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Query: UMLS:C0011860 (type 2 diabetes)
 57,723 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Circadian oscillators play an indispensable role in the coordination of physiological processes with the cyclic changes in the physical environment. A significant number of recent clinical and molecular studies suggest that circadian biology may play an important role in the regulation of adipose and other metabolic tissue functions. In this discussion, we present the hypothesis that circadian dysfunction may be involved in the pathogenesis of obesity, type 2 diabetes, and the metabolic syndrome.
Obesity (Silver Spring) 2007 Mar
PMID:Circadian rhythms and the regulation of metabolic tissue function and energy homeostasis. 1737 1

Conflicting results have been reported regarding whether the PPARgamma2 Pro12Ala polymorphism plays a role in the risk of type 2 diabetes (T2D), suggesting genetic heterogeneity. To investigate this issue, a meta-analysis of 41 published and 2 unpublished studies (a total of 42,910 subjects) was conducted. Ala12 carriers had a 19% T2D risk reduction, but this association was highly heterogeneous (p = 0.005). A great proportion (48%) of heterogeneity was explained by the controls' BMI, with risk reduction being greater when BMI was lower. Risk reduction of Ala12 carriers in Asia (35%) was higher than in Europe (15%, p = 0.02) and tended to be higher than in North America (18%, p = 0.10). Difference between Asians and Europeans was no longer significant (p = 0.15) after adjusting for the controls' BMI. Studies from Europe were still heterogeneous (p = 0.02) with risk reduction in Ala12 carriers being progressively smaller (test for trend in the odds ratios, p = 0.02) from Northern (26% reduction, p < 0.0001) to Central (10%, p = 0.04) and Southern (0%, p = 0.94) Europe. In conclusion, in our meta-analysis, the reduced risk of T2D in Ala12 carriers is not homogeneous. It is greater in Asia than in Europe and, among Europeans, it is higher in Northern Europe, barely significant in Central Europe, and nonexistent in Southern Europe.
Obesity (Silver Spring) 2007 May
PMID:Heterogeneous effect of peroxisome proliferator-activated receptor gamma2 Ala12 variant on type 2 diabetes risk. 1749 82

We recently showed that long-term weight reduction changes the gene expression profile of adipose tissue in overweight individuals with impaired glucose tolerance (IGT). One of the responding genes was X-chromosomal tenomodulin (TNMD), a putative angiogenesis inhibitor. Our aim was to study the associations of individual single nucleotide polymorphisms and haplotypes with adiposity, glucose metabolism, and the risk of type 2 diabetes (T2D). Seven single nucleotide polymorphisms from two different haploblocks were genotyped from 507 participants of the Finnish Diabetes Prevention Study (DPS). Sex-specific genotype effects were observed. Three markers of haploblock 1 were associated with features of adiposity in women (rs5966709, rs4828037) and men (rs11798018). Markers rs2073163 and rs1155794 from haploblock 2 were associated with 2-hour plasma glucose levels in men during the 3-year follow-up. The same two markers together with rs2073162 associated with the conversion of IGT to T2D in men. The risk of developing T2D was approximately 2-fold in individuals with genotypes associated with higher 2-hour plasma glucose levels; the hazard ratios were 2.192 (p = 0.025) for rs2073162-A, 2.191 (p = 0.027) for rs2073163-C, and 1.998 (p = 0.054) for rs1155974-T. These results suggest that TNMD polymorphisms are associated with adiposity and also with glucose metabolism and conversion from IGT to T2D in men.
Obesity (Silver Spring) 2007 May
PMID:Tenomodulin is associated with obesity and diabetes risk: the Finnish diabetes prevention study. 1749 83

Despite minimal invasive orientation in restorative dentistry, in Romania the necessary for extensive restorative treatment in posterior teeth is still high. The silver amalgam still remains a social treatment option for such situation. The purpose of this study was to analyze the efficiency of a new method for analytical determination of the volume of restoration in posterior teeth, knowing that the risk for coronal fracture depends on the size of restoration. The study correlated the results obtained through this method with the real values (mathematically determined) of restorations and the anatomical crowns volumes in order to assess the risk fracture. Amalgam restorations of different types and sizes were placed in 24 extracted premolars and molars. A good global correlation was observed between the true and calculated value (98.321%). The best correlation was observed for MOD restorations (93.042%) while the worst coefficient was obtained for MO restorations (83.378%). The medium restorations presented o correlation of 99.288% and the extensive restorations had an index around 96.957%. This method is based on physics principles and objective measurement resulting in a good correlation with the real dimensions of cavities. Therefore it could be used to assess the risk of crown fracture in teeth with amalgam restorations.
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PMID:[Study regarding coronal fracture probability in posterior amalgam restorations]. 1757 68

Short nucleotide repetitions (STRs) are commonly used as genetic markers; thus their detection and analysis constitutes a very important tool for the mapping of genetic diseases, as well as for gathering information about genetic polymorphisms at the population level. STRs can be detected with agarose- or acrylamide-based electrophoretic techniques, followed by visualization of the DNA sample with ethidium bromide, silver nitrate, or fluorophore labeling. In this work, we analyzed genomic DNA from five individuals affected with type II diabetes mellitus (T2DM) and five controls (unaffected individuals) in order to know the most precise and reproducible technique for the analysis of the existing polymorphism in the STR DG10S478 of the TCF7L2 gene. The combination of PCR with labeling of the products with the CY5 fluorophore, followed by detection on an ALFexpress sequencer, offered the required resolution to detect the variability in this STR, based solely on size analysis. Our methodology offers similar accuracy and reproducibility at lower costs than existing methods based on the sequencing of PCR products, and is a faster alternative when applied to genotyping studies.
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PMID:Electrophoretic techniques applied to the detection and analysis of the human microsatellite DG10s478. 1816 73

Obesity and type 2 diabetes constitute leading public health problems worldwide. Studies have shown that insulin resistance affiliated with these conditions is associated with skeletal muscle lipid accumulation, while the latter is associated with mitochondrial dysfunctions. However, the initiation and regulation of mitochondrial biogenesis rely heavily on approximately 1000 nuclear-encoded mitochondrial regulatory proteins. In this study, we targeted the ubiquinol-cytochrome c reductase core protein I gene, a nuclear-encoded component of mitochondrial complex III, for its association with subcutaneous fat depth (SFD) and skeletal muscle lipid accumulation (SMLA) using cattle as a model. Four promoter polymorphisms were identified and genotyped on approximately 250 Wagyu x Limousin F2 progeny. Statistical analysis revealed that two completely linked polymorphic sites, g.13487C>T and g.13709G>C (r2 = 1), were significantly associated with both SFD (p < 0.01) and SMLA (p < 0.0001). The difference between TTCC and CCGG haplotypes was 0.178 cm for SFD and 0.624 scores for SMLA. Interestingly, the former haplotype produced higher promoter activities than the latter by 43% to 49% in three cell lines (p < 0.05). In addition to Rett syndrome and breast/ovarian cancer observed in other studies, we report evidence for the first time, to our knowledge, that overexpression of ubiquinol-cytochrome c reductase core protein I might affect mitochondrial morphology and/or physiology and lead to development of obesity and related conditions.
Obesity (Silver Spring) 2007 Dec
PMID:Functional UQCRC1 polymorphisms affect promoter activity and body lipid accumulation. 1819 95

Secreted from white adipose tissue, circulating concentrations of adiponectin are reduced in the presence of metabolic and cardiovascular disease such as obesity and type 2 diabetes. The aim of this systematic review is to assess the body of evidence critically for the effects of exercise on adiponectin levels. Literature searches using the Medline, CINAHL, Cochrane Controlled Trials registry, EMBASE, and SportDiscus databases were conducted from 1966 to September 2006 using keywords pertaining to "adiponectin" and "exercise." Thirty-three trials met the inclusion criteria. Study designs consisted of 5 cross-sectional studies, 7 trials of acute exercise, 11 uncontrolled trials, 2 non-randomized controlled trials, and 8 randomized controlled trials (RCTs). Exercise of varying prescription has been shown to increase serum adiponectin in 38% of RCTs, demonstrating small-to-moderate effect sizes (ESs). One study reported a dose-response effect of resistance training intensity and the augmentation of adiponectin. Inconsistent support in the literature exists for increasing adiponectin levels after short-term exposure to robust aerobic or resistance training of moderate-to-high intensities. Particular attention should be directed toward high-risk cohorts, in whom augmentation of the anti-inflammatory cytokine adiponectin may assume critical importance.
Obesity (Silver Spring) 2008 Feb
PMID:Effects of exercise on adiponectin: a systematic review. 1823 30

The transcription factor 7-like 2 (TCF7L2) rs7903146 T allele was previously associated with type 2 diabetes (T2D) and decreased BMI whereas haplotypes carrying the rs7903146 C and rs10885406 A alleles (HapA) were associated with increased BMI. The functional relevance of TCF7L2 polymorphisms and their effects on T2D and obesity remained to be further investigated. In white European populations, we found that the rs7903146 T allele was more associated with T2D in 3,547 non-obese individuals (odds ratio (OR) = 1.88 (1.69-2.10)) than in 1,110 class III obese subjects (OR = 1.24 (1.03-1.50)). No direct effect of the rs7903146 C allele and HapA was found on any form of obesity in 3,507 normal glucose tolerant (NGT) individuals, 1,106 pedigrees with familial obesity and 5,512 individuals from the French general population. However, in T2D subjects, the rs7903146 C allele was less prevalent in the 1,111 non-obese individuals (55.2%) compared to 659 class III obese subjects (67.5% OR = 1.69 (1.46-1.95)). Functional studies showed that the rs7903146 T allele is less prone to be bound by protein factors than the C allele in 3T3-L1, HepG2 and beta-TC3 cell lines and that TCF7L2 expression decreases in subcutaneous adipose tissue from NGT obese T/T carriers under calorie restriction. In conclusion, TCF7L2 is not a risk factor for obesity in European populations, but its effect on T2D risk is modulated by obesity. Furthermore, our data suggest that the rs7903146 T allele may be possibly functional and associated with a nominal decrease in TCF7L2 expression in adipose tissue of individuals under calorie restriction.
Obesity (Silver Spring) 2008 Feb
PMID:Effects of TCF7L2 polymorphisms on obesity in European populations. 1823 63

We sought to assess the relationship between the metabolic syndrome, abdominal obesity, and glucose deterioration amongst patients with type 2 diabetes. Our prospective cohort consisted of 164 adult patients with established diabetes who have a history of poor glycemic control, have just completed an intensive intervention aimed at improved control, and have demonstrated reduced HbA1c prior to enrollment. Waist circumference and presence of metabolic syndrome were assessed at baseline, and patients were followed up (median 24 months) for assessment of the study outcome, namely, time-to-hyperglycemic relapse, predefined as HbA1c >8% and >1% rise over baseline. Kaplan-Meier estimates of relapse-free glucose maintenance and multivariable Cox regression models were used for quantifying the independent effects of the metabolic syndrome and waist circumference on risk of glucose deterioration. The mean baseline waist circumference was 42.9 5.5 inches. Prevalence of the metabolic syndrome was 80%. During follow-up, 39 patients (24%) experienced hyperglycemic relapse. The metabolic syndrome was not associated with time-to-relapse (P = 0.15). The waist circumference component by itself, however, was associated with increased likelihood of hyperglycemic relapse with an unadjusted hazard ratio of 3.4 (95% confidence interval (CI) 1.2-9.7) and a hazard ratio of 3.2 (95% CI 1.1-9.1) after adjusting for age, gender, insulin use, weight change, and physical activity level. The National Cholesterol Education Program Adult Treatment Panel III (NCEP ATPIII) metabolic syndrome had limited ability to predict glucose deterioration in this type 2 diabetes cohort. Waist circumference by itself, however, is a strong predictor of future glucose control, and may be a parsimonious tool for risk stratification. BMI may also be a useful predictive tool.
Obesity (Silver Spring) 2008 Apr
PMID:Waist circumference, not the metabolic syndrome, predicts glucose deterioration in type 2 diabetes. 1827 89

The objective of this paper is to evaluate adaptations in hepatic mitochondrial protein mass, function and efficiency in a rat model of high-fat diet-induced obesity and insulin resistance that displays several correlates to human obesity. Adult male rats were fed a high-fat diet for 7 weeks. Mitochondrial state 3 and state 4 respiratory capacities were measured in liver homogenate and isolated mitochondria by using nicotinamide adenine dinucleotide, flavin adenine dinucleotide and lipid substrates. Mitochondrial efficiency was evaluated by measuring proton leak kinetics. Mitochondrial mass was assessed by ultrastructural observations and citrate synthase (CS) activity measurements. Mitochondrial oxidative damage and antioxidant defence were also considered by measuring lipid peroxidation, aconitase and superoxide dismutase (SOD) specific activity. Whole body metabolic characteristics were obtained by measuring 24-h oxygen consumption (VO2), carbon dioxide production (VCO2), respiratory quotient (RQ) and nonprotein respiratory quotient (NPRQ), using indirect calorimetry with urinary nitrogen analysis. Whole body glucose homeostasis was assessed by measuring plasma insulin and glucose levels after a glucose load. Adult rats fed a high-fat diet for 7 weeks, exhibit not only obesity, insulin resistance and hepatic steatosis, but also reduced respiratory capacity and increased oxidative stress in liver mitochondria. Our present results indicate that alterations in the mitochondrial compartment induced by a high-fat diet are associated with the development of insulin resistance and ectopic fat storage in the liver. Our results thus fit in with the emerging idea that mitochondrial dysfunction can led to the development of metabolic diseases, such as obesity, type 2 diabetes mellitus and nonalcoholic steatohepatitis.
Obesity (Silver Spring) 2008 May
PMID:Alterations in hepatic mitochondrial compartment in a model of obesity and insulin resistance. 1827 91


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