Archive for December, 2009

Autonomic dysfunction in presymptomatic and early symptomatic Huntington’s disease

Tuesday, December 29th, 2009

Kobal J, Melik Z, Cankar K, Bajrovic FF, Meglic B, Peterlin B, Zaletel M. Autonomic dysfunction in presymptomatic and early symptomatic Huntington’s disease.Acta Neurol Scand: DOI: 10.1111/j.1600-0404.2009.01251.x.© 2009 The Authors Journal compilation © 2009 Blackwell Munksgaard.Objectives [ndash] Although autonomic dysfunction was found in advanced Huntington’s disease (HD) patients it is not clear whether there is autonomic dysfunction in presymptomatic and early symptomatic HD.Material & methods [ndash] Different cardiovascular autonomic tests were performed in 14 presymptomatic HD mutation carriers (PHD), 11 early symptomatic HD patients (EHD) and in 25 sex and age matched controls.Results [ndash] We found attenuated response to simple mental arithmetic test (relative heart rate in PHD and EHD was 10% lower than in controls; diastolic pressure was 10.6% lower in EHD than in controls; P < 0.05) and exaggerated response to the late phase of cold pressor test (relative heart rate was 10% higher in PHD and 7% higher in EHD than in controls; P < 0.05). The rest of the cardiovascular autonomic tests did not reveal significant differences between patients and controls.Conclusions [ndash] Our results suggest that subtle autonomic dysfunction occurs even in PHD and EHD.

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Neutral and acidic oligosaccharides in preterm infants: a randomized, double-blind, placebo-controlled trial.

Saturday, December 26th, 2009
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Neutral and acidic oligosaccharides in preterm infants: a randomized, double-blind, placebo-controlled trial.

Am J Clin Nutr. 2009 Dec 23;

Authors: Westerbeek EA, van den Berg JP, Lafeber HN, Fetter WP, Boehm G, Twisk JW, van Elburg RM

BACKGROUND: Serious infectious morbidity is high in preterm infants. Enteral supplementation of prebiotics may reduce the incidence of serious infections, especially infections related to the gastrointestinal tract. OBJECTIVE: The objective was to determine the effect of enteral supplementation of a prebiotic mixture consisting of neutral oligosaccharides ((SC)GOS/(LC)FOS) and acidic oligosaccharides (AOS) on serious infectious morbidity in preterm infants. DESIGN: In a randomized controlled trial, preterm infants (gestational age <32 wk and/or birth weight <1500 g) received enteral supplementation of 80% (SC)GOS/(LC)FOS and 20% AOS (1.5 g . kg(-1) . d(-1)) or placebo (maltodextrin) between days 3 and 30 of life. Serious infectious morbidity was defined as a culture positive for sepsis, meningitis, pyelonephritis, or pneumonia. The analysis was performed by intention-to-treat and per-protocol, defined as >/=50% supplementation dose during the study period. RESULTS: In total, 113 preterm infants were included. Baseline and nutritional characteristics were not different between groups. In the intention-to-treat analysis, the incidence of >/=1 serious infection, >/=1 serious endogenous infection, or >/=2 serious infectious episodes was not significantly different in the (SC)GOS/(LC)FOS/AOS-supplemented and placebo groups. In the per-protocol analysis, there was a trend toward a lower incidence of >/=1 serious endogenous infection and >/=2 serious infectious episodes in the (SC)GOS/(LC)FOS/AOS-supplemented group compared with the placebo group (P = 0.09 and P = 0.07, respectively). CONCLUSIONS: Enteral supplementation of (SC)GOS/(LC)FOS/AOS does not significantly reduce the risk of serious infectious morbidity in preterm infants. However, there was a trend toward a lower incidence of serious infectious morbidity, especially for infections with endogenous bacteria. This finding suggests a possible beneficial effect that should be evaluated in a larger study. This trial was registered at isrctn.org as ISRCTN16211826.

PMID: 20032496 [PubMed - as supplied by publisher]

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Gene-nutrient interactions in the metabolic syndrome: single nucleotide polymorphisms in ADIPOQ and ADIPOR1 interact with plasma saturated fatty acids to modulate insulin resistance.

Saturday, December 26th, 2009
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Gene-nutrient interactions in the metabolic syndrome: single nucleotide polymorphisms in ADIPOQ and ADIPOR1 interact with plasma saturated fatty acids to modulate insulin resistance.

Am J Clin Nutr. 2009 Dec 23;

Authors: Ferguson JF, Phillips CM, Tierney AC, Pérez-Martínez P, Defoort C, Helal O, Lairon D, Planells R, Shaw DI, Lovegrove JA, Gjelstad IM, Drevon CA, Blaak EE, Saris WH, Leszczynska-Golabek I, Kiec-Wilk B, Risérus U, Karlström B, Miranda JL, Roche HM

BACKGROUND: Progression of the metabolic syndrome (MetS) is determined by genetic and environmental factors. Gene-environment interactions may be important in modulating the susceptibility to the development of MetS traits. OBJECTIVE: Gene-nutrient interactions were examined in MetS subjects to determine interactions between single nucleotide polymorphisms (SNPs) in the adiponectin gene (ADIPOQ) and its receptors (ADIPOR1 and ADIPOR2) and plasma fatty acid composition and their effects on MetS characteristics. DESIGN: Plasma fatty acid composition, insulin sensitivity, plasma adiponectin and lipid concentrations, and ADIPOQ, ADIPOR1, and ADIPOR2 SNP genotypes were determined in a cross-sectional analysis of 451 subjects with the MetS who participated in the LIPGENE (Diet, Genomics, and the Metabolic Syndrome: an Integrated Nutrition, Agro-food, Social, and Economic Analysis) dietary intervention study and were repeated in 1754 subjects from the LIPGENE-SU.VI.MAX (SUpplementation en VItamines et Minéraux AntioXydants) case-control study (http://www.ucd.ie/lipgene). RESULTS: Single SNP effects were detected in the cohort. Triacylglycerols, nonesterified fatty acids, and waist circumference were significantly different between genotypes for 2 SNPs (rs266729 in ADIPOQ and rs10920533 in ADIPOR1). Minor allele homozygotes for both of these SNPs were identified as having degrees of insulin resistance, as measured by the homeostasis model assessment of insulin resistance, that were highly responsive to differences in plasma saturated fatty acids (SFAs). The SFA-dependent association between ADIPOR1 rs10920533 and insulin resistance was replicated in cases with MetS from a separate independent study, which was an association not present in controls. CONCLUSIONS: A reduction in plasma SFAs could be expected to lower insulin resistance in MetS subjects who are minor allele carriers of rs266729 in ADIPOQ and rs10920533 in ADIPOR1. Personalized dietary advice to decrease SFA consumption in these individuals may be recommended as a possible therapeutic measure to improve insulin sensitivity. This trial was registered at clinicaltrials.gov as NCT00429195.

PMID: 20032495 [PubMed - as supplied by publisher]

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Fasting urine pH is independent of insulin sensitivity.

Saturday, December 26th, 2009
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Fasting urine pH is independent of insulin sensitivity.

Am J Clin Nutr. 2009 Dec 23;

Authors: Workeneh B, Abbasi F, Reaven G

BACKGROUND: It has recently been suggested that a low urine pH be added to the abnormalities linked to insulin resistance. This conclusion is based on the finding of a low urine pH in individuals with clinical syndromes associated with insulin resistance and not on studies in which a direct measure of insulin sensitivity was shown to be significantly related to differences in urine pH. OBJECTIVE: To address this issue, we quantified insulin-mediated glucose uptake (IMGU) by using the insulin suppression test in 96 apparently healthy, nondiabetic individuals and defined its relation to fasting urine pH. DESIGN: Urine samples were collected and analyzed from a cohort of healthy subjects within a narrow body mass index range who were recruited to determine insulin sensitivity. RESULTS: There was an approximate 6-fold variation in values for IMGU in this population, with no relation to urine pH (r = 0.02). Furthermore, there was no relation between body mass index, as a surrogate estimate of insulin resistance, and urine pH (r = 0.06). CONCLUSION: On the basis of these findings, we question the view that a low urine pH be added to the abnormalities linked to insulin resistance in low-risk populations.

PMID: 20032494 [PubMed - as supplied by publisher]

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TCF7L2 rs7903146-macronutrient interaction in obese individuals’ responses to a 10-wk randomized hypoenergetic diet.

Saturday, December 26th, 2009
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TCF7L2 rs7903146-macronutrient interaction in obese individuals’ responses to a 10-wk randomized hypoenergetic diet.

Am J Clin Nutr. 2009 Dec 23;

Authors: Grau K, Cauchi S, Holst C, Astrup A, Martinez JA, Saris WH, Blaak EE, Oppert JM, Arner P, Rössner S, Macdonald IA, Klimcakova E, Langin D, Pedersen O, Froguel P, Sørensen TI

BACKGROUND: Transcription factor 7-like 2 (TCF7L2) rs7903146 associates with type 2 diabetes and may operate via impaired glucagon-like peptide 1 secretion, which is stimulated more by fat than by carbohydrate ingestion. OBJECTIVE: The objective was to examine the interaction between TCF7L2 rs7903146 and dietary fat and carbohydrate [high-fat, low-carbohydrate: 40-45% of energy as fat (HF); compared with low-fat, high-carbohydrate: 20-25% of energy as fat (LF)] in obese individuals’ responses to a 10-wk hypoenergetic diet (-600 kcal/d). DESIGN: European, obese participants (n = 771) were randomly assigned to receive an HF or an LF diet. Body weight, fat mass (FM), fat-free mass (FFM), waist circumference (WC), resting energy expenditure (REE), fasting fat oxidation in percentage of REE (FatOx), homeostasis model assessed insulin release (HOMA-beta), and HOMA-insulin resistance (HOMA-IR) were determined at baseline and after the intervention; 739 individuals were genotyped for rs7903146. RESULTS: Average weight loss was 6.9 kg with the LF and 6.6 kg with the HF (difference between diets, NS) diet. Among individuals who were homozygous for the T-risk allele, those in the HF diet group experienced smaller weight losses (Deltaweight) (2.6 kg; P = 0.009; n = 622), smaller DeltaFFM (1.6 kg; P = 0.027; n = 609), smaller DeltaWC (3.3 cm; P = 0.010; n = 608), and a smaller DeltaHOMA-IR (1.3 units; P = 0.004; n = 615) than did the LF diet group. For C allele carriers, there were no differences between the HF and LF diet groups. For the HF diet group, each additional T allele was associated with a reduced loss of FM (0.67 kg; P = 0.019; n = 609). TCF7L2 rs7903146 was not associated with DeltaREE, DeltaFatOx, DeltaHOMA-beta, or dropout. CONCLUSION: Our results suggest that obese individuals who are homozygous for the TCF7L2 rs7903146 T-risk allele are more sensitive to LF than to HF weight-loss diets.

PMID: 20032493 [PubMed - as supplied by publisher]

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Late introduction of complementary feeding, rather than duration of breastfeeding, may protect against adult overweight.

Saturday, December 26th, 2009
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Late introduction of complementary feeding, rather than duration of breastfeeding, may protect against adult overweight.

Am J Clin Nutr. 2009 Dec 23;

Authors: Schack-Nielsen L, Sørensen TI, Mortensen EL, Michaelsen KF

BACKGROUND: Early nutrition may affect the risk of overweight in later life. OBJECTIVE: The objective was to explore the effect of the duration of breastfeeding (BF) and age at introduction of complementary feeding (CF) on body mass index (BMI) during childhood through adulthood. DESIGN: The study was based on a subsample of the Copenhagen Perinatal Cohort established in 1959-1961 (n = 5068). Information on BF and available information on CF (age of introduction of “spoon-feeding,” “vegetables,” “egg,” “meat,” and “firm food”) and several covariates were collected in infancy and linked with information on BMI from follow-up examinations in childhood and adulthood at age 42 y. RESULTS: The median (10th, 90th percentiles) durations of any BF and age at introduction of spoon-feeding were 2.50 (0.23, 6.50) and 3.50 (2.00, 6.00) mo, respectively. After 1 y of age and throughout childhood and adolescence, no association between BF and BMI was found in regression models also adjusted for age at introduction of spoon-feeding and covariates. The risk of overweight at age 42 y decreased or tended to decrease with increasing age (in mo) at introduction of spoon-feeding [odds ratio (OR): 0.94; 95% CI: 0.86, 1.02], vegetables (OR: 0.90; 95% CI: 0.81, 0.98), meat (OR: 0.93; 95% CI: 0.87, 1.00), and firm food (OR: 0.92; 95% CI: 0.86, 0.98) but not egg (OR: 0.98; 95% CI: 0.91, 1.05). CONCLUSION: The findings of this study suggest that introduction of CF at a later age (within the range of 2 to 6 mo) is protective against overweight in adulthood but do not support a protective effect of a longer duration of BF.

PMID: 20032492 [PubMed - as supplied by publisher]

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Safety and Efficacy of Ezetimibe Added to Atorvastatin Versus Up Titration of Atorvastatin to 40 mg in Patients ≥65 Years of Age (from the ZETia in the ELDerly [ZETELD] Study)

Friday, December 25th, 2009

Publication year: 2009
Source: The American Journal of Cardiology, In Press, Corrected Proof, Available online 23 December 2009
Franklin, Zieve , Nanette K., Wenger , Ori, Ben-Yehuda , Christian, Constance , Steven, Bird , …

Few clinical studies have focused on the efficacy of lipid-lowering therapies in patients ≥65 years of age. The percentage of change from baseline in low-density lipoprotein (LDL) cholesterol and the percentage of patients achieving prespecified LDL cholesterol levels after 12 weeks of ezetimibe 10 mg plus atorvastatin versus up titration of atorvastatin were assessed in subjects ≥65 years old with hyperlipidemia and at high risk of coronary heart disease. After stabilization of atorvastatin 10-mg therapy, 1,053 patients, ≥65 years old, at high risk of coronary heart disease, with and without atherosclerotic vascular disease and a LDL cholesterol level that was…

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The role of CTGF in the diabetic rat retina and its relationship with VEGF and TGF-β2, elucidated by treatment with CTGFsiRNA

Thursday, December 24th, 2009

Purpose: The critical association of connective tissue growth factor (CTGF) with diabetic retinopathy (DR) remains to be clarified. We detected alterations in the gene and protein expression of CTGF and related cytokines, including vascular endothelial growth factor (VEGF) and transforming growth factor-[beta]2 (TGF-[beta]2), and their response to small interfering RNA (siRNA) targeting the CTGF (CTGFsiRNA) in the retina of diabetic rats. The relationships between CTGF, VEGF and TGF-[beta]2 levels, as well as the degree of apoptosis in the diabetic retina, were also investigated.Methods: Diabetes was induced in rats by the [beta]-cell toxin streptozotocin (STZ). Retinas were obtained from control and diabetic rats and similar animals treated with CTGFsiRNA by intravitreal injection. mRNA level and protein expression of CTGF, VEGF and TGF-[beta]2 were measured by reverse transcription-polymerase chain reaction (RT-PCR) and Western blotting, and located by immunohistochemistry. Retinal apoptosis was detected by TUNEL staining.Results: The levels of CTGF, VEGF and TGF-[beta]2 and the number of TUNEL-positive nuclei were significantly higher in diabetic retinas than in control retinas (p < 0.01). The level of CTGF rose at 8 weeks, earlier than levels of VEGF and TGF-[beta]2, which rose at 12 weeks after the onset of diabetes. The difference was significant (p < 0.05). siRNA-mediated inhibition of CTGF mRNA inhibited retinal VEGF and TGF-[beta]2 and also resulted in a significant decrease in apoptosis. Significant correlations were found between CTGF and VEGF (p = 0.009), CTGF and TGF-[beta]2 (p = 0.01), and apoptosis and these three cytokines (p < 0.01) in the rat retina early in diabetes.Conclusions: These results suggest that the diabetes-mediated increase in CTGF upregulates VEGF and TGF-[beta]2 expression and induces apoptosis in the retina. This elevation may be inhibited by treatment with CTGFsiRNA. Connective tissue growth factor may serve as a potential target for the prevention and treatment of DR.

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Transient regression of choroidal neovascularization membrane after vitrectomy in age-related macular degeneration with vitreomacular traction syndrome

Thursday, December 24th, 2009

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With Appreciation.

Wednesday, December 23rd, 2009
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With Appreciation.

Am J Clin Nutr. 2010 Jan;91(1):241-245

Authors:

PMID: 20023073 [PubMed - as supplied by publisher]

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