BACKGROUND: Many studies have recently shown that leptin can promote angiogenesis via endothelial leptin receptors and induce oxidative stress in endothelial cells; These findings suggest the relationship between cardiovascular risk and blood leptin concentration. In the present study, we investigated the relationship between leptin concentration and carotid intima-medial thickness (CIMT) as an indicator of early atherosclerosis in adults. METHEODS: The study subjects comprised 138 (45 men and 93 women; mean age 42.4+/-7.5 years; mean BMI 24.0+/-2.7 kg/m2) without history of diabetes, hypertension or cardiovascular disease. We measured CIMT by high resolution ultrasonography and plasma leptin levels by radioimmunoassay. RESULTS: 1) No significant differences in age, BMI or CIMT between male and female subjects were noted, but the leptin levels in female were significantly higher than those in males. (8.42+/-5.90 ng/mL vs. 3.08+/-1.00 ng/mL, p<0.001) 2) CIMT showed a significant positive correlation with age (r=0.31, p< 0.001), BMI (r=0.25, p<0.01) and level (r=0.42, p<0.05) in simple regression analysis. 3) When male and female subjects were each divided into 3 groups by leptin concentration, no significant difference in CIMT among female subjects was found. In male subjects, CIMT was significantly higher in the highest tertile of leptin level than in the other 2 groups (0.65+/-0.03 mm vs. 0.56+/-0.07 mm and 0.53+/-0.07 mm, p<0.01) after adjustment for BMI and age. However, this difference was not significant after adjustment for smoking. 4) CIMT (0.61+/-0.05 mm vs. 0.53+/-0.07 mm, p<0.01) and leptin concentrations (3.57+/-2.13 ng/mL vs. 2.20+/-1.39 ng/mL, p<0.05) were significantly higher in male smokers than in male non-smokers. CONCLUSION: Our results demonstrated significant correlation of CIMT to plasma leptin level before adjustment for smoking. A possible explanation is the permissive action of smoking on the atherogenic effect of leptin. However, further studies to elucidate the relationships and interactions among smoking, leptin level and the development of atherosclerosis will be needed.
Adult* ; Atherosclerosis ; Cardiovascular Diseases ; Endothelial Cells ; Female ; Humans ; Hypertension ; Leptin* ; Male ; Oxidative Stress ; Plasma* ; Radioimmunoassay ; Receptors, Leptin ; Smoke ; Smoking ; Ultrasonography

BACKGROUND: The genetic and environmental factors involved in the development of obesity and several candidate genes have been suggested to have an influence on energy and fuel metabolism. However, the specific genetic defects responsible for human obesity have not been identified yet. It is likely that a combination of polymorphisms in one or more candidate genes may affect energy metabolism and the development of obesity. We performed this study to determine the role of 45 bp insertion in the uncoupling protein (UCP)2 exon 8 and Trp64Arg polymorphism of beta3-adrenergic receptor ( 3-AR) gene in the regulation of body weight and the pattern of fat distribution. METHODS: In 114 subjects (male: 40, female: 74, mean body mass index: 24.1+/-2.7 kg/m2, 80 subjects with normal glucose tolerance, 34 subjects with impaired glucose tolerance), body fat distribution patterns were assessed by anthropometric measurement, bioelectric impedance analysis and computed tomogram. The genotypes of UCP genes were determined by polymerase chain reaction (PCR), and mutation in 3-AR gene by PCR followed by enzymatic digestion. RESULTS: In UCP2 genes, the frequency of deletion homozygote (DD) was 59.4%, heterozygote (DI) was 3.5% and insertion homozygote (II) was 3.1% Meanwhile, in 3-AR, the frequency of TrpTrp was 67.9%, TrpArg was 29.5% and ArgArg was 2.7%. In the lean group (subjects with a BMI less than 25 kg/m2), the frequencies of insertion allele and Arg64 allele were not significantly different than those among the overweight subjects (BMI > or = 25 kg/m2). There was not significant difference in clinical, biochemical or body fat distribution patterns between the groups according to UCP2 polymorphism. In the case of the polymorphism in 3-AR gene, the subjects with ArgArg homozygotes had lower HDL-cholesterol level (p<0.05). For the individuals over 40 years of age, BMI was greater among those with the deletion homozygotes and Arg64 allele, as compared to other groups according to the combination of UCP2 and 3-AR genotypes (p<0.05). CONCLUSION: These results suggest that genetic variations in UCP2 and 3-AR can synergistically affect metabolic rate and susceptibility to weight gain, thereby and contribute to the change in body weight in later life.
Adult* ; Alleles ; Body Fat Distribution ; Body Mass Index ; Body Weight ; Digestion ; Electric Impedance ; Energy Metabolism ; Exons ; Female ; Genetic Variation ; Genotype ; Glucose ; Heterozygote ; Homozygote ; Humans ; Metabolism ; Obesity* ; Overweight ; Polymerase Chain Reaction ; Weight Gain

As the number of elderly population increases, the proportion of edentulous patients is increasing, and the demand for traditional dentures will also increase. Arranging the artificial teeth according to the relationship and shape of the upper and lower alveolar ridge is an important factor increasing the stability of the denture. This case is a 79 year old female patient who wishes to make denture covered by national health insurance for psychological and economical reasons. With the alveolar bone severely atrophic, the dental CAD software was used for accurate diagnosis and the posterior teeth were arranged in a cross bite according to the interalveolar crest line angle by the program. After completion, the denture showed adequate stability and maintenance in periodic examinations and treatment, and the patient also expressed high satisfaction.
Aged ; Alveolar Process ; Denture, Complete ; Dentures ; Diagnosis ; Female ; Humans ; Malocclusion ; National Health Programs ; Rehabilitation* ; Tooth ; Tooth, Artificial

OBJECTIVES: Gestational diabetes mellitus (GDM) affects 2%-4% of the all pregnant women, and it is a major risk factor for development of type 2 DM. We performed this cross-sectional study to determine whether there were defects in insulin secretory capacity or insulin sensitivity in women with previous GDM. METHODS: On 6-8 weeks after delivery, 75 g oral glucose tolerance test was performed in 36 women with previous GDM and 19 non-pregnant control women matched with age and weight. Intravenous glucose tolerance test was performed on 10-14 weeks after delivery. Insulin secretory capacity measured as the acute insulin response to glucose (AIRg) and insulin sensitivity as minimal model derived sensitivity index (S(I)) were obtained. AIRg x S(I) (beta-cell disposition index) was used as an index of beta-cell function. RESULTS: Women with previous GDM were classified into normal glucose tolerance (postpartum-NGT, n=19) and impaired glucose tolerance (postpartum-IGT, n=17). Postpartum fasting glucose levels were significantly higher in postpartum-IGT compared to postpartum-NGT and control (P<0.05). AIRg x S(I) was significantly lower in postpartum-IGT compared to control (P<0.05). S(I) was lower in postpartum-NGT and postpartum-IGT compared to control, but the difference did not have the statistical significance. Frequency of parental history of type 2 diabetes was significantly greater in postpartum-IGT compared to postpartum-NGT (P<0.05). CONCLUSION: Women with previous GDM showed impaired insulin secretion although their glucose tolerance states were restored to normal. It suggests impaired early insulin secretion may be a major pathophysiologic factor for development of type 2 DM, and this defect may be genetically determined.
Cross-Sectional Studies ; Diabetes Mellitus, Type 2 ; Diabetes, Gestational* ; Fasting ; Female ; Glucose ; Glucose Tolerance Test ; Humans ; Insulin Resistance ; Insulin* ; Insulin-Secreting Cells ; Parents ; Postpartum Period ; Pregnancy ; Pregnant Women ; Risk Factors