Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011854 (type 1 diabetes)
 20,749 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Acute phase proteins have been suggested to be increased in patients with type 1 diabetes. The aim of this study was to evaluate the relationship between serum C-reactive protein (CRP) and intima-media thickness (IMT) and functions of the common carotid artery (CCA) in children and adolescents with type 1 diabetes. Serum CRP levels were measured in 65 children and adolescents with diabetes (33 girls and 32 boys; mean age, 12.7 +/- 3.8 years; range, 7-18; duration of diabetes, 6.9 +/- 3.6 years). Age and diabetes duration, as well as major cardiovascular risk factors including anthropometric and metabolic parameters, were matched between girls and boys. The relations of serum CRP levels to CCA structure and functions were measured by ultrasonography as IMT, cross-sectional compliance, cross-sectional distensibility, diastolic wall stress (DWS), and incremental elastic modulus (IEM). There was no significant difference for serum CRP levels between girls and boys (3.7 +/- 1.3 vs 3.2 +/- 0.4 mg/L; p > 0.05). CRP was positively correlated with IMT (r = 0.49, p = 0.001), IEM (r = 0.24, p = 0.05), DWS (r = 0.58, p < 0.001), and body mass index (BMI) (r = 0.28, p = 0.05). In a multivariate regression model, we included CRP and metabolic and anthropometric parameters such as duration of diabetes, HbA1c, BMI, waist:hip ratio, age, and systolic and diastolic blood pressure as independent variables in the model for CCA structure and functions. CRP emerged as an independent correlation for mean IMT (beta = 0.51, p < 0.001) and DWS (beta = 0.61, p < 0.001). According to our findings, CRP was associated with CCA structure and functions in children and adolescents with type 1 diabetes.
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PMID:Evidence for an association between type 1 diabetes and premature carotid atherosclerosis in childhood. 1663 45

Diabetes is an emblematic example of a heterogeneous disease. Systemic inflammation has emerged as a prominent factor in the type 2 diabetes pathoetiology, but it remains ill-defined in type 1 diabetes. There is a wide spectrum of associations between inflammatory responses and diabetic syndromes. At one end of this spectrum, there is type 1 diabetes for which there is convincing evidence that chronic inflammation of pancreatic islets is a central aspect of disease pathogenesis. At the opposite end, is type 2 diabetes that is clearly associated with systemic inflammation, which could be either the cause or simply mark the underlying pathology. Accumulating evidence has substantiated that a subgroup of adult patients clinically diagnosed with type 2 diabetes exhibit autoantibody responses to islet autoantigens. The presence of these immunologic abnormalities is associated with a severe insulin secretory defect and the absence of signs of systemic inflammation as documented by plasma C-reactive protein and fibrinogen levels that are comparable with those of control populations. Islet autoantibody evaluation should be part of the diagnostic assessment for clinically diagnosed type 2 diabetes not only because it might predict the rate of progression to insulin requirement in adult populations but also to identify a pathogenically distinct disease phenotype characterized by the absence of systemic inflammation and its related disorders. A more appropriate characterization of this subgroup of clinically diagnosed type 2 diabetes, diabetes of autoimmune pathogenesis, will promote future research into the etiology, natural history, and treatment.
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PMID:The heterogeneity of diabetes: unraveling a dispute: is systemic inflammation related to islet autoimmunity? 1732 78

We investigated a patient with type 1 diabetes mellitus undergoing pancreatic islets transplantation. In this patient, we evaluated the clinical usefulness of serial measurement of serum S100A8/A9 complex levels for detecting acute inflammatory responses associated with rejection of transplanted pancreatic islets. The serum S100A8/A9 complex was a more sensitive marker for acute inflammation associated with islet transplant rejection than the serum C-reactive protein. Thus, the serial measurement of the serum S100A8/A9 complex concentration is useful for monitoring the patients with pancreatic islet transplantation.
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PMID:A case with transient increases in serum S100A8/A9 levels implying acute inflammatory responses after pancreatic islet transplantation. 1796 15

Progressive renal function decline begins in one third of patients with microalbuminuria and type 1 diabetes. This study examined whether this decline is associated with elevated excretion of inflammatory markers in urine. Five inflammatory markers (IL-6, IL-8, monocyte chemoattractant protein-1, interferon-gamma-inducible protein (IP-10), and macrophage inflammatory protein-1delta) were measured in urine samples from the First Joslin Study of the Natural History of Microalbuminuria in Type 1 Diabetes, a cohort recruited in 1991. Samples were obtained from 43 participants with microalbuminuria and stable renal function (nondecliners), from 28 with microalbuminuria and early progressive renal function decline (decliners), and from 74 with normoalbuminuria and stable renal function (reference). Urinary concentrations of all five inflammatory markers were significantly higher in decliners than in nondecliners, who were similar to the reference group. Multivariate analysis revealed that those with more than two markers elevated were more than five times as likely to have early progressive decline of renal function. In contrast, serum concentrations of C-reactive protein, IL-8, and macrophage inflammatory protein-1delta did not differ between decliners and nondecliners. These results support the hypothesis that inflammatory processes in the kidney contribute to the progression of nephropathy in patients with type 1 diabetes.
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PMID:Association of urinary inflammatory markers and renal decline in microalbuminuric type 1 diabetics. 1825 62

We examined whether alterations in vascular endothelial function and early structural changes in atherosclerosis are associated with microvascular complications in patients with type 1 diabetes mellitus (DM). Flow-mediated dilation (FMD) of the brachial artery and carotid intima-media thickness (IMT) measurement were performed in 70 young adults (aged 19 to 35 yr), 48 with type 1 DM, and 22 normal controls. Patients with diabetes had a lower peak FMD response (7.8+/-3.9 vs. 11.1+/-1.9%, p<0.001) and increased IMT (0.51+/-0.10 vs. 0.42+/-0.07 mm, p<0.001) compared with controls. Twenty (41.7%) of the patients had microvascular complications including neuropathy, nephropathy, or retinopathy. In these complicated diabetic patients, we found a lower FMD response (6.1+/-2.5 vs. 9.9+/-3.5%, p=0.001) compared with diabetics without microvascular complications. The presence of microvascular complications was also associated with older age and longer duration of the disease. However, no differences were observed in IMT, body size, blood pressure, HbA1c, C-reactive protein, low-density lipoprotein or high-density lipoprotein cholesterol levels between complicated and non-complicated patients. Endothelial dysfunction and early structural atherosclerotic changes are common manifestations in type 1 DM, and endothelial dysfunction is thought to be an early event in the atherosclerotic process and important in the pathogenesis of microvascular complications.
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PMID:Endothelial dysfunction and microvascular complications in type 1 diabetes mellitus. 1830 3

Functional disturbances in microcirculation in juvenile type 1 diabetes (T1D) are believed to underlie, in part, the later occurrence of cardiovascular complications. Some epidemiologic studies suggested greater risk of microvascular complications in those with T1D-risk genotypes of human leukocyte antigen (HLA). We investigated whether HLA-DQ2/8, which is linked to highest T1D morbidity, influences microvascular function in young diabetic patients. Cutaneous microvascular endothelium-dependent and independent reactivity and HLA genotypes were assessed in young patients (age: 9-21 y) with T1D (duration: 2-20 y). HLA-DQ2/8 was identified in 29 of 75 patients. The DQ2/8 and non-DQ2/8 groups were similar in age, body mass index, diabetes duration, glycosylated hemoglobin, and C-reactive protein (CRP). Compared with the non-DQ2/8 group, the DQ2/8 group showed decreased endothelium-dependent responses (p = 0.03 after adjustment for age, diabetes duration, glycosylated hemoglobin, and CRP) and elevated soluble intercellular adhesion molecule-1 (p = 0.05). In these but not in non-DQ2/8 patients, CRP correlated with both systolic (r = 0.76; p < 0.001) and diastolic (r = 0.50; p = 0.01) blood pressure. HLA-DQ2/8 is associated with endothelial microvascular dysfunction in young patients with T1D, and future studies are needed to provide mechanistic insights. The findings could explain in part the previously reported epidemiologic link between T1D-risk HLA and microvascular complications.
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PMID:Cutaneous microvascular dysfunction is associated with human leukocyte antigen-DQ in youths with type 1 diabetes. 1835 50

The prevalence of diabetes worldwide is increasing rapidly in association with the increase in obesity. Complications are a major fear of patients with diabetes. Complications of diabetes affect many tissues and organs, causing retinopathy, nephropathy, neuropathy, cardiovascular diseases, peripheral vascular diseases, stroke, and periodontal pathologies. Immunologic abnormalities are associated with type 1 and type 2 diabetes and diabetic complications. T cell abnormalities are believed to be the major cause of autoimmune disease in type 1 diabetes, leading to the destruction of pancreatic islets. In type 2 diabetes, inflammation and activation of monocytes are postulated to be important for enhancing insulin resistance and may contribute to the loss of insulin secretory function by islet cells. Many factors can enhance insulin resistance, including genetics, a sedentary lifestyle, obesity, and other conditions, such as chronic inflammation or infection. Increases in inflammation, such as activation of monocytes and increased levels of inflammatory markers, e.g., C-reactive protein, plasminogen activator inhibitor-1, and other cytokines, were reported in insulin-resistant states without diabetes. One possible mechanism is that abnormal levels of metabolites, such as lipids, fatty acids, and various cytokines from the adipose tissue, activate monocytes and increase the secretion of inflammatory cytokines, enhancing insulin resistance. According to this model, obesity activates monocytes and enhances insulin resistance, increasing the risk for type 2 diabetes. Abnormalities in innate immunity might also participate in the development of diabetic complications. In general, hyperglycemia is the main initiator of diabetic retinopathy, nephropathy, and neuropathy, and it participates in the development of diabetic cardiovascular diseases. Although the precise role of inflammation in the development of diabetic microvascular diseases is still unclear, it is likely that inflammation induced by diabetes and insulin resistance can accelerate atherosclerosis in patients with diabetes. Also, it was shown that conditions with an inflammatory basis, such as obesity and type 2 diabetes, can contribute to periodontal disease, suggesting that periodontal abnormalities may be partly influenced by inflammatory changes. Further research is required to confirm the role of inflammation and the onset of diabetes, microvascular diseases, and periodontal pathologies.
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PMID:The role of inflammatory cytokines in diabetes and its complications. 1867 7

Recent work shows a high prevalence of low testosterone and inappropriately low luteinizing hormone (LH) and follicle stimulating hormone (FSH) concentrations in type 2 diabetes. This syndrome of hypogonadotrophic hypogonadism (HH) is associated with obesity in patients with type 2 diabetes. However, the duration of diabetes or HbA1c are not related to HH. Furthermore, recent data show that HH is not associated with type 1 diabetes. C-reactive protein concentrations have been shown to be elevated in patients with HH and are inversely related to plasma testosterone concentrations. This inverse relationship between plasma free testosterone and C- reactive protein concentrations in patients with type 2 diabetes suggests that inflammation may play an important role in the pathogenesis of this syndrome. This is of interest since inflammatory mechanisms may have a cardinal role in the pathogenesis of insulin resistance. It is also relevant that in the mouse, deletion of the insulin receptor in neurons leads to HH in addition to a state of systemic insulin resistance. It has also been shown that insulin facilitates the secretion of gonadotrophin releasing hormone (GnRH) from neuronal cell cultures. Thus, HH may be the result of insulin resistance at the level of the GnRH secreting neuron. Low testosterone concentrations are also related to an increase in total and regional adiposity. This review discusses these issues and attempts to make the syndrome relevant as a clinical entity. Clinical trials are required to determine whether testosterone replacement alleviates insulin resistance and inflammation. In addition, low testosterone levels are associated with an increase in cardiovascular events. Testosterone therapy may therefore, reduce cardiovascular risk. This important aspect requires further investigation.
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PMID:Hypogonadotrophic hypogonadism in type 2 diabetes. 1882 Dec 86

The purpose of this study was to estimate incidence of type 1 diabetes mellitus (T1DM) among children and young adults aged 0-25 years and to assess growth, glycaemic control, complications, risk factors and mortality associated diabetes mellitus,based on prospective registration of patients in Karnataka Diabetes Registry during the period 1995-2008. Complications were determined in subgroups serving as cohorts by screening tests and based on physicians' report. There were 1040 patients (514 boys and 526 girls) registered during the period 1995-2008. The overall incidence/prevalence of T1 DM (per 100,000 persons) was 3.8(0.32/10(5)/year) [males 3.7(0.3110(5)/year) and females 4(0.33/10(5)/year)]. On cross-sectional analysis of different cohorts, 88% (90/102) were below 50th percentile height, 95% (114/120) were <50th percentile of weight. Thirty-nine patients (10.7%) had poor glycaemic control (A1c>9%), The prevalence of different complications were as follows: Neuropathy 5.2% (12/230), retinopathy 8.4% (14/166), nephropathy 8.6% (20/230), hypertension 2.6% (6/230). Hypercholesterolaemia and hypertriglyceridaemia were found in 20.2% (24/119) and 41.7% (48/115) cases respectively and 18.1% (19/105) had low HDL. The percentage of patient with micro-albuminuria, high sensitive C-reactive protein were 29.6% (n=233) and 44.4% (20/45) respectively. Poor glycaemic control, hypertension and duration were strong consistent predictors of all complications. Twenty patients died during the period of which 10 deaths were related to diabetes. Though the incidence of diabetes in the young is low in our population compared to the western population, the burden of diabetes is high due to large population in our country. In spite of our best efforts there are still a huge gap between the standard of care and practice. Majority of type 1 diabetics are not reaching the ideal glycaemic targets.
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PMID:Incidence of type 1 diabetes mellitus and associated complications among children and young adults: results from Karnataka Diabetes Registry 1995-2008. 1936 93

The purpose of the study was to investigate bone mineral density (BMD) in children with type 1 diabetes (DM1) and to establish the relationships between BMD, physical activity, glycemic control, and markers of systemic oxidative stress and inflammation. We studied 30 children with DM1, aged 4.7-18.6 years, and 30 healthy subjects, matched by sex, age, and body mass index (BMI). Mean duration of DM1 was 5.4 +/- 3.4 years and mean glycosylated hemoglobin (HbA(1c)) level over 12 months was 9.8 +/- 1.5%. Lumbar and total bone mineral density (BMD, g/cm(2)) were measured by dual-energy X-ray absorptiometry (DXA). We calculated the apparent volumetric lumbar BMD (BMDvol, g/cm(3)) and total mineral content adjusted for age and height (BMCadj), and measured plasma intercellular adhesion molecule-1 (ICAM-1), high sensitivity C-reactive protein (hs-CRP), and urinary 8-iso-prostaglandin F(2a) (F(2)-IsoPs). Calcium (Ca) intake was assessed by questionnaire and physical activity by questionnaire and accelerometer (ActiGraph, count/h). Total BMCadj and lumbar BMDvol were significantly lower in children with DM1 than in controls (101.8 +/- 7.7 vs. 107 +/- 5.7%, P = 0.005; 0.32 +/- 0.08 vs. 0.36 +/- 0.09 g/cm(3), P = 0.05, respectively). These differences were mostly caused by the differences in boys. Plasma ICAM-1 and hs-CRP levels were significantly higher in the DM1 group compared to the controls. Ca intake and urine F(2)-IsoPs levels were similar between the groups. Diabetic boys were less active than controls (18231 +/- 6613 vs. 24145 +/- 7449 count/h, P = 0.04). In the DM1 group, lumbar BMDvol correlated inversely with urinary F(2)-IsoPs (r = -0.5; P = 0.005) and plasma ICAM-1 levels (r = -0.4; P = 0.02), and also with HbA(1c) levels after adjustment for age (r = -0.45; P < 0.05). Total BMCadj correlated inversely with HbA(1c) levels (r = -0.4; P = 0.02). We conclude that children with DM1, particularly boys, have lower BMD. Poor glycemic control, elevated markers of oxidative stress, and inflammation are associated with lower BMD.
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PMID:Lower bone mineral density in children with type 1 diabetes is associated with poor glycemic control and higher serum ICAM-1 and urinary isoprostane levels. 1937 18


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