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Purpose: Fasting or postprandial hypertriglyceridemia is considered an independent cardiovascular disease (CVD) risk factor. The intestinal fatty acid binding protein (FABP2) is involved in the intracellular transport and metabolism of fatty acids. The presence of the Ala54Thr polymorphism of the FABP2 gene appears to be involved in postprandial hypertriglyceridemia. We explored the possible association of the Ala54Thr polymorphism with fat intolerance in apparently healthy, fasting, normolipidemic subjects with normal body-mass index and without diabetes. Methodology: A total of 158 apparently healthy individuals were classified as fat tolerant (n = 123) or intolerant (n = 35) according to their response (plasma triglycerides) to an oral abbreviated tolerance test with blood samples taken at 0, 2 and 4 h. At 0 h, all subjects ingested 26.3 g of fats. Presence of the Ala54Thr polymorphism of the FABP2 gene was evaluated by polymerase chain reaction⁻restriction fragment length (PCR⁻RFLP). Results: The group with fat intolerance (postprandial hypertriglyceridemia group) showed an increased frequency of the Thr54Thr genotype when compared with the group with normal fat tolerance (control group) (23% vs. 4%, respectively, OR: 16.53, 95% CI: 4.09⁻66.82, p: 0.0001, pc: 0.0003). Carriers of at least one Thr54 allele were up to six times more prevalent in the fat intolerant group than in the non-carriers. (OR: 6.35; 95% CI: 1.86⁻21.59, p: 0.0003, pc: 0.0009). The levels of plasma triglycerides (Tg) at 4 h after the test meal were higher in carriers of at least one 54Thr allele than in carriers of the Ala54 allele (p < 0.05). Conclusions: There is a significant association between postprandial hypertriglyceridemia and the presence of at least one 54Thr allele of the FABP2 gene. In addition, subjects with this genotype showed an increased ratio of Tg/HDL-cholesterol. This parameter is a marker of increased CVD risk and insulin resistance.

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Xanthelasmas are localized accumulation of lipid deposits on the eyelids. Lesions are typically asymptomatic and treatment is often sought for cosmetic purposes. Unfortunately, there is paucity of strong evidence in the literature for the effective treatment of normolipidemic xanthelasmas. A literature search using the term "xanthelasma" was carried out in PubMed and Medline databases. Only articles related to treatment were considered and analyzed for their data. Commonly cited treatments include topical trichloroacetic acid, liquid nitrogen cryotherapy, and various lasers including carbon dioxide, Er:YAG, Q-switched Nd:YAG, and pulse dye laser. However, traditional surgical excision has also been used. This article reviews these currently accepted modalities of treatment.

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The study was designed to assess the effect of different strawberry extracts on glucose levels, lipid profiles, and oxidative stress in nicotinamide-streptozotocin (NIC-STZ) induced diabetic rats. The associated changes were evaluated through biochemical, molecular, and histological assays. Diabetes was induced by intraperitoneal injection of STZ to albino Wistar rats after treatment with nicotinamide. Aqueous, hydroalcoholic, and alcoholic strawberry extracts were administrated orally to diabetic rats. Treatment of strawberry extracts improved lipid profile, liver function, and serum creatinine and led to a significant increase in antioxidant status in diabetic rats. Real-time PCR expression analysis of genes from the liver of animals treated with strawberry extracts exhibited downregulation of several fatty acid synthesis genes, transcription factors, such as Sterol regulatory Element Binding Transcription factor (SREBP) and Nuclear Factor-κß (NF-κß), and inflammatory markers, like Interleukin 6 (IL6) and Tumor Necrosis Factor-α (TNF-α). Strawberry extracts also upregulated liver Peroxisome Proliferator Activated Receptor-γ (PPAR-γ). Histological examination confirmed the nephroprotective and ß-cell regeneration/protection effects of strawberry extracts. The present study demonstrates several beneficial effects of strawberry extracts along with its probable mechanism of action.

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We report the case of a 25-year-old woman presenting with left hip pain. A lesion was found in the proximal femoral metaphysis. Benign bone tumor, such as intraosseous lipoma or liposclerosing myxofibrous tumor, was suspected based on simple radiographs and magnetic resonance images. Curettage of the lesion and bone grafting was performed. Histologic findings reflected primary intraosseous xanthoma of the proximal femur. Laboratory tests revealed the patient to be normolipidemic, while immunoelectrophoretic fractionation of lipoproteins revealed normal values for alpha, pre-beta, beta, and chylomicrons. At the one-year follow-up, there was no evidence of local recurrence. This is the first reported case of primary intraosseous xanthoma of the proximal femur in a normolipidemic patient.

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Mutations in the genes low-density lipoprotein (LDL) receptor-related protein-6 (LRP6) and myocyte enhancer factor 2A (MEF2A) were reported in families with coronary artery disease (CAD). We intend to determine the mutational spectrum of these genes among hyperlipidemic and normolipidemic CAD families. Forty probands with early-onset CAD were recruited from 19 hyperlipidemic and 21 normolipidemic Chinese families. We sequenced all exons and intron-exon boundaries of LRP6 and MEF2A, and found a novel heterozygous variant in LRP6 from a proband with normolipidemic CAD. This variant led to a substitution of histidine to tyrosine (Y418H) in an evolutionarily conserved domain YWTD in exon 6 and was not found in 1025 unrelated healthy individuals. Co-segregated with CAD in the affected family, LRP6Y418H significantly debilitated the Wnt3a-associated signaling pathway, suppressed endothelial cell proliferation and migration, and decreased anti-apoptotic ability. However, it exhibited no influences on low-density lipoprotein cholesterol uptake. Thus, mutation Y418H in LRP6 likely contributes to normolipidemic familial CAD via impairing endothelial cell functions and weakening the Wnt3a signaling pathway.

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We report the case of a 25-year-old woman presenting with left hip pain. A lesion was found in the proximal femoral metaphysis. Benign bone tumor, such as intraosseous lipoma or liposclerosing myxofibrous tumor, was suspected based on simple radiographs and magnetic resonance images. Curettage of the lesion and bone grafting was performed. Histologic findings reflected primary intraosseous xanthoma of the proximal femur. Laboratory tests revealed the patient to be normolipidemic, while immunoelectrophoretic fractionation of lipoproteins revealed normal values for alpha, pre-beta, beta, and chylomicrons. At the one-year follow-up, there was no evidence of local recurrence. This is the first reported case of primary intraosseous xanthoma of the proximal femur in a normolipidemic patient.

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