Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020473 (hyperlipidemia)
 15,891 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Oxyhemoglobin dissociation curves (ODC) were performed on blood from diabetic and nondiabetic subjects with and without hypertriglyceridemia. P50 at in vivo pH was slightly lower than normal in normolipemic diabetics (25.7 versus 26.6 mmHg, p less than 0.05), in spite of increased red cell 2,3-diphosphoglycerate concentration (15.4 versus 14.4 mumole/g Hg, p less than 0.025). P50 at in vivo pH in diabetics with moderately elevated very low density lipoproteins (VLDL)--Type IV hyperlipoproteinemia (HLP)--was likewise found to be slightly lower than normal (25.5 versus 26.6 mmHg, p less than 0.05). In contrast, diabetics with pronounced hyperlipemia due to accumulation of chylomicrons (type I HLP) or due to accumulation of chylomicrons (type I HLP) or due to accumulation of chylomicrons as well as VLDL (type V HLP) showed markedly increased hemoglobin--oxygen affinity (P50:21.1 versus 26.6 mmHg, p less than 0.001). The change in the ODC of normolipemic diabetics is considered to be an expresssion of the presence of an increased proportion of a hemoglobin fraction (Hb Alc) with increased oxygen affinity. The additional change in the ODC of the hyperlipemic patients is thought to be secondary to accumulation of triglyceride-rich particles for the following reasons: (1) a similar increase in oxygen affinity of hemoglobin was demonstrated in familial type I HLP of nondiabetic subjects; (2) normal red cells increased their oxygen affinity when incubated in lactescent plasma; (3) in both acquired types I and V HLP the disappearance of HLP was followed by a normalization of the ODC.
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PMID:Hyperlipoproteinemia, diabetes, and oxygen affinity of hemoglobin. 1 60

Oxyhemoglobin dissociation curves were performed from blood of subjects with pancreatitis associated with Type V and Type I hyperlipoproteinemia. The hemoglobin-oxygen affininty was markedly increased with P50 varying from 22.3 to 17.7 mmHg. As the hyperlipoproteinemia subsided the clinical and laboratory signs of pancreatic affection disappeared. The increased hemoglobin-oxygen affinity and decreased flow of red cells due to hyperchylomicronemia in the microcirculation may lead to tissue hypoxia, which may act as a precipitating injurious factor leading to pancreatitis during severe hyperlipemia.
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PMID:Increased hemoglobin-oxygen affinity in patients with pancreatitis associated with type I and V hyperlipoproteinemia. 2 74

Efficient entry of synthetic polymers inside cells is a central issue in polymeric drug delivery. Though polymers are widely believed to interact nonspecifically with plasma membrane, we present unexpected evidence that amphiphilic block copolymers, depending on their aggregation state, can distinguish between caveolae- and clathrin-mediated endocytosis. A block copolymer of poly(ethylene oxide) (PEO) and poly(propylene oxide) (PPO), Pluronic P85 (P85), below critical micelle concentration (CMC) exists as single molecule coils (unimers) and above CMC forms 14.6 nm aggregated micelles with a hydrophobic PPO core and hydrophilic PEO shell. The internalization pathways of P85 in mammalian cells were elucidated using endocytosis inhibitors and colocalization with endocytosis markers (clathrin-specific antibodies and transferrin for clathrin and caveolin-1-specific antibodies and cholera toxin B for caveolae). Altogether, our results indicate that P85 unimers internalize through caveolae-mediated endocytosis, while P85 micelles internalize through clathrin-mediated endocytosis. Furthermore, at concentrations above 0.01% P85 inhibits caveolae-mediated endocytosis (cholera toxin B), while having little or no effect on the clathrin-mediated endocytosis (transferrin). Selective interaction of Pluronic with caveolae may explain its striking pharmacological activities including inhibition of drug efflux transport, activation of gene expression, and dose-dependent hyperlipidemia.
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PMID:Different internalization pathways of polymeric micelles and unimers and their effects on vesicular transport. 1872 94