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The presence of eruptive xanthomas is associated with lipid disorders, particularly hypertriglyceridaemia. Intensified hypertriglyceridaemia >10 mmol/l (880 mg%) is a major risk factor for acute pancreatitis. The presented case concerns a 40-year-old man with skin lesions in the form of eruptive xanthomas, accompanied by hypertriglyceridaemiae, complicated by acute pancreatitis, and diagnosed with type 2 diabetes with glycated haemoglobin 9.7 g/dl. Seeding of skin lesions appeared 2–3 months before hospitalization and was observed in the direction of molluscum contagiosum.
Apolipoprotein CIII is a major protein component of chylomicrons and very low density lipoproteins (VLDL) and it is important in the regulation of triglyceride metabolism. Sst 1 polymorphism in the apolipoprotein CIII gene (APO CIII) has been recognized as a factor influencing levels of plasma triglycerides. We examined APO CIII Sac I (Sst I) variants and serum lipids profile in 175 subjects. DNA samples were analyzed by polymerase chain reaction (PCR) followed by Sac I (Sst I) digestion. The frequency of S2 allele was found to be three times higher among men with enhanced plasma triglyceride (TG) compared to men with normal TG levels (16,2% vs. 5,2%). Subjects with the S1S2 genotype compared to S1S1 homozygotes had higher plasma triglycerides and cholesterol levels (190 ± 155 mg/dl vs. 139 ± 90 mg/dl, p=0,035; 234 ± 60 mg/dl vs. 214 ± 37, p=0,04 respectively). These results indicate that a relationship between S2 allele of APO CIII gene and enhanced TG levels occur in studied population.
The study evaluated the effects of Mimusa pudica (M. pudica) leaf extract on type 2 diabetes in rats fed high fructose diet (HFD). Rats were fed either control diet or HFD for 14 days, following which the diet was fortified with M. Pudica at a dose of 500 mg/kg BW. After 8 weeks, HFD caused deleterious metabolic effects, including increased body weight, hyperglycemia, hyperinsulinemia, dyslipidemia and liver dysfunction. Further, rats fed HFD alone showed increased activities of hepatocellular enzymes in plasma and lipid deposition in liver. Treatment with M. pudica significantly reduced the body weight, improved insulin sensitivity, managed the dyslipidemia and reduced liver damage towards normal. Histopathology of the liver confirmed the changes induced by HFD and the M. pudiac treatment significantly reversed towards normality. These data suggest that M. pudica treatment improve insulin sensitivity and attenuates fat accumulation in liver.
Lipoprotein lipase (LPL) is a key enzyme in the metabolism of lipoproteins and their balanced distribution in the plasma. A deficiency of this enzyme due to gene mutations leads to severe dyslipidemia. In this report, we describe the major LPL gene mutations that are prevalent in the French-Canadian population of Québec and the nature of dyslipidemia caused by the resulting enzyme deficiency. We discuss the possibility that dyslipidemia caused by LPL deficiency may enhance oxidative stress in the blood cells, bring about increased fluidity of the membrane components of these cells and increase the susceptibility of their mitochondrial DNA to structural alterations. Some preliminary experimental results in verification of this hypothesis are presented.
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Biological role of liver X receptors

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