RESUMEN
AIMS: Diabetes mellitus is the most common metabolic disorder in Kuwait. Anemia is a known outcome of diabetes and its related complications. This study examined the prevalence of anemia in diabetic subjects in Kuwait as well as any association between the presence of anemia with Hemoglobin A1c and diabetes complications. METHODS: The study subjects were diabetic patients with complete records and two or more visits at Dasman Diabetes Institute. Patient's data included demographics, complications, medications and laboratory results. Descriptive statistics were applied using SPSS. RESULTS: Of 1580 included diabetic patients; the prevalence of anemia was 28.5% (95% CI: 26.3, 30.8). Diabetic females had a higher rate of anemia compared to males (35.8% vs. 21.3% respectively, p<0.001). There was no association between diabetes control (HbA1c) and anemia in both genders (p=0.887). Patients with elevated serum creatinine and microalbuminuria were more likely to be anemic (p<0.001). Diabetic patients with anemia had higher presence of peripheral neuropathy and diabetic foot (p<0.001). CONCLUSION: This study shows high prevalence of anemia in diabetic patients, particularly in those with diabetic complications. These results should prompt treatment centers to include anemia investigation and management within their diabetes treatment protocols to reduce morbidity in diabetes.
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Anemia/epidemiología , Diabetes Mellitus/epidemiología , Adolescente , Adulto , Anciano , Albuminuria/sangre , Albuminuria/epidemiología , Anemia/sangre , Anemia/diagnóstico , Biomarcadores/sangre , Creatinina/sangre , Diabetes Mellitus/sangre , Diabetes Mellitus/diagnóstico , Pie Diabético/epidemiología , Nefropatías Diabéticas/sangre , Nefropatías Diabéticas/epidemiología , Neuropatías Diabéticas/epidemiología , Femenino , Hemoglobina Glucada/análisis , Hemoglobinas/análisis , Humanos , Kuwait/epidemiología , Masculino , Registros Médicos , Persona de Mediana Edad , Prevalencia , Estudios Retrospectivos , Factores de Riesgo , Distribución por Sexo , Adulto JovenRESUMEN
BACKGROUND: Fractalkine (CX3CL1) is involved in the development of numerous inflammatory conditions including metabolic diseases. However, changes in the circulatory fractalkine levels in type-2 diabetes (T2D) and their relationship with inflammatory chemokines/cytokines remain unclear. The aim of the study was to determine the T2D-associated modulations in plasma fractalkine levels and investigate their relationship with circulatory chemokines/cytokines. METHODS: A total of 47 plasma samples were collected from 23 T2D and 24 non-diabetic individuals selected over a wide range of body mass index (BMI). Clinical metabolic parameters were determined using standard commercial kits. Fractalkine and chemokines/cytokines were measured using Luminex X-MAP® technology. C-reactive protein (CRP) was measured by ELISA. The data were compared using unpaired t-test and the dependence between two variables was assessed by Pearson's correlation coefficient (r). RESULTS: Plasma fractalkine levels were significantly higher (P = 0.005) in T2D patients (166 ± 14.22 pg/ml) as compared with non-diabetics (118 ± 8.90 pg/ml). In T2D patients, plasma fractalkine levels correlated positively (P ≤ 0.05) with inflammatory chemokines/cytokines including CCL3 (r = 0.52), CCL4 (r = 0.85), CCL11 (r = 0.51), CXCL1 (r = 0.67), G-CSF (r = 0.91), IFN-α2 (r = 0.97), IL-17A (r = 0.79), IL-1ß (r = 0.97), IL-12P70 (r = 0.90), TNF-α (r = 0.58), and IL-6 (r = 0.60). In non-diabetic individuals, fractalkine levels correlated (P ≤ 0.05) with those of CCL4 (r = 0.49), IL-1ß (r = 0.73), IL-12P70 (r = 0.41), and TNF-α (r = 0.50). Notably, plasma fractalkine levels in T2D patients associated with systemic inflammation (CRP) (r = 0.65, P = 0.02). CONCLUSIONS: The altered plasma fractalkine levels associate differentially with inflammatory chemokines/cytokines in T2D patients which may have implications for T2D immunopathogenesis.
RESUMEN
OBJECTIVE: Recent studies have demonstrated a protective role for IL-33 against obesity-associated inflammation, atherosclerosis and metabolic abnormalities. IL-33 promotes the production of T helper type 2 (Th2) cytokines, polarizes macrophages towards a protective alternatively activated phenotype, reduces lipid storage and decreases the expression of genes associated with lipid metabolism and adipogenesis. Our objective was to determine the level of serum IL-33 in non-diabetic and diabetic subjects, and to correlate these levels with clinical (BMI and body weight) and metabolic (serum lipids and HbA1c) parameters. METHODS: The level of IL-33 was measured in the serum of lean, overweight and obese non-diabetic and diabetic subjects, and then correlated with clinical and metabolic parameters. RESULTS: Non-lean subjects had significantly (P = 0.01) lower levels of IL-33 compared to lean controls. IL-33 was negatively correlated with the BMI and body weight in lean and overweight, but not obese (non-diabetic and diabetic), subjects. IL-33 is associated with protective lipid profiles, and is negatively correlated with HbA1c, in non-diabetic (lean, overweight and obese) but not diabetic subjects. CONCLUSIONS: Our data support previous findings showing a protective role for IL-33 against adiposity and atherosclerosis, and further suggest that reduced levels of IL-33 may put certain individuals at increased risk of developing atherosclerosis and insulin resistance. Therefore, IL-33 may serve as a novel marker to predict those who may be at increased risk of developing atherosclerosis.
Asunto(s)
Índice de Masa Corporal , Interleucinas/sangre , Metabolismo de los Lípidos , Metaboloma , Adulto , Biomarcadores , Peso Corporal , Diabetes Mellitus/sangre , Diabetes Mellitus/metabolismo , Hemoglobina Glucada/metabolismo , Humanos , Interleucina-33 , Lípidos/sangre , Persona de Mediana Edad , Obesidad/sangre , Obesidad/metabolismo , Adulto JovenRESUMEN
BACKGROUND: Expression profile of the toll like receptors (TLRs) on PBMCs is central to the regulation of proinflammatory markers. An imbalance in the TLRs expression may lead to several types of inflammatory disorders. Furthermore, the dynamic regulation of inflammatory activity and associated impaired production of cytokines by peripheral blood mononuclear cells (PBMCs) in obese individulas remain poorly understood. Therefore, we determined the perturbation in TLRs (TLR2 and TLR4), their adaptor proteins (MyD88, IRAK1 and TRAF6) expression in PBMCs/subcutaneous adipose tissue (AT) as well as inflammatory cytokines changes in obese individuals. METHODS: mRNA expression levels of TLR2, TLR4, IL-6, TNF-α and adaptor proteins were determined by RT-PCR. TLR2, TLR4 and adaptor proteins expression in AT was determined by immunohistochemistry. RESULTS: Obese and overweight individuals showed significantly increased expression of TLR2, TLR4 and MyD88 in both PBMCs and AT as compared with lean individuals (P < 0.05). Interestingly, we found a remarkably higher expression of TLRs in obese and overweight individuals with type 2 diabetes (P < 0.05). Increased expression of TLR2, TLR4, MyD88 and IRAK1 correlated with body mass index (BMI) (TLR2: r = 0.91; TLR4: r = 0.88, P <0.0001; MyD88: r = 0.95, P < 0.0001; IRAK1 r = 0.78, P < 0.002). TLRs' expression was also correlated with fasting blood glucose (FBG) (TLR2: r = 0.61, P < 0.002; TLR4: r = 0.52, P < 0.01) and glycated haemoglobin (HbA1c) ( TLR2: r = 0.44, P <0.03; TLR4: r = 0.48, P < 0.03). Transcript levels of IL-6 and TNF-α were highly elevated in obese subjects compared to lean subjects. There was a strong association of TLRs' expression in PBMCs with TNF-α (TLR2: r = 0.92; TLR4: r = 0.92; P < 0.0001) and IL-6 (TLR2: r = 0.91, P < 0.0001; TLR4: r = 0.81; P < 0.001). Similarly adaptor proteins were significantly correlated with TNF-α (MyD88: r = 0.9, P < 0.0001; IRAK1: r = 0.86; P < 0.0002) and IL-6 (MyD88: r = 0.91, P < 0.0001; IRAK1: 0.77; P < 0.002). CONCLUSIONS: TLRs and adapter proteins were overexpressed in PBMCs from obese subjects, which correlated with increased expression of TNF-α and IL-6. This association may explain a potential pathophysiological link between obesity and inflammation leading to insulin resistance.