Plasma triglyceride, increased

Reduced plasma triglycerides, increased S-hydro-xybutyrate, and increased plasma uric acid were noted over 6 days of administration of DCA as a hypoglycemic agent. Although there is no conclusive evidence, DCA is proposed to cause neurotoxic effects in humans based on the fact that DCA inhibits its own metabolism. These effects are expected to occur at therapeutic doses, 25-100 mg kg... 

Inhibits HMG-Co-A reductase, the enzyme that catalyzes the early step in cholesterol synthesis. Decreases LDL cholesterol, VLDL cholesterol, and plasma triglycerides, increases HDL cholesterol. 

Familial lipoprotein lipase deficiency is characterized by a massive accumulation of chylomicrons and a corresponding increase in plasma triglycerides or a type I lipoprotein pattern. Presenting manifestations include repeated attacks of pancreatitis and abdominal pain, eruptive cutaneous xanthomatosis, and hepatosplenomegaly beginning in childhood. Symptom severity is proportional to dietary fat intake, and consequently to the elevation of chylomicrons. Accelerated atherosclerosis is not associated with this disease. 

Metformin is the only biguanide available in the United States. It enhances insulin sensitivity of both hepatic and peripheral (muscle) tissues. This allows for increased uptake of glucose into these insulin-sensitive tissues. Metformin consistently reduces A1C levels by 1.5% to 2%, FPG levels by 60 to 80 mg/dL, and retains the ability to reduce FPG levels when they are very high (>300 mg/dL). It reduces plasma triglycerides and low-density lipoprotein (LDL) cholesterol by 8% to 15% and modestly increases high-density lipoprotein (HDL) cholesterol (2%). It does not induce hypoglycemia when used alone. 

Pioglitazone decreases plasma triglycerides by 10% to 20%, whereas rosiglitazone tends to have no effect. Pioglitazone does not cause significant increases in LDL cholesterol, whereas LDL cholesterol may increase by 5% to 15% with rosiglitazone. 

A patient with a history of recurring attacks of pancieathis, eruptive xanthomas, and increased plasma triglyceride levels (2000 mg/dL) associated with chylomicrons, most likely has a deficiency in... 

Lipoproteins are an important class of serum proteins in which a spherical hydrophobic core of triglycerides or cholesterol esters is surrounded by an amphipathic monolayer of phospholipids, cholesterol and apolipoproteins (fatbinding proteins). Lipoproteins transport lipid in the circulation and vary in size and density, depending on their proteindipid ratio (Figure 7.3). Lipoprotein metabolism is adversely affected by obesity low-density lipoprotein (LDL)-cholesterol and plasma triglyceride are increased, together with decreased high-density lipoprotein (HDL)-cholesterol concentrations. 

D. Lipoprotein lipase. Fenohbrate is a hypotriglyc-eridemic drug that lowers plasma triglycerides by increasing the activity of hpoprotein lipase, the enzyme responsible for disassembly of triglycerides in serum lipoproteins (VLDL, IDL and chylomicrons). 

Mechanism of Action An antihyperlipidemic that enhances synthesis of lipoprotein lipase and reduces triglyceride-rich lipoproteins and VLDLs. Therapeutic Effect Increases VLDL catabolism and reduces total plasma triglyceride levels. Pharmacokinetics Well absorbed from the GI tract. Absorption increased when given with food. Protein binding 99%. Rapidly metabolized in the liver to active metabolite. Excreted primarily in urine lesser amount in feces. Not removed by hemodialysis. Half-life 20 hr. 

Mechanism of Action An HMG-CoA reductase inhibitor that interferes with cholesterol biosynthesis by preventing the conversion of HMG-CoA reductase to meva-lonate, a precursor to cholesteroh Therapeutic Effect Lowers serum LDL and VLDL cholesterol and plasma triglyceride levels increases serum HDL concentration. Pharmacokinetics Poorly absorbed from the G1 tract. Protein binding 50%. Metabolized in the liver (minimal active metabolites). Primarily excreted in feces via the biliary system. Not removed by hemodialysis. Half-life 2.7 hr. 

Mechanism of Action An antihyperlipidemicthat interferes with cholesterol biosynthesis by inhibiting the conversion of the enzyme hydroxymethylglutaryl-CoA (HMG-CoA) to mevalonate, a precursor to cholesterol. Therapeutic Effect Decreases LDL cholesterol, VLDL, and plasma triglyceride levels, increases HDL concentration. Pharmacokinetics Protein binding 88%. Minimal hepatic metabolism. Primarily eliminated in the feces. Half-life 19 hr (increased in patients with severe renal dysfunction). 

Simvastatin has been shown to reduce both normal and elevated low-density lipoprotein (LDL) cholesterol concentrations. Apolipoprotein B, VLDL cholesterol and plasma triglycerides also reduce and can produce increase in HDL cholesterol. 

The effect of di(2-ethylhexyl) phthalate in diet (2% for 21 days) on lipoprotein metabolism in male Wistar rats was evaluated (Mocchiutti Bernal, 1997). The observed reduction in plasma triglyceride levels was associated with (and attributed to) increased activity of extrahepatic lipoprotein lipase. 

Alterations in the composition of the plasma lipids caused by estrogens are characterized by an increase in the high-density lipoproteins (HDL), a slight reduction in the low-density lipoproteins (LDL), and a reduction in total plasma cholesterol levels. Plasma triglyceride levels are increased. Estrogens decrease hepatic oxidation of adipose tissue lipid to ketones and increase synthesis of triglycerides. 

Aldesleukin can cause lipid disorders. Recurrent and marked hypocholesterolemia with reduced high- and low-density lipoproteins, and slight increases in plasma triglycerides have been observed after high-dose aldesleukin... 

In six patients with renal transplants treated with sirolimus, mean total plasma cholesterol, triglyceride, and apolipoprotein concentrations increased (1067). The authors suggested that sirolimus increases lipase activity in adipose tissue and reduces lipoprotein lipase activity, resulting in increased hepatic synthesis of triglycerides, increased secretion of VLDL, and increased hypertriglyceridemia. 

However, the reductase inhibitors clearly induce an increase in high-affinity LDL receptors. This effect increases both the fractional catabolic rate of LDL and the liver s extraction of LDL precursors (VLDL remnants), thus reducing plasma LDL (Figure 35-2). Because of marked first-pass hepatic extraction, the major effect is on liver. Preferential activity in liver of some congeners appears to be attributable to tissue-specific differences in uptake. Limited reduction of LDL levels in patients who lack functional LDL receptors indicates that decreases in de novo cholesterologenesis also contribute to cholesterol reduction. Modest decreases in plasma triglycerides and small increases in HDL also occur. 

Wistar) (GO) Other 7.5 (decreased plasma triglyceride levels) foci of necrotic cells, increased hepatic triglyceride levels, vesiculation and dispersion of ribosomal granules in the endoplasmic reticulum, increased AST) 1969... 

Twelve hours after ingestion of a single dose of white phosphorus, significant increases in liver triglyceride and decreases in plasma triglyceride levels were observed (Ghoshal et... 

A disorder of lipid metabolism, in which absence of lipoprotein lipase activity due to an absolute apoC-II deficiency results in marked hypertriglyceridemia (Type I phenotype), has been reviewed elsewhere (N8). There are some unexplained differences in the clinical picture and plasma lipoprotein pattern between apoC-II deficiency and primary lipoprotein lipase deficiency. In apoC-II deficiency, symptoms appear to be milder (but recurrent abdominal pain, caused apparently by acute pancreatitis, is a frequently reported symptom). Patients do not show xanthomas or hepatomegaly, and few have splenomegaly (all features of lipoprotein lipase deficiency). Diagnosis is by electrophoresis of the C apolipoproteins, and a plasma triglyceride concentration usually 1000-3000 mg/dl (N8). There may be an increase in plasma VLDL concentration, whereas in classical lipoprotein lipase deficiency plasma VLDL concentration is nearly normal (N8). 

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