Impact of obesity on glucose and lipid profiles in adolescents at different age groups in relation to adulthood.
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BACKGROUND: As obesity is rapidly becoming a major medical and public health problem, the aim of our study was to determine: 1) if obesity in Caucasian adolescents at 5 different Tanner stages are associated with obesity in adulthood and its obesity-associated abnormal glucose and lipid profiles, 2) the type of fat distribution is associated with glucose and lipid profile abnormalities, and 3) the risk level and the age of appearance of these abnormalities. METHODS: For the first study, data analyses were from a case-control study of adolescents classified according to their BMI; a BMI >or= 85th percentile for age and sex as overweight, and those with a BMI >or= 95th percentile as obese. Subjects with a BMI < 85th percentile were classified as controls. WC:AC ratio of waist circumference to arm circumference was used as an indicator of a central pattern of adiposity. Two other indices of central adiposity were calculated from skinfolds: Central-peripheral (CPR) as subscapular skinfold + suprailliac skinfold)/ (triceps skinfold + thigh skinfold) and ratio of subscapular to triceps skinfold (STR). The sum of the four skinfolds (SUM) was calculated from triceps, subscapular, suprailliac and thigh skinfolds. SUM provides a single measure of subcutaneous adiposity. Representative adult subjects were used for comparison. Glucose and lipid profiles were also determined in these subjects. Abnormal glucose and lipid profiles were determined as being those with fasting glucose >or= 6.1 mmol/l and lipid values >or= 85th percentile adjusted for age and sex, respectively. Prevalence and odds ratio analysis were used to determine the impact of obesity on glucose and lipid profiles at each Tanner stages for both sexes. Correlation coefficient analyses were used to determine the association between glucose and lipid profiles and anthropometric measurements for both sexes. The second study evaluated in a retrospective-prospective longitudinal way if: 1) obesity in adolescence is associated with obesity in adulthood and 2) the nature of obesity-associated risk factors. Incidence and odds ratio analysis were used to determine the impact of obesity on glucose and lipid profiles at 7 different age groups from 9 to 38 years old in both sexes between 1974 to 2000. RESULTS: Overall, glucose and lipid profiles were significantly (P < 0.01) associated with all anthropometric measurements either in male and female adolescents. WC:AC, CPR, STR and SUM are stronger predictors of both glucose and lipid profiles than BMI. Obese and overweight adolescents of Tanner stages III and higher are at increased risk of having an impaired glucose and lipid profiles than normal subjects with odds ratios of 5.9 and higher. Obesity in adolescents of 13-15 years old group is significantly (P < 0.01) associated with obesity in adulthood (with odds ratios of at least 12 for both men and women) and abnormal glucose (odds ratio of >or= 8.6) and lipid profiles (odds ratio of >or= 11.4). CONCLUSIONS: This study confirmed that adolescents aged between 13 and 15 years old of both sexes with a BMI >or= 85th percentile are at increased risk of becoming overweight or obese adults and presenting abnormal glucose and lipid profiles as adults. This emphasizes the importance of early detection and intervention directed at treatment of obesity to avert the long-term consequences of obesity on the development of cardiovascular diseases. (+info)
Increased central artery stiffness in impaired glucose metabolism and type 2 diabetes: the Hoorn Study.
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Impaired glucose metabolism (IGM) and type 2 diabetes (DM-2) are associated with high cardiovascular disease risk. Increases in peripheral and central artery stiffness may represent pathophysiologic pathways through which glucose tolerance status leads to cardiovascular disease. Peripheral artery stiffness increases with deteriorating glucose tolerance status, whereas this trend remains unclear for central artery stiffness. Therefore, we investigated the associations between glucose tolerance status and estimates of central arterial stiffness. We performed a population-based study of 619 individuals (normal glucose metabolism, n=261; IGM, n=170; and DM-2, n=188) and assessed central artery stiffness by measuring total systemic arterial compliance, aortic pressure augmentation index, and carotid-femoral transit time. After adjustment for sex, age, heart rate, height, body mass index, and mean arterial pressure, DM-2 was associated with decreased total systemic arterial compliance, increased aortic augmentation index, and decreased carotid-femoral transit time. IGM was borderline significantly associated with decreased total systemic arterial compliance. Respective regression coefficients (95% confidence intervals) for IGM and DM-2 compared with normal glucose metabolism were -0.05 (-0.11 to 0.01) and -0.13 (-0.19 to -0.07) mL/mm Hg for total systemic arterial compliance; 1.1 (-0.2 to 2.5) and 1.6 (0.2 to 3.0) percentage points for aortic augmentation index; and -0.85 (-5.20 to 3.49) and -4.95 (-9.41 to -0.48) ms for carotid-femoral transit time. IGM and DM-2 are associated with increased central artery stiffness, which is more pronounced in DM-2. Deteriorating glucose tolerance is associated with increased central and peripheral arterial stiffness, which may partly explain why both DM-2 and IGM are associated with increased cardiovascular risk. (+info)
Glucose metabolism in early onset versus late onset Alzheimer's disease: an SPM analysis of 120 patients.
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The aims of this cross-sectional study were (i) to compare the overall glucose metabolism between early onset and late onset Alzheimer's disease in a large sample of patients; and (ii) to investigate the pattern of glucose metabolism as a function of dementia severity in early onset versus late onset Alzheimer's disease, using a statistical parametric mapping (SPM) analysis. Subjects consisted of four groups: 74 patients with early onset Alzheimer's disease, 46 patients with late onset of the disease, and two control groups age matched to each patient group. All the subjects underwent 2-[(18)F]fluoro-2-deoxy-d-glucose (FDG)-PET under the same scanning conditions. Severity of dementia was rated with the Clincial Dementia Rating (CDR). Voxel-based SPM99 was used for statistical analyses. Overall glucose hypometabolism of early onset Alzheimer's disease patients was much greater in magnitude and extent than that of late onset patients, though both groups were similar in dementia severity: the early onset group showed more severe hypometabolism in parietal, frontal and subcortical (basal ganglia and thalamus) areas. When the decline of glucose metabolism was compared as a function of CDR stage, the slope was steeper in early onset than in late onset Alzheimer's disease. The rapid decline occurred at CDR 0.5-1 in the early onset group, whereas similar changes occurred at CDR 2-3 in the late onset group. The greater hypometabolism in early onset than in late onset patients is required to reach the same severity of dementia, probably reflecting greater functional reserve in younger than in older subjects. Alternatively, the metabolic decline curve suggests that the early onset patients may take a more rapid course in the reduction of glucose metabolism than the late onset patients. (+info)
Evaluation of glucose metabolism profile in coronary disease. Prospective study in hospitalized patients.
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BACKGROUND: In 1995, it was estimated that 4% of the adult population had a diagnosis of diabetes mellitus. The trend is for growing prevalence, with a prediction of 300 million individuals with diabetes diagnosed in 2025. There seems to be a large number of asymptomatic individuals with undiagnosed disorders of glucose metabolism. These disorders, whether diabetes mellitus or conditions considered as prediabetic, including impaired glucose tolerance or impaired fasting glucose, represent an important risk factor for coronary disease and worsen the prognosis of established disease. The aim of this study was to evaluate the prevalence of glucose metabolism disorders in individuals admitted to hospital with coronary disease and to determine whether a significant number of these patients had previously undiagnosed diabetes or prediabetic conditions. METHODS: We conducted a prospective study of 44 consecutive patients admitted to the Cardiology Department with a diagnosis of coronary disease, whether previously established or established at the time of admission. We measured morning plasma glucose in all patients, after at least eight hours fasting, and all except those with a previous diagnosis of diabetes underwent an oral glucose tolerance test with 75 g of glucose before hospital discharge. For classification of glucometabolic state, we used the values defined by the World Health Organization (1999). RESULTS: The mean age of our cohort was 64.2+/-13.6 years. The most prevalent disorder was diabetes, with 19 patients (43.2%). Of these, 12 patients (27.3%) had a previous diagnosis of diabetes and 7 patients (15.9%) were unaware that they had the disease. We identified isolated impaired glucose tolerance in 11 patients (25%), isolated impaired fasting glucose in one patient (2.3%) and combined impaired glucose tolerance and impaired fasting glucose in another (2.3%). The remaining 12 patients (27.3%) revealed normal glycemia values. CONCLUSIONS: Glucose metabolism disorders including diabetes and impaired glucose tolerance have a high prevalence in coronary patients. This population includes a significant number of asymptomatic patients with undiagnosed diabetes or undetected prediabetic conditions. A systematic evaluation of the glucometabolic state of individuals with coronary disease during hospitalization, using an oral glucose tolerance test, may enable earlier identification of these disorders and implementation of measures to reduce their future impact. (+info)
Brain white-matter volume loss and glucose hypometabolism precede the clinical symptoms of Huntington's disease.
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We studied the anatomic and functional changes in various brain areas during the course of Huntington's disease (HD) in a large cohort of mutation-positive individuals (n = 71) encompassing the complete range of disability (presymptomatic through stage V), and in healthy controls, for the purpose of defining both degenerative and dysfunctional brain changes in the same subjects. METHODS: We used an MRI and unsupervised multiparametric segmentation procedure based on a relaxometric approach to measure in vivo brain volumes in 71 subjects with presymptomatic to advanced HD. The same population was evaluated by 18F-FDG PET to assess variations in brain glucose metabolism. To predict age at onset in unaffected mutation carriers, we considered the estimated number of years from each subject's age to manifested HD symptoms, for a given expanded triplet number. RESULTS: Age-adjusted analyses confirmed that the 71 subjects as a group, as well as the subgroup of 24 unaffected presymptomatic subjects at risk for HD, had significantly smaller gray-matter and white-matter volumes and larger cerebrospinal fluid volumes than did controls (P < 0.0001). In the 24 presymptomatic subjects, we observed a significant inverse linear correlation between white-matter volume reduction and the estimated time to symptom onset (r2= 0.39; P = 0.0011). Both clinically unaffected subjects at risk for HD and symptomatic patients had significantly decreased glucose uptake in the cortex (frontal and temporal lobes) and striatum (caudate and putamen). HD subjects who were followed up longitudinally showed progressive white-matter reduction in the preclinical subjects (n = 10) and decreased glucose uptake in the cortex and striatum in affected (n = 21) and preclinical (n = 10) subjects. CONCLUSION: White-matter volume loss may precede gray-matter atrophy and may be associated with neuronal dysfunction in early disease. (+info)
Pharmaceutical prospects of phytoestrogens.
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Interest in the physiologic and pharmacologic role of bioactive compounds present in plants has increased dramatically over the last decade. Of particular interest in relation to human health are the classes of compounds known as the phytoestrogens, which embody several groups of non-steroidal estrogens, including isoflavones and lignans that are widely distributed within nature. The impact of dietary phytoestrogens on normal biologic processes was first recognized in sheep. Observations of sheep grazing on fields rich in clover and cheetahs fed high soy diets in zoos suggested that flavonoids and related phytochemicals can affect mammalian health. Endogenous estrogens have an important role not only in the hypothalamic-pituitary-gonadal axis, but also in various non-gonadal systems, such as cardiovascular systems, bone, and central nervous systems, and lipid metabolism. There have been several clinical studies of hormone replacement therapy (HRT) in post-menopausal women to examine whether HRT has beneficial effects on the cardiovascular system, bone fractures, lipid metabolism, and Alzheimer's disease. In addition, estrogen contributes to the development of some estrogen-dependent cancers, such as breast cancer and prostate cancer and the number of patients with these cancers is increasing in developed countries. Although recent mega-studies showed negative results for classical HRT in the prevention of some of these diseases, the molecules that interact with estrogen receptors are candidate drugs for various diseases, including hormone-dependent cancers. This review focuses on the molecular properties and pharmaceutical potential of phytoestrogens. (+info)
Abnormal glucose tolerance and insulin resistance in polycystic ovary syndrome amongst the Taiwanese population- not correlated with insulin receptor substrate-1 Gly972Arg/Ala513Pro polymorphism.
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BACKGROUND: Insulin resistance and glucose dysmetabolism in polycystic ovary syndrome (PCOS) are related with the polymorphisms in the genes encoding the insulin receptor substrate (IRS) proteins, especially Gly972Arg/Ala513Pro polymorphism being reported to be associated with type-2 diabetes and PCOS. We intended to assess the prevalence of abnormal glucose tolerance (AGT) and insulin resistance in Taiwanese PCOS women. We also tried to assess whether the particular identity of Gly972Arg/Ala513Pro polymorphic alleles of the IRS-1 gene mutation can be used as an appropriate diagnostic indicator for PCOS. METHODS: We designed a prospective clinical study. Forty-seven Taiwanese Hoklo and Hakka women, diagnosed with PCOS were enrolled in this study as were forty-five healthy Hoklo and Hakka women as the control group. Insulin resistance was evaluated with fasting insulin, fasting glucose/insulin ratio, and homeostasis model assessment index for insulin resistance (HOMAIR). The genomic DNA of the subjects was amplified by PCR and digested by restriction fragmented length polymorphism (RFLP) with Bst N1 used for codon 972 and Dra III for codon 513. RESULTS: AGT was found in 46.8% of these PCOS patients and was significantly related to high insulin resistance rather than the low insulin resistance. Those patients with either insulin resistance or AGT comprised the majority of PCOS affected patients (AGT + fasting insulin > or =17: 83%, AGT + glucose/insulin ratio > or =6.5: 85.1%, AGT + HOMAIR > or = 2: 87.2%, and AGT + HOMAIR > or = 3.8: 72.3%). None of the tested samples revealed any polymorphism due to the absence of any Dra III recognition site or any Bst N1 recognition site in the amplified PCR fragment digested by restriction fragmented length polymorphism. CONCLUSION: There is significantly high prevalence of AGT and insulin resistance in PCOS women, but Gly972Arg and Ala513Pro polymorphic alleles of IRS-1 are rare and are not associated with the elevated risk of PCOS amongst Taiwanese subjects. This is quite different from the similar study in phylogenetically diverged Caucasian subjects. (+info)
Development of cookie test for the simultaneous determination of glucose intolerance, hyperinsulinemia, insulin resistance and postprandial dyslipidemia.
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A new cookie test was developed for the simultaneous evaluation of multiple risk factors such as glucose intolerance, hyperinsulinemia, insulin resistance and postprandial dyslipidemia. The cookie consisting of 75 g carbohydrate and 25 g fat is ingested and the blood samples are obtained at 0, 1 and 2 hours later. When the two carbohydrate sources, liquid glucose and test cookie, were compared as a glucose load within 3 months, the 2 hr plasma glucose levels were not statistically different, proposing the use of the same criteria at 2 hour glucose level for the diagnosis of diabetes and impaired glucose tolerance (IGT) in subjects without exocrine pancreatic dysfunction. In addition, hyperinsulinemia, insulin resistance (AUC insulin, and/or AUC insulin X AUC glucose), and postprandial hyperlipidemia (DeltaTG, Triglyceride; DeltaRLP, remnant like particles) have been simultaneously uncovered. Reactive hypoglycemia with adverse epigastric discomfort was observed in 26.3% of the control subjects with liquid glucose, while it was observed in only 1 case (5.3%) without any symptom with cookie tests. In fact, one reactive hypoglycemia out of 5 with liquid glucose turned out to be IGT with cookie test. In 64 subjects with lifestyle-related diseases, cookie test revealed hyperinsulinemia and insulin resistance in 56% respectively, postprandial hyperlipidemia in 39%, diabetes and IGT in 22-23% of each of the subjects and all showed at least one abnormal value. In contrast, in university students with exercise habit, all showed normal results with cookie test. In addition, improved insulin sensitivity over non-exercise group was obverved. In summary, the cookie test provided more informations compared with OGTT using liquid glucose and with fewer side effects. Simultaneous evaluation of glucose intolerance, hyperinsulinemia, insulin resistance, and postprandial hyperlipidemia was also possible. (+info)