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To assess the association of metabolic syndrome (MetS) with Alzheimer disease (AD).

The effect of sonification on d-fructose hydrogenation over several heterogeneous catalysts was investigated. The reaction rate and selectivity were studied at different temperatures, pressures, and ultrasonic power inputs. The ultrasonic effects were clearly catalyst dependent. The sonification during the hydrogenation reaction significantly enhanced reaction rate over Cu/SiO2. In the case of Raney-Ni, just moderate improvements of reaction rates were observed under ultrasound and a slight decrease of catalyst activity by sonification was obtained over Cu/ZnO/Al2O3. Although the choice of catalyst significantly influenced selectivity, no positive influence of acoustic irradiation on selectivity was achieved. The influence of pressure and temperature over Raney-Ni type catalyst was studied under sonification as well. High pressures and temperatures brought just moderate enhancements of reaction rates, while the variation of nominal ultrasonic power input significantly affected the catalyst activity. A catalyst deactivation study was conducted by recycling the catalyst. Acoustic irradiation significantly prevented catalyst deactivation compared to experiments in silent conditions. The effect of ultrasound on catalyst surface was confirmed by means of scanning electron microscopy (SEM).

A tailor-made autoclave setup for simultaneous acoustic irradiation and hydrogenation was used in the hydrogenation of fatty acids and carbohydrates. The aim was not to perform actual sonochemistry but to retard deactivation of the catalyst by means of acoustic irradiation. The catalyst used was a Raney nickel one that tends to deactivate quite rapidly from batch to batch. The results indicated that in the case of the aqueous system (xylose hydrogenation to xylitol) the effect is clear. In the case of the fatty acids one actually observed an enhancement of the reaction rate: with recycled catalyst the second and third batch proceeded somewhat faster than the first one.
© 2003 Society of Chemical Industry

The hydrogenation kinetics of 2,2-dimethylol-1-butanal (TMP-aldol) and 2,2-dimethylol-1-propanal (TME-aldol) over a supported nickel catalyst were determined with experiments carried out in a batchwise operating autoclave at 50−90 °C and 40−80 bar hydrogen. Water was used as the solvent. TMP- and TME-aldol were hydrogenated with 100% selectivity to the corresponding triols. The effects of the catalyst activation procedure and the formaldehyde concentration on the hydrogenation kinetics were studied with thermogravimetry, X-ray photoelectron spectroscopy, and hydrogenation experiments. Catalyst reduction at a high temperature (400 °C) under hydrogen flow was favorable because of a more effective reduction of nickel oxides. Formaldehyde had a considerable retarding effect on the aldol hydrogenation:  the hydrogenation rate was low until all of the formaldehyde was hydrogenated to methanol. The hydrogenation rate of TME-aldol was found to be significantly lower than that of TMP-aldol at low temperatures and pressures (60 °C and 40 bar), whereas equally high rates for both aldol molecules were observed at the highest temperature and pressure studied. A kinetic model including the inhibitory effect of formaldehyde as well as real hydrogen solubility data was proposed for the aldol hydrogenation. The model is comprised of adsorption, desorption, and surface reaction steps. The rate equations based on the model were able to describe the experimentally recorded hydrogenation kinetics of TMP- and TME-aldol.

To investigate whether the APOE-4 allele is associated with weight loss in patients with AD or in nondemented elderly subjects.

OBJECTIVE: To study cognitive function in an elderly population with persistent impaired glucose tolerance (IGT). RESEARCH DESIGN AND METHODS: Fasting and postload 2-h plasma glucose and insulin levels were determined at baseline in a population-based sample of 1,300 people and repeated an average of 3.5 years later in 980 subjects. At follow-up, cognitive function was evaluated in subjects with persistent normal glucose tolerance (NGT; n = 506) and IGT (n = 80) with a brief neuropsychological test battery. RESULTS: Subjects with persistent IGT scored lower in the Mini-Mental State Examination (MMSE) and in the Buschke Selective Reminding Test long-term memory scores. Multiple linear regression analysis revealed that age, education, and insulin levels (either fasting or 2-h value) were associated with the MMSE score in subjects with persistent IGT. Other potential risk factors for impaired cognitive function were not significantly associated with the MMSE score. CONCLUSIONS: Our study showed that persistent IGT in the elderly is associated with mildly impaired cognitive function, and hyperinsulinemia may account for this association.

OBJECTIVE: To investigate the effect of the islet promoter region variant (G-->A) at nucleotide -30 of the glucokinase (GCK) gene on insulin levels in subjects with normal glucose tolerance (NGT), impaired glucose tolerance (IGT), and NIDDM. RESEARCH DESIGN AND METHODS: The study population included 294 subjects with NGT, 83 subjects with IGT, and 36 subjects with NIDDM. Oral glucose tolerance tests (OGTTs) were performed in all subjects, and intravenous glucose tolerance tests (IVGTTs) were performed in subjects with NGT. The islet promoter region of the GCK gene was amplified with polymerase chain reaction and screened for the variant (-30) using single-strand conformation polymorphism analysis. RESULTS: The islet promoter variant (-30) of the GCK gene was found in 17% of subjects with NGT, 23% of subjects with IGT, and 14% of patients with NIDDM (NS between the groups). Fasting, 1-h, and 2-h insulin levels, measured by OGTT, did not differ between subjects with and without this variant in any of the three groups. Furthermore, first-phase insulin secretion, determined by an IVGTT in subjects with NGT, did not associate with presence of the islet promoter region variant (-30) of the GCK gene. CONCLUSIONS: These results indicate that the variant (-30) of the islet promoter region of the GCK gene does not have a significant effect on insulin secretion in Finnish subjects with NGT, IGT, or NIDDM.

Impaired glycogen synthesis after insulin stimulation accounts for most of the insulin resistance in patients with non-insulin-dependent diabetes mellitus (NIDDM). The glycogen synthase gene (GYS1), which encodes the rate-limiting enzyme for glycogen synthesis, is a promising candidate gene for NIDDM. Therefore, we screened all 16 exons of this gene by single-strand conformation polymorphism analysis in 40 patients with NIDDM (age 67 ± 2 years, body mass index 28.2 ± 0.6 kg/m2) from Taipalsaari, eastern Finland. The Gly464Ser variant (exon 11) and a silent polymorphism TTC342TTT (exon 7) have been reported previously. In addition, we found a new variant Gln71His (exon 2) and a new amino acid polymorphism Met416Val (exon 10). An additional sample of 65 patients with NIDDM and 82 normoglycaemic men (age 54 ± 1 years, body mass index 26.3 ±1.4 kg/m2) were screened. The allele frequency of the TTC342TTT silent substitution was 0.29 in both NIDDM and normoglycaemic subjects. The Gln71His and Gly464Ser variants were found in 1 (1 %) and 3 (3 %) subjects, respectively, of the 105 NIDDM patients and in none of the 82 normoglycaemic men. The Met416Val polymorphism was found in 16 (15 %) of the 105 NIDDM patients and in 14 (17 %,) of the 82 control subjects (all heterozygous). The Met416Val polymorphism was not associated with insulin resistance in two groups of normoglycaemic subjects. In conclusion, the new Gln71His and Met416Val substitutions and other variants of the glycogen synthase gene are unlikely to make a major contribution to insulin resistance and NIDDM in diabetic patients from eastern Finland. [Diabetologia (1997) 40: 1313-1319]

Insulin resistance and impaired insulin secretion are thought to be the primary defects in the pathogenesis of non-insulin-dependent diabetes mellitus (NIDDM). Disproportionately increased proinsulin relative to insulin levels are suggested to be an early indicator of a failing pancreas. We examined the relationship of fasting specific insulin, proinsulin, and 32, 33 split proinsulin concentrations, and the proinsulin: insulin ratio to the risk of developing NIDDM 3.5 years later in 65–74-year-old non-diabetic Finnish subjects participating in a populationbased study (n=892) on diabetes and heart disease. Altogether 69 subjects developed NIDDM over a 3.5-year follow-up (cases). The cases were compared to randomly-selected gender-matched control subjects (n=69) and control subjects matched for gender, glucose tolerance status (normal or impaired), and body mass index (n=69). There were no differences in insulin concentrations between cases and random or matched control subjects [median and interquartile range; 123 (77–154), 108 (74–143), 118 (83–145) pmol/l, p=0.271]. Random control subjects had lower proinsulin and 32,33 split proinsulin concentrations and split proinsulin: insulin ratios compared to cases [5.7 (3.8–9.0) vs 7.3 (4.8–10.0) pmol/l, p=0.005; 7.3 (4.5–13.0) vs 10.4 (7.1–18.0) pmol/l, p=0.002; 0.073 (0.057–0.110) vs 0.097 (0.060–0.135), p=0.003]. Matched control subjects had lower proinsulin concentrations and proinsulin: insulin ratios compared to cases [5.9 (4.0–7.7) vs 7.3 (4.8–10.0) pmol/l, p=0.019; 0.048 (0.035–0.071) vs 0.064 (0.045–0.100), p=0.008]. When cases were compared to matched control subjects a 1 SD increase in baseline proinsulin: insulin ratio was associated with a 1.37-fold risk (p=0.020) of developing diabetes. Moreover, this association was independent of fasting glucose concentration at baseline. Thus, in elderly prediabetic subjects disproportionately increased proinsulin concentration, an indicator of defective insulin secretion, is associated with conversion to diabetes over a short time period.

Skeletal muscle and adipose tissue hexokinase II is a promising candidate gene for non-insulin-dependent diabetes mellitus (NIDDM) and insulin resistance. Therefore, we investigated the association of alleles at four polymorphic loci in this gene with NIDDM and insulin resistance in 110 Finnish diabetic patients with NIDDM and in 97 Finnish control subjects with normal glucose tolerance and a negative family history of diabetes. The four polymorphic nucleotide substitutions (silent) in the coding region of the hexokinase II gene were: GAC 251 GAT (exon 7), AAC 692 AAT and CCG 736 CCC (exon 15), and CTG 766 CTA (exon 16). Allele frequencies of each of these polymorphisms did not differ between patients with NIDDM and control subjects. In addition, subjects who were homozygous for the less frequent allele of each of the four polymorphisms had a similar degree of insulin resistance, as determined by the euglycaemic clamp technique, as did the subjects who were homozygous for the common allele in both control subjects and in patients with NIDDM. In conclusion, polymorphisms in the hexokinase II gene are not associated with the risk of NIDDM or insulin resistance in the Finnish population.

Risk factors measured in a cross-sectional study in subjects aged 65–74 years living in eastern Finland were correlated with the risk of developing diabetes 3.5 years later. Sixty-nine of 892 initially non-diabetic subjects developed diabetes during the follow-up. Subjects who subsequently developed diabetes had multiple adverse changes in risk factor levels before the diagnosis of diabetes. Subjects who developed diabetes had higher body mass index and waist-hip ratio as well as higher levels of fasting and 2-h plasma glucose and insulin and higher prevalence of family history of diabetes than those who remained healthy. Furthermore, prevalence of hypertension and levels of diastolic blood pressure and total triglycerides were higher and HDL cholesterol lower among subjects who developed diabetes than among those who remained healthy. The highest risk of developing diabetes was associated with impaired glucose tolerance (World Health Organisation criteria) (odds ratio = 9.8,95% confidence interval = 6.1–5.8). The risk of developing diabetes was 3.7 (3.2–6.1) among subjects in the highest quartile of 2-h insulin distribution, 3.5 (2.0–6.1) in those with triglycerides greater than 2.5 mmol/l,2.7 (1.5–4.6) in those with waist-hip ratio greater than 1.0,2.5 (1.5–4.4) in those with HDL cholesterol less than 1.0 mmol/l, 2.1 (1.2–3.6) in those with body mass index greater than 30 kg/m2, 1.9 (1.1–3.3) among those in the highest quartile of fasting insulin distribution, 1.8 (1.0–3.1) in those having hypertension, and 1.7 (1.0–2.9) in those with a family history of diabetes. The risk of diabetes increased by clustering of risk factors related to insulin resistance (impaired glucose tolerance, triglycerides >2.5 mmol/l, HDL cholesterol <1.0, hypertension) so that the risk was 3.6-fold in those having one risk factor and 59-fold in those having all four risk factors compared to subjects having no risk factors. In conclusion, cardiovascular risk factors related to insulin resistance are predictors of diabetes in the elderly.

Background: Menopause is associated with worsening of cardiovascular (CV) risk factors that can be counteract by physical exercise. Between angiotensin-converting enzyme (ACE) insertion/deletion (I/D) polymorphism, the deletion variant (DD) is related to higher levels of circulating angiotensin II. We evaluated the effect of a short term endurance exercise program on CV remodeling, by means of 2-D echocardiography, among healthy, sedentary, postmenopausal women with ACE I/D genotypes. Methods: Fifty-three women (mean age 56 ± 4 years) underwent a 4 months moderate intensity walking training, eliciting an effort equal to 11-12 according the rating of perceived exertion scale (RPE). Partecipants' attendance at physical exercise program was 85.90 ± 10.75%. The ACE genotype was ascertained by polimerase chain reaction (DD in 20; ID in 27) before (T0) and after training (T1), along with laboratory, anthropometric and echocardiographic measurements. Results: We observed in both groups a significant reduction in systolic and diastolic blood pressure, weight and body mass index, along with a significant increase in left ventricular ejection fraction and diastolic function. Only ID group showed a significant decrease in heart rate and relative wall thickness [RWT ± SD] (T0 0.42 ± 0.06 – T1 0.40 ± 0.05, P 0.04), with a significant increase in left ventricular mass index [LVMI, g/m(2.7) ± SD] (T0 44.58 ± 11.28 – T1 47.34 ± 9.94, P 0.004) and in right ventricular systolic function, assessed by tricuspid annular plane systolic excursion [TAPSE, mm ± SD] (T0 22.52 ± 0.3 – T1 22.96 ± 0.3, P 0.03). Conclusions: Short term aerobic exercise program ameliorates CV profile in healthy, sedentary, postmenopausal women and is associated with positive left ventricular remodeling in ID patients. Enhanced ACE activity, as in DD genotype, could reduce this phenomenon. Thus, ACE polymorphism could account for the individual cardiac remodeling response to physical exercise and should be considered in order to optimize CV prevention measures.