RESUMEN
The acute phase reactions, associated with injury, inflammation, or sepsis, markedly affect the concentration and composition of plasma lipids and lipoproteins. Hepatic production of triglycerides and very low density lipoprotein formation are increased, but do not necessarily result in high plasma triglyceride levels. In contrast, all conditions lower plasma cholesterol by decreasing its content in both low-density and high-density lipoproteins. In addition, substantial changes in protein and lipid composition of lipoproteins are observed that may redefine the function of these particles, but also increase their atherogenic and inflammatory properties.
Asunto(s)
Reacción de Fase Aguda/sangre , Lípidos/sangre , Lipoproteínas/sangre , Hígado/metabolismo , HDL-Colesterol/sangre , HDL-Colesterol/química , LDL-Colesterol/sangre , LDL-Colesterol/química , Humanos , Lipoproteínas VLDL/sangre , Lipoproteínas VLDL/química , Triglicéridos/biosíntesis , Triglicéridos/sangreRESUMEN
The metabolism of D-glucose and/or D-fructose was investigated in pancreatic islets from control rats and hereditarily diabetic GK rats. In the case of both D-glucose and D-fructose metabolism, a preferential alteration of oxidative events was observed in islets from GK rats. The generation of 3HOH from D-[5-3H]glucose (or D-[5-3H]fructose) exceeded that from D-[3-3H]glucose (or D-[3-3H]fructose) in both control and GK rats. This difference, which is possibly attributable to a partial escape from glycolysis of tritiated dihydroxyacetone phosphate, was accentuated whenever the rate of glycolysis was decreased, e.g., in the absence of extracellular Ca(2+) or presence of exogenous D-glyceraldehyde. D-Mannoheptulose, which inhibited D-glucose metabolism, exerted only limited effects upon D-fructose metabolism. In the presence of both hexoses, the paired ratio between D-[U-14C]fructose oxidation and D-[3-3H]fructose or D-[5-3H]fructose utilization was considerably increased, this being probably attributable, in part at least, to a preferential stimulation by the aldohexose of mitochondrial oxidative events. Moreover, this coincided with the fact that D-mannoheptulose now severely inhibited the catabolism of D-[5-3H]fructose and D-[U-14C]fructose. The latter situation is consistent with both the knowledge that D-glucose augments D-fructose phosphorylation by glucokinase and the findings that D-mannoheptulose, which fails to affect D-fructose phosphorylation by fructokinase, inhibits the phosphorylation of D-fructose by glucokinase.