Search PubMed⌕ Search

Biomedical subjects

J A Paniagua

Publications and source records attributed to J A Paniagua.

17 recordsLinked to original sources
PubMed2005

A carbohydrate-rich diet reduces LDL size in QQ homozygotes for the Gln 192Arg polymorphism of the paraoxonase 1 gene.

Paraoxonase 1 (PON 1) is an esterase with antioxidant properties that is present in HDL. Gln192Arg polymorphism (also named Q192R or Q/R) of the PON 1 gene that encodes this protein defines two alleles (Q and R). The R allele has been associated with higher cardiovascular risk. LDL size and susceptibility to oxidation also have been identified as cardiovascular risk factors. Our objective was to determine whether genetic variations in the Gln192Arg polymorphism influence LDL size and susceptibility to oxidation after the consumption of diets with different fat content. In our experiments, the participants (n = 98) underwent three 4-wk diets--one, saturated fat-enriched (SAT); another, monounsaturated fat-enriched (MONO); and a third, carbohydrate-enriched (CHO). We observed that LDL were smaller in the QQ group after the CHO diet vs. the SAT (P < 0.01) and MONO diets (P < 0.03). No differences in LDL size were found in QR/RR subjects. When we analyzed lag time of oxidation of LDL, we found that when carriers of the R allele (QR/RR) received the MONO diet, the lag period of LDL oxidation was longer as compared with the CHO diet. Otherwise, we found no differences in QQ homozygotes when we evaluated the lag time of oxidation of LDL after the three diets. These results suggest that the Glnl92Arg polymorphism of the paraoxonase gene influences LDL size and susceptibility to oxidation in response to diet.

Adolescent↗
PubMed2005

Oxidized-LDL levels are changed during short-term serum glucose variations and lowered with statin treatment in early Type 2 diabetes: a study of endothelial function and microalbuminuria.

AIMS: To investigate the role of HMG-CoA reductase inhibitor (statin) treatment during serum glucose variations on plasma oxidized LDL (ox-LDL) levels in obese patients with early Type 2 diabetes mellitus (T2D) and its relationship to endothelial biomarkers. METHODS: In a double-blind, randomized crossover study, 15 obese diet-treated T2D patients received cerivastatin (0.4 mg/day) or placebo for 3 months. Circulating ox-LDL levels were measured fasting and during a euglycaemic-hyperinsulinaemic clamp (approximately 5.5 mmol/l; EHC) and a hyperglycemic clamp (approximately 20 mmol/l; HC). An endothelium-dependent flow-mediated dilation (FMD) study was carried out and urinary albumin excretion (UAE) was measured at rest and during EHC. S-ICAM, s-VCAM and basal prothrombotic factors were also measured. RESULTS: During cerivastatin treatment, basal circulating ox-LDL levels decreased by 48% (P<0.001) compared with placebo. Serum ox-LDL levels decreased during EHC and remained unchanged during HC compared with the fasting state; with cerivastatin treatment these levels were lower compared with placebo both in the fasting state and during the clamp studies. FMD was higher with cerivastatin than with placebo (P<0.001) and the increments in FMD correlated with decrements in serum ox-LDL levels (r=0.78, P=0.001). Microalbuminuria increased during EHC but this was blunted during cerivastatin therapy compared with placebo (P<0.05). Basal sICAM-1 and sVCAM-1 levels decreased (P<0.01 and P<0.05, respectively). CONCLUSIONS: In early obese Type 2 diabetic patients, serum ox-LDL levels are influenced by short-term serum glucose variations and lowered with cerivastatin therapy. During cerivastatin treatment, improved flow-mediated endothelium-dependent dilation was associated with decrements in circulating ox-LDL levels and the hyperinsulinaemia-induced urinary albumin excretion was blunted.

Adult↗
PubMed2004

Postprandial lipemia is modified by the presence of the polymorphism present in the exon 1 variant at the SR-BI gene locus.

It has recently been reported that carriers of the less common allele at the scavenger receptor class B type I (SR-BI) exon 1 polymorphism are more susceptible to the presence of saturated fatty acid in the diet because of a greater increase in LDL cholesterol. Our aim was to determine if this polymorphism could also influence postprandial lipoprotein metabolism, because the SR-BI has been described as a possible mediator in the intestinal absorption of triacylglycerols. Forty-seven normolipidemic volunteers who were homozygous for the E3 allele at the APOE gene were selected [37 homozygous for the common genotype (1/1) at the SR-BI exon 1 polymorphism and 10 heterozygous (1/2)]. They were given a fat-rich meal containing 1 g fat and 7 mg cholesterol per kg body weight and vitamin A 60,000 IU/m2 body surface. Fat accounted for 60% of calories, and protein and carbohydrates accounted for 15% and 25% of energy respectively. Blood samples were taken at time 0, every 1 h until 6 h, and every 2.5 h until 11 h. Total cholesterol and triacylglycerols in plasma, and cholesterol, triacylglycerols and retinyl palmitate in triacylglycerol-rich lipoproteins (large and small triacylglycerol-rich lipoproteins) were determined. Postprandial responses for triacylglycerols and retinyl palmitate in small triacylglycerol-rich lipoproteins were higher in 1/1 individuals than in 1/2 individuals. No other significant differences were noted. Our data show that the presence of the genotype 1/2 is associated with a lower postprandial lipemic response.

Adult↗
PubMed2003

A reduction in dietary saturated fat decreases body fat content in overweight, hypercholesterolemic males.

BACKGROUND AND AIM: The effect of the quality of dietary fat on body composition is unknown. Our objective was to determine whether body composition is modified by the isocaloric substitution of a diet rich in saturated fat by a diet high in monounsaturated fat (Mediterranean diet) or a carbohydrate-rich diet in overweight subjects with hypercholesterolemia. METHODS AND RESULTS: The study involved 34 hypercholesterolemic males aged 18-63 years with a body mass index (BMI) of 28.2 (2.6), all of whom consumed a diet rich in saturated fat (SAT) for 28 days. They were then randomly divided into two groups of 17 subjects and underwent two dietary periods of 28 days each in a crossover design: a Mediterranean diet high in monounsaturated fat (MONO) and a carbohydrate-rich diet (CHO). The order of the diets was different for the two group. The CHO diet contained 57% CHO and 28% total fat (< 10% saturated fat, 12% monounsaturated fat and 6% polyunsaturated fat); the Mediterranean diet contained 47% CHO and 38% fat (< 10% saturated fat, 22% monounsaturated fat--75% of which was provided by olive oil- and 6% polyunsaturated fat). The variables measured at the end of each dietary intervention period were: 1) body composition by means of bioelectrical impedance; 2) plasma lipoproteins using enzymatic techniques; and 3) fatty acids in cholesterol esters by means of gas chromatography. BMI and the waist/hip ratio remained the same during the three dietary periods. A decrease in fat was observed when changing from a saturated fat diet (23.3 (6.3) kg) to a Mediterranean diet (20.8 (7.2) kg) (p < 0.05), or a carbohydrate-rich diet (20.6 (6.7) kg) (p < 0.05). Lean mass increased when changing from a SAT diet (58.4 (7.0) kg) to a CHO diet (60.2 (7.0) kg) (p < 0.05). CONCLUSION: The isocaloric substitution of a saturated fat-rich diet by a Mediterranean or carbohydrate-rich diet decreases total body fat in hypercholesterolemic males.

Adipose Tissue↗
PubMed2002

The SstI polymorphism of the apo C-III gene is associated with insulin sensitivity in young men.

AIMS/HYPOTHESIS: Insulin resistance is considered to be a risk factor for diabetes and coronary heart disease and is determined by the interaction between genetic and environmental factors. The SstI polymorphism in the apolipoprotein C-III gene has been related to the presence of different features of the insulin resistance syndrome. We investigate if this mutation influences the peripheral effect of insulin in healthy young subjects (30 men and 29 women) eating a westernised diet. METHODS: We investigated peripheral insulin sensitivity with the insulin suppression test after a 28-day westernised high-saturated fat diet (38% total fat and 18% saturated fat with 115 mg of cholesterol per 1000 Ju). RESULTS: Steady state plasma glucose values were lower in S1-S1 compared with S1-S2 men (p=0.018 by ANOVA), but not in women (p=0.723). CONCLUSION/INTERPRETATION: There was no difference between carriers and non-carriers of the S2 allele in relation to incidence and sensitivity; although on subgroup analysis there was an effect in men but not in women.

Adult↗
PubMed2002

Cerivastatin improves insulin sensitivity and insulin secretion in early-state obese type 2 diabetes.

In a double-blind, placebo-controlled, randomized crossover study, 15 stable mild hyperglycemic patients without treatment and with features of metabolic syndrome were treated with cerivastatin (0.4 mg/day) or placebo for 3 months. The insulin sensitivity index during the euglycemic-hyperinsulinemic clamp (EHC; 5.4 mmol/l; 80 mU x m(-2) x min(-1)) was increased by cerivastatin treatment (66.39 +/- 3.9 nmol x lean body mass [LBM](-1) x min(-1) x pmol(-1) x l(-1)) as compared with placebo (58.37 +/- 3.69 nmol x LBM(-1) x min(-1) x pmol(-1) x l(- 1); P < 0.01) by 13.7%. Glucose oxidation during EHC was significantly higher with statin treatment (16.1 +/- 1.37 micromol x LBM(-1) x min(-1)) as compared with placebo (14.58 +/- 1.48 micromol x LBM(-1) x min(-1); P < 0.05). During hyperinsulinemia (approximately 800 pmol/l) in EHC steady-state, lipid oxidation was significantly decreased and respiratory quotient was significantly increased with statin treatment (0.33 +/- 0.05 mg x LBM(-1) x min(- 1), 0.94 +/- 0.01) as compared with placebo (0.48 +/- 0.06 mg x LBM(-1) x min(-1), 0.91 +/- 0.01; P < 0.01 and P < 0.05, respectively). During statin treatment, the first-phase insulin response increased from 2.07 +/- 0.28 to 2.82 +/- 0.38 pmol x l(-1) x pmol(-1) (P < 0.05). The second phase of insulin responses examined by C-peptide and insulin levels averaged during the hyperglycemic clamp (20 mmol/l) was unchanged. In conclusion, this study demonstrates that 0.4 mg cerivastatin therapy improves first-phase insulin secretion and increases insulin-mediated glucose uptake and respiratory quotient in the early state of obese type 2 diabetes.

Blood Glucose↗
PubMed2000

Increased high-density lipoprotein-3 binding to leukocytes following weight loss and improved glycemic control in type 2 diabetic patients.

This study evaluates the effect on high-density lipoprotein (HDL) binding activity in cultured granulocytes before and after metabolic control of non-insulin-dependent diabetes mellitus ([NIDDM] type 2 diabetes) patients. In 20 type 2 diabetic patients, diabetic control was accomplished by administration of oral antidiabetic agents and dietary restrictions. Adequate metabolic control was reflected by a decrease in the fasting glucose, glycosylated hemoglobin (HbA1c), mean insulin, and body mass index (BMI). After control of the diabetes, the mean HDL3 cholesterol was increased from 0.918 +/- 0.05 to 1.008 +/- 0.05 mmol/L (P < .05) and apolipoprotein AI (apo AI) was increased from 103 +/- 5.8 to 115 +/- 5.1 mg/dL (P < .01). The HDL3 maximum specific binding was higher after versus before diabetic control, 77 +/- 6 versus 122 +/- 8 ng/mg cell protein (P < .01). This increase was related to an increase in maximum binding ([Bmax] from 4.97 x 10(-10) to 8.3 x 10(-10) mol/L, P < .001), and no significant changes were observed in the Kd (from 1.47 x 10(-7) v 2.04 x 10(-7) mol/L). These results suggest that the metabolic control of type 2 diabetes increases HDL3 binding activity.

Adult↗
PubMed1999

[The diet rich in monounsaturated fat modifies in a beneficial way carbohydrate metabolism and arterial pressure].

OBJECTIVE: Two dietary regimens recommended for the reduction of coronary risk, by way of their effects on lipid profile, are the diet low in saturated fat and a diet rich in monounsaturated fats (MUFA). However the effects of these diets on carbohydrate metabolism in healthy subjects are not well known. The objective of this study was to compare the effect of both diets on various parameters of carbohydrate metabolism. METHODS: 41 healthy young males were submitted to 3 consecutive diets, each for a duration of 4 weeks. The first diet was rich in saturated fat (SAT) (38% fat, 20% saturated). The second was rich in carbohydrates following the recommendations of the NCEP-I (National Cholesterol Education Program type I) (28% fat, 47% carbohydrates). The last one was a diet rich in monounsaturated fatty acids (38% fat, 22% MUFA). At the end of each dietary period, blood pressure (BP) and blood levels of glucose, insulin and free fatty acids were determined. 29 subjects were also submitted to an oral glucose tolerance test (OGTT) at the end of each diet. RESULTS: The SAT diet induced the highest levels of insulin after the OGTT. The consumption of the MUFA diet determined the lowest levels of fasting blood glucose (-0.60 mmol/l [13%], p < 0.0002), insulin (-9 microUl/ml [47%], p < 0.0002) and free fatty acids (-0.11 mmol/l [24%], p = 0.006), compared to the NCEP-I diet. Systolic and diastolic blood pressure were higher in the NCEP-I diet than during the other periods (SBP: +6 mmHg compare with SAT [5%], p = 0.0001; and +5 mmHg compare with MUFA [4%], p = 0.0001; DBP: +20 mmHg compare with MUFA [27%], p = 0.0001) and +6 mmHg compared with SAT [8%], p = 0.0001). CONCLUSION: Of the diets most commonly used for the treatment and prevention of arteriosclerosis, a diet rich in monounsaturated fats is the most beneficial for the healthy population from the point of view of carbohydrate metabolism and blood pressure.

Adult↗
PubMed1998

Plasma lipid response to hypolipidemic diets in young healthy non-obese men varies with body mass index.

Lipid response to dietary fat is highly variable among individuals of a population. The aim of this study was to establish whether being overweight is one of the factors that determines this response. Forty-one non-obese healthy men were divided into two groups according to body mass index as follows: controls, <25 kg/m2; overweight, >25 kg/m2 but <30 kg/m2. After consuming a saturated fat-rich diet (SAT diet: 38% fat, 20% saturated) for 4 wk, subjects were switched to a low fat diet [National Cholesterol Education Program (NCEP)-I diet: 28% fat, 10% saturated] for 4 wk and then to a monounsaturated fat-rich diet (MUFA diet: 38% fat, 22% monounsaturated) for 4 wk. Data were analyzed by Student's t test and two-way ANOVA for repeated measures. After consuming the NCEP-I diet, the overweight subjects had a smaller decrease relative to the SAT diet period in plasma total cholesterol [-0.30 vs. -0.67 mmol/L (-7 vs. -16%), P < 0.02] and low density lipoprotein-cholesterol concentrations [-0.24 vs. -0.55 mmol/L (-9 vs. -21%), P < 0.04] than controls. However, in the overweight subjects, the MUFA diet produced a greater decrease in plasma triglycerides than in the controls relative to the SAT diet period [-0.36 vs. -0.03 mmol/L (-26 vs. -4%), P < 0.006] and to the NCEP-I diet period [-0.29 vs. 0. 01 mmol/L (-22 vs. 1%), P < 0.01). Plasma cholesterol concentrations changed to a lesser extent, and triglyceride concentration to a greater extent, in overweight but non-obese young men than in those of normal weight in response to changes in dietary fat composition. Our data suggest that in the diet treatment of obese hyperlipemic subjects, it is more important for them to lose weight than to change the fat composition of their diets.

Adult↗
PubMed1998

Bezafibrate and lovastatin decrease the oxidizability of low-density lipoproteins in heart transplant recipients with hyperlidemia.

BACKGROUND: Oxidized low-density lipoprotein plays an important role in the development of atherosclerosis. We evaluated the effect of two lipid-lowering drugs, bezafibrate and lovastatin, on the susceptibility of low-density lipoproteins for oxidation in vitro in 21 heart transplant recipients with hyperlipidemia. METHODS: Patients were given the same diet for 3 months, and after that they were randomized to lovastatin or bezafibrate for a period of 8 weeks and then crossed over to an additional 8 weeks of either bezafibrate or lovastatin. Baseline parameters were also compared with those of a control group of healthy subjects and after both periods of pharmacologic treatment. RESULTS: The low-density lipoproteins of transplant recipients presents a shorter lag time than in control subjects (64+/-3 vs 80+/-4 minutes, respectively). This parameter increases after both bezafibrate and lovastatin treatment (83+/-5 and 80+/-4 minutes, respectively). Moreover, we did observe a negative correlation between insulinemia and the lag time of oxidation after bezafibrate treatment (r = -0.5014, P < .021) and between the polyunsaturated fatty acids/monounsaturated fatty acids ratio in low-density lipoprotein cholesterol esters and lag time after lovastatin treatment (r = -0.4631, P < .04). CONCLUSIONS: Bezafibrate and lovastatin decrease the oxidizability of low-density lipoproteins in heart transplant recipients with hyperlipemia.

Bezafibrate↗
PubMed1995

The effect of cyclosporine and methylprednisolone on plasma lipoprotein levels in rats.

The aim of this study was to evaluate in rats the effects of cyclosporine, methylprednisolone, and the combination of both (CyP) on plasma lipids and lipoproteins levels. Three groups received a low doses of cyclosporine, methylprednisolone, and CyP (cyclosporine, 15 mg/kg/day; methylprednisolone, 1 mg/kg/day; and CyP, 15 plus 1 mg/kg/day of cyclosporine and methylprednisolone, respectively). Three additional groups received high doses (cyclosporine, 30 mg/kg/day; methylprednisolone, 2 mg/kg/day; and CyP, 30 plus 2 mg/kg/day of cyclosporine and methyprednisolone, respectively). The administration of cyclosporine produced an increase in plasma levels of triglycerides, very low density lipoprotein (VLDL) triglycerides, low-density lipoprotein (LDL) cholesterol and in total cholesterol/HDL cholesterol and LDL cholesterol/high-density lipoprotein (HDL) cholesterol ratios. In addition, cyclosporine decreased plasma HDL cholesterol and HDL2 cholesterol levels. The administration of methylprednisolone produced an increase in triglycerides and VLDL triglycerides and a decrease in HDL cholesterol and HDL2 cholesterol levels. Total cholesterol/HDL cholesterol and LDL cholesterol/HDL cholesterol ratios did not change after administration of methylprednisolone. The association of both drugs resulted in a greater increase in triglycerides and VLDL triglycerides than the separated administration of either cyclosporine or methylprednisolone alone. In rats receiving cyclosporine the increase in triglycerides and VLDL triglycerides may be due to a significant decrease in plasma lipoprotein lipase activity.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1984

Effect of phorbol ester TPA on macrophage metabolic activity.

Metabolically active macrophages are known to play a role in tumor immune surveillance, not only as effector cells but also as collaborators in T cell mediated immune response. The present work reports that non-toxic concentrations of the tumor promoter TPA, stimulate the adherence of murine peritoneal macrophages after short time incubation, while TPA pretreatment for periods longer than 4 hrs suppresses phagocytosis, RNA and protein synthesis by these cells. Although inhibition of macrophage metabolic activity could play an additional role in tumor promotion, the enhancing and depressing effects of TPA on the immune system must be weighed before it can be assumed that TPA acts in vivo primarily to depress the immune system.

Animals↗
PubMed1984

Depressed lymphoproliferative response in mixed leukocyte reaction after Mis-locus alloimmunization.

The proliferation of BALB/C lymphocytes preimmunized with Mis or H-2 incompatible cells in response to alloantigens was studied. The results show that preimmunization with Mis-incompatible spleen cells inhibits the lymphoproliferative response against alloantigens whereas preimmunization with H-2 incompatible spleen cells enhances it. It is suggested that Mis coded determinants activate suppressor mechanisms responsible for the unresponsiveness of these preimmunized lymphocytes against alloantigens.

Animals↗
PubMed1982

[Not Available].

Explore the source record for details and available documents.

History of Medicine↗
PubMedDate not supplied

[Not Available].

Explore the source record for details and available documents.

History, Early Modern 1451-1600↗
PubMedDate not supplied

[Temporal cerebellar atrophy following phenytoin therapy].

Epilepsy is considered among the causes of acquired cerebellar degeneration. It is broadly discussed if its real cause would be seizures, the cerebral hypoxia related to them, or different drugs used in epilepsy treatment, such as phenytoin or carbamazepine. We report on a young male diagnosed of partial seizures and treated with carbamazepine, who began to receive phenytoin after the meningioma removing. He suffered then a progressive cerebellar degeneration according to CT and MR controls during a 18 months follow-up. Serum phenytoin levels were always normal and the patient never presented symptoms related to acute toxicity. We consider phenytoin is the main cause of the cerebellar atrophy noted in our patient; the short time in which it developed makes us think that there is an special susceptibility in cerebellum cells to phenytoin toxicity.

Anticonvulsants↗