Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011860 (type 2 diabetes)
 57,723 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

This study was performed to compare concentrations of pro-inflammatory cytokines, such as interleukin 6 (IL-6), tumor necrosis factor alpha (TNF-alpha) as well as acute-phase protein, such as C-reactive protein (CRP) between subjects with normal glucose tolerance (NGT) and impaired glucose tolerance (IGT). The purpose of this study was to verify whether the pro-inflammatory cytokine-induced acute-phase response is a pathogenic mechanism in type 2 diabetes in elderly Korean women. A total of 1737 elderly subjects aged over 60 years participated in a population based study in Seoul, Korea (SWS Study 1999). Amongst them, a total of 232 non-smoking and non-diabetic female subjects aged 60-89 years was randomly selected and compared with each other. Higher serum high-sensitivity CRP (hs-CRP) concentrations were shown in subjects with IGT than those with normal glucose tolerance (median 1.2 versus 0.9, P < 0.05). Moreover, a relationship between serum hs-CRP concentrations and many components of the metabolic syndrome were detected. Serum pro-inflammatory cytokine IL-6 or TNF-alpha concentrations, however, were neither increased in subjects with IGT nor closely correlated with the components of the metabolic syndrome. In multiple regression analysis with stepwise selection method using hs-CRP as a dependent variable, it was found that white blood cell (WBC) counts, body mass index (BMI), fasting insulin, post-load 2h glucose, hematocrit and LDL cholesterol were significant independent variables. Our study confirms that increased acute-phase reaction is associated with impaired glucose tolerance and the metabolic syndrome in elderly Korean women. However, the hypothesis that pro-inflammatory cytokine-induced systemic inflammation is an early metabolic defect prior to onset of type 2 diabetes, is not supported in our study of elderly Korean women.
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PMID:Comparison of serum concentrations of C-reactive protein, TNF-alpha, and interleukin 6 between elderly Korean women with normal and impaired glucose tolerance. 1506 2

Remarkable proportions of individuals diagnosed with major depressive disorder (MDD) have comorbid metabolic disturbances (i.e., obesity, type 2 diabetes mellitus (T2DM), hypertension, dyslipidemia), and vice versa. Accumulating evidence suggests that common pathophysiologic pathways such as a chronic, low-grade, proinflammatory state mediate this frequent co-occurrence. However, it remains unclear what traits precede the onset and increase the risk for these pathologic states. The aim of our review was to evaluate the evidentiary base supporting the hypothesis that the increased hazard for metabolic disturbance in MDD subpopulations (and vice versa) is mediated in part by endophenotypic variations in sleep architecture. We conducted a PubMed search of all English-language literature with the following search terms: sleep disturbance, circadian rhythm, inflammation, metabolic syndrome, obesity, MDD, mood disorder, prodrome, T2DM, cytokine, interleukin, hypertension, dyslipidemia, and hypercholesterolemia. Longitudinal and meta-analysis data indicate that specific variations in sleep architecture (i.e., decreased slow-wave sleep [SWS], increased rapid eye movement [REM] density) precede the onset of depressive symptomatology for a subpopulation of individuals. The same sleep architecture variations also are associated with obesity, T2DM, and hypertension. Decreased SWS and increased REM density is correlated with an increase in proinflammatory cytokines (e.g., IL-6, tumor necrosis factor, etc.). This proinflammatory state has been independently shown to be associated with MDD and metabolic disturbances. Taken together, our review suggests that sleep architecture variation of increased REM density and decreased SWS may be an endophenotypic trait, which serves to identify a subpopulation at increased risk for depressive symptoms and metabolic disturbances. Future research is needed to discern the predictive value, sensitivity, and specificity of using sleep architecture variation as a biomarker for MDD and metabolic disturbances. Validation of this marker would have broad clinical implications, such as primary, secondary, and tertiary preventative health strategies.
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PMID:Sleep architecture variation: a mediator of metabolic disturbance in individuals with major depressive disorder. 2400 95