEW; however, SM-glycolipid produced a significantly greater hypoglycemia. Although SEB, SEW, and SM-glycolipid all produced significant increases in adipose tissue glucose oxidation a decreasing trend in effectiveness was observed, while the SM-lipid A was without effect. However, adding detoxified hydrolysates of endotoxin to SM-lipid A produced a significant increase in glucose oxidation. In conclusion, lipid A is the primary endotoxin moiety mediating both the lethal effects of endotoxin and its hypoglycemic action. However, maximal expression of insulinlike action requires the presence of all three portions of endotoxin. Topics: Adrenalectomy; Animals; Blood Glucose; Endotoxins; Glucose; Glycolipids; Hypoglycemia; Insulin; Lead; Lipid A; Male; Oxidation-Reduction; Polysaccharides, Bacterial; Rats; Salmonella; Salmonella enteritidis	1983

Article

Year

Systemic hypoglycemia following central injection of endotoxin in mice.

Brain research, 1985, Jul-29, Volume: 339, Issue:2

Intracerebroventricular microinjection of endotoxin in mice resulted in powerful hypoglycemia. The effect was reproduced by the biologically active moiety of endotoxin, lipid A, and prevented by coadministration of the polycationic peptide antibiotic polymyxin B (PMB) or by detoxification of endotoxin by means of mild alkaline hydrolysis. Central treatment with PMB also attenuated the hypoglycemic response to systemic administration of endotoxin or lipid A. These results suggest a direct role of the CNS in the mechanism of endotoxin hypoglycemia.

Topics: Animals; Endotoxins; Escherichia coli; Hypoglycemia; Injections, Intraventricular; Lipid A; Male; Mice; Mice, Inbred ICR; Polymyxin B

1985

Relation of endotoxin structure to hypoglycemic and insulinlike actions.

Circulatory shock, 1983, Volume: 11, Issue:1

Various endotoxin preparations were used to determine which portion of endotoxin, lipid A, polysaccharide, or lipid-associated protein (LAP), mediates the hypoglycemic and insulinlike action in rats. Salmonella enteriditis Boivin (SEB), complete endotoxin, and S enteriditis Westphal (SEW), lacking LAP, were equally lethal to endotoxin-sensitized rats; however, S minnesota (SM) glycolipid (lipid A plus 16% polysaccharide) was comparatively more toxic. Toxic effects were prevented by alteration of lipid A through alkaline hydrolysis or polymixin B treatment. SM-lipid A (0.02% polysaccharide) was less toxic than SM-glycolipid. Similar hypoglycemic effects were produced by SEB and SEW; however, SM-glycolipid produced a significantly greater hypoglycemia. Although SEB, SEW, and SM-glycolipid all produced significant increases in adipose tissue glucose oxidation a decreasing trend in effectiveness was observed, while the SM-lipid A was without effect. However, adding detoxified hydrolysates of endotoxin to SM-lipid A produced a significant increase in glucose oxidation. In conclusion, lipid A is the primary endotoxin moiety mediating both the lethal effects of endotoxin and its hypoglycemic action. However, maximal expression of insulinlike action requires the presence of all three portions of endotoxin.

Topics: Adrenalectomy; Animals; Blood Glucose; Endotoxins; Glucose; Glycolipids; Hypoglycemia; Insulin; Lead; Lipid A; Male; Oxidation-Reduction; Polysaccharides, Bacterial; Rats; Salmonella; Salmonella enteritidis

1983